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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[从人血清脂蛋白(a)中提取载脂蛋白(a)]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930109]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[王大宝,潘晓平,严钱勤,唐峻岭]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>王大宝,潘晓平,严钱勤,唐峻岭</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930109]]></guid><cfi:id>129</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[热损伤与烧伤后红细胞膜特性改变的差异]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930110]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[孟凡寅,方之扬,许红,张志鸿,陈仕明]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>孟凡寅,方之扬,许红,张志鸿,陈仕明</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930110]]></guid><cfi:id>128</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[人多反应性抗体重链V区基因克隆和序列分析]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930111]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[张劲松,叶敏]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>张劲松,叶敏</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930111]]></guid><cfi:id>127</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[人白血病抑制因子基因cDNA的克隆及分析]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930112]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[涂强,王永俊,李文,谢宝树,朱元晓,阎玉河,余竟源,兰兰,林万明]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>涂强,王永俊,李文,谢宝树,朱元晓,阎玉河,余竟源,兰兰,林万明</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19930112]]></guid><cfi:id>126</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[FOS/JUN Mediates EndOthelin-1 Gene Expression Induced by Phorbol Ester in Endothelial Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940520]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Gel shift of electrophoresis and Northern and Western blotting analysis were used to detect the effect of c-iun antibody on the interact between AP-1 site of ET-1 gene and nuclear proteins as well as the effect of TPA on c-fos/c-jun gene expression. The results showed that AP-1 binding activity in vascular endothelial cells was stimulated by c-fos/c-jun, whose expression was induced by TPA, and that the electrophoretic mobility of band of DNA-protein complexes was altered by the antibody against c-jun. These results suggest that ET-1 gene expression induced by TPA is mediated by c-fos/c-jun.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wen Jinkun,Hu Jing,Qiao Yaming,Zhang Chenhui,Zhou Airu and Tang Jian]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wen Jinkun,Hu Jing,Qiao Yaming,Zhang Chenhui,Zhou Airu and Tang Jian</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940520]]></guid><cfi:id>125</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A Rapid and Reliable Method for Direct Sequencing of PCR Products]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940521]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A simple, rapid and reliable sequencing method for double stranded PCR products is described. This method presented utilizing the unique property of T7 DNA polymerase which remains active at low temperature to allow the sequencing reaction performed at low temperature. Excellent sequencing results have been obtained by this method for various PCR products .]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wang Liang,Zhang Jinsan,Zhu Dan,Yin Luo,Wang Xiuqin and Wu Min]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wang Liang,Zhang Jinsan,Zhu Dan,Yin Luo,Wang Xiuqin and Wu Min</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940521]]></guid><cfi:id>124</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Determination of the Content of AchE in the Plasma of Patients With PNH]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940522]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The contents of AchE in plasma and erythrocyte membrane of patients with PNH were determined by ELISA. The results show that the content of AchE is low in PNH erythrocyte membrane but high in plasma when it is compaired with that in normal.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Xu Caimin,Lu Hong,Pan Huazhen and Zhang Zhinan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Xu Caimin,Lu Hong,Pan Huazhen and Zhang Zhinan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940522]]></guid><cfi:id>123</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Experimental Research on Naked DNA Gene Therapy of Parkinson's Disease]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940421]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<i>In vivo</i> naked DNA gene transfer method was used in gene therapy of Parkinson's disease (PD). The complex of rat tyrosine hydroxy-lase (TH) expression plasmid and Lipofectin was injected stereotaxically into striatum of PD rat model. The asymmetric rotational behavior was reduced substantially and quickly. On the third day after injection, drug-induced rotation decreased 50% compared with pretreatment scores. Immunohistochemical staining showed TH-positive nerve cells in striatum of injection side, which indicated that TH gene was uptaked and expressed by nerve cells. These preliminary results have general implications for the application of naked DNA transfer techpique in gene therapy of human neurological disease and specific implications for PD.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Cao Lei,Zheng Zhongcheng,Liu Xinyuan,Liu Zhenguo,Zhao Yingchun,Chen Shengdi,Jiang Zhihua and Zhou Changfu]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Cao Lei,Zheng Zhongcheng,Liu Xinyuan,Liu Zhenguo,Zhao Yingchun,Chen Shengdi,Jiang Zhihua and Zhou Changfu</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940421]]></guid><cfi:id>122</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A New Assay for Kinase Activity: The Determination of Protein Kinase Using Capillary Electrophoresis]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940322]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A new assay of protein kinase A using capillary electrophoresis has been established.It is a universal and useful method for kinase activity. The method based on principle that substrate (kemptide)and product (phosphorylated kemptide) are easily seperated by capillary electrophoresis and the enzyme activity can be calculated on the integrated area. A continous sampling technique which can analyse more than 10 samples in one run has also been developed.The new method is easy to operate and its accuracy and sensitivity are higher than that of conventional isotopic method.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wan Qian,Chen Changzheng,Li Boliang and Xia Qichang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wan Qian,Chen Changzheng,Li Boliang and Xia Qichang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940322]]></guid><cfi:id>121</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Quantum Calculation for the Coordination Modes of Substrates Binding on Nitrogenase Active-Center]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940219]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[EHMO studies of N<sub>2</sub> and C<sub>2</sub>H<sub>2</sub> coordination-activation led to the conclusion that the iron-molybdenum cofactor of nitrogenase might be able to give a special treat to its special substrate, i. e. N≡N. The exogenous substrates except N<sub>2</sub> are apparently not to get into the cage of the active-center and / or to manoeuvre as freely as N≡N inside the cage with the proposed structural settings.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Liu Aimin,Zhou Taijin,Zhang Hongtu,Wan Huilin and Cai Qirui]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Liu Aimin,Zhou Taijin,Zhang Hongtu,Wan Huilin and Cai Qirui</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940219]]></guid><cfi:id>120</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Measurement of Surface Charge Numbers of Purple Membrane]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940220]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The pH-dependent surface charge densities of the acetylated and the native purple membrane were determined by the ESR spin lable method. The spin probe is CAT<sub>12</sub>. The number of surface charges shieded by acetylation was adapted as a criterion to calculate the surface charge numbers on both sides of the purple membrane from surface pH 4─11. The result shows that the total surface negative charge numbers are 9 per bacteriorhodopsin at surface pH 5─9 but increases both above surface pH 9 and below surface pH 5. It supports strongly  the  model  based on five  divalent cation binding sites on the surface of purple membrane.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wang Guangyu,Hu Kunsheng and Zhang Hengtao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wang Guangyu,Hu Kunsheng and Zhang Hengtao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940220]]></guid><cfi:id>119</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The First Sixteen N-teriminal Amino Acids of Firefly Luciferase involve in Catalytic Activity]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940117]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The full-length intronless firefly luciferase gene and its deletion mutant which lacked 48 nucleotides from the initiation codon (ATG) were inserted into the high expression secretion vector. pIN-Ⅲ-ompA3. and introducedinto <i>E. coli</i> cells in which high level and no luciferase activity were detected, respectively.This result shows that the first sixteen N-terminal amino acids of firefly luciferase involve in catalytic activity.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Lu Jianrong,Yang Jian and Jin Zhenhua]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Lu Jianrong,Yang Jian and Jin Zhenhua</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940117]]></guid><cfi:id>118</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Studies of the Immobilized Extracellular Cate-chol 1,2-Dioxygenase]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940118]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The extracellular catechol 1, 2-dioxygenase was immobilized. The apparent activity of the immobilized extracellular catechol 1, 2-dioxygenase was high. and range of use was extended. The pH-activity profile was altered by immobilization, and optimal PH from 6.0-9.0 was observed. Immobilization was shown to increase the thermal stability of the enzyme.The pureness and concentration of biotrans-formation of catechol to <i>cis, cis</i>-muconic acid were high. The product was easily separatedfrom enzyme. The immobilized method of extracellular catechol 1,2-dioxygenase was novel and simple.  The results presented show that the immobilization of extracellular catechol 1,2-dioxygenase offers an attractive means for the production of cis, cis-muconic acid.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Li Li and Li Qin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Li Li and Li Qin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19940118]]></guid><cfi:id>117</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Continuous Expression of FMR-1 Homologous Gene During Rat Brain Development]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950622]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The expression of FMR-1 homologous gene was investigated in rat brains from fetus to postnatal one month by Northern blot hybridization. The continuous transcripting during the whole stage and the higher expression level in late developing stage supported that FMR-1 gene plays an important role during the late CNS development in embryo.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Ji Hong,Huang Tao,Shen Yan and Wu Guanyun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Ji Hong,Huang Tao,Shen Yan and Wu Guanyun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950622]]></guid><cfi:id>116</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Primary Determination on Receptor Subunit Binding Ability of IL-2 Mutants by IL-2 Partial Antagonists]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950422]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Two partial antagonists of human interleukin-2(IL-2):15 Val-IL-2,126Asp-IL-2 and an IL-2 receptor a subunit binding deficient mutant 62Leu-IL-2 have been obtained by site-directed mutagenesis, 62Leu-IL-2 could exhibit significant stimulation on CTLL-2 cells. When 15Val-IL-2 or l26Asp-IL-2 was incubated together with CTLL-2 cells in addition to 62Leu-IL-2,the stimulative ability of 62Leu-IL-2 was distinctly inhibited.In consideration with the interaction of IL-2 with IL-2 receptor subunits,15Val-IL-2 or l26Asp-IL-2 can be used for the primary determination on receptor subunit binding ability of IL-2 mutants.  Furthermore，this idea may also be applied in some other  ligand-receptor systerns.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wang Zhiyong,Zheng Zhongcheng,Xu Jingfen and Liu Xinyuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wang Zhiyong,Zheng Zhongcheng,Xu Jingfen and Liu Xinyuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950422]]></guid><cfi:id>115</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Relationship Between the Three Enzymatic Activities of Camphorin and Its Single Tryptophan Residue]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950219]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Recent study indicated that camphorm,a new ribosome-inactivating protein (RIP),contained only one tryptophan residue. This single tryptophan residue had obviously different relation with the three enzymatic activities of camphorin.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Qin Ling,Ling Jun,Ruan Kangcheng and Liu Wangyi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Qin Ling,Ling Jun,Ruan Kangcheng and Liu Wangyi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950219]]></guid><cfi:id>114</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Single Primer Pre-incorporation PCR and Ampliflcation of Antlhody Variable Region Gene]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950123]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Using 5′- primers corresponding to leader sequence,3′- primers to constant region,and conventional PCR protocol,only 4 out of 10 variable region cDNAs of the 5 monoclonal antibodies were amplified.A novel protocol was designed and tested which included one more time phase of reaction:94℃ 1 min,37℃ 6-8min,1-3 cycles,with 5′-primer but no 3′-primer.Conventional PCR cvcles started after 3′- primer was supplemented.As a result,all 10 variable region cDNAs were successfully amplified.This novel protocol was named “single primer preincorporation PCR”.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Lan Fenghua,Masato Umeda and Keizo Inoue]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Lan Fenghua,Masato Umeda and Keizo Inoue</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950123]]></guid><cfi:id>113</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Effect of Calcium Ion on the Conformation of the Hemolytic Toxin from the Venom of <i>Agkistrodon halys Pallas</i>]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950124]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The study on the interaction of BPLA<sub>2</sub> with Ca<sup>2＋</sup> by fluorescence spectroscopy indicated that Ca<sup>2＋</sup> was very important to BPLA<sub>2</sub>.In the prescence of Ca<sup>2＋</sup> ,the environment around the Trp residue in BPLA<sub>2</sub> became more hydrophobic upon the binding of the substrate to the enzyme,resulting in 9 nm blue shift of the Trp fluorescence emission spectrum. But such a phenomenon was not observed in the absence of Ca<sup>2＋</sup>.The experiment indicated that there was a hydrophobic region in BPLA<sub>2</sub> molecule. Ca<sup>2＋</sup> might increase the hydrophobility of this region. Further，it was also found that the binding of Ca<sup>2＋</sup> to the enzyme was related to the single His residue of the enzyme.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Zheng Le,Feng Bo,Zhou Yuanchong and Ruan Kangcheng]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Zheng Le,Feng Bo,Zhou Yuanchong and Ruan Kangcheng</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19950124]]></guid><cfi:id>112</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning of Glial Cell Line-Derived Neurotrophic Factor Gene and Purification of Expressed Product]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960621]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The coding sequence of glial cell linederived neurotrophic factor (GDNF) was amplified from human genomic DNA by PCR method.Recombinant GDNF was expressed in <i>E. coli</i> and purified.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Chen Yan,Zhang Ying,Li Jinzhao,Deng Wei,Xia Lingchao and Qiu Rong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Chen Yan,Zhang Ying,Li Jinzhao,Deng Wei,Xia Lingchao and Qiu Rong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960621]]></guid><cfi:id>111</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Experimental Gene Therapy for Human Colorectal Carcinoma Cells by Cell Type-specific Expression of Suicide Genes]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960424]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The expression plasmid PCEA-TK or pCEA-CD was constructed by ligating the CEA gene promoter to suicide gene such as HSV-TK (herpes simplex virus thymidine kinase) gene or EC-CD (<i>E. coli</i> cytosine deaminase) gene. A human colorectal carcinoma cell line LoVo or a human uterine cervical cancer cell line HeLa was co-transfected with pSV2-neo and PCEA-TK (or PCEA-CD). After selection with G418, the transgenetic cell clones (hoVo/CEA-TK,LoVo/CEA-CD, HeLa/CEA-TK and HeLa/CEA-CD) were obtained. There was no significant difference in either morphology or cell growth curve between suicide gene transduced cells and wild type cells. But LoVo/CEA-TK (or LoVo/CEA-CD) cells were 2000(or 700) times more sensitive to the cytotoxicity of prodrug  ganciclovir(or S-Fluorocytosine)than parental LoVo cells. However, HeLa/CEA-TK or HeLa/CEA-CD cells were still resistant to Ganciclovir (or 5-Fluorocytosine). These results showed the possibility of gene therapy for human colorectal carcinoma by cell type-specific expression of suicide genes.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Jiang Qiong,Ge Kai,Xu Dehua,Zheng Zhongcheng and Liu Xinyuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Jiang Qiong,Ge Kai,Xu Dehua,Zheng Zhongcheng and Liu Xinyuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960424]]></guid><cfi:id>110</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Identification of Integration of Foreign Gene in Transgenic Pigs]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960322]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Foreign porcine growth hormone genes were introduced into Hubei white pigs. Inorder to avoid possible homology in metallothionein-Ia gene promoter between sheep and porcine, two PCR primers were designed and located on the regions of sheep metallothionein Ia gene promoter and porcine growth hormone gene, respectively. This reflects the exact results by PCR detection. The results of DNA blotting indicated that 6 of 43 offsprings showed positive integration.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Liu Guisheng,Chen Qingxuan,Wang Jing,Wei Qingxin and Chen Yongfu]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Liu Guisheng,Chen Qingxuan,Wang Jing,Wei Qingxin and Chen Yongfu</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960322]]></guid><cfi:id>109</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Expression of Triplet Ribozyme Targeting <i>Bombyx Mori</i> Nuclear Polyhedrosis Virus (BmNPV) Immediate Early Gene mRNA in Bm-N Cell]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960124]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In order to evaluate the effect of ribozymes on suppressing BmNPV, triplet ribozyme (R426) targeting the BmNPV immediate early gene (IE) was designed. <i>In vitro</i> cleavage experiment showed that R426 transcript was able to cleave the target sequence specifically. Expression experiment indicated that R426 extracted from Bm-N cell can also cleave the target specifically and cause about 30% reduction of BmNPV polyhedra in transfected cell.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Zhang Xiaolan,Chen Nongan,Lu Changde and Qi Guorong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Zhang Xiaolan,Chen Nongan,Lu Changde and Qi Guorong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19960124]]></guid><cfi:id>108</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Functional Expression of Human Epidermal Growth Factor Receptor (EGF-R) in Membrane of <i>E.coli</i>]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970621]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[An <i>E.coli</i> strain which could express domain Ⅲ of the extracellular region of the human EGF-R(EGF-RⅢ) in its membrane had been obtained. The results of EGF receptor radiobinding assay showed that <sup>125</sup>I-EGF could bind specifically to the intact bacterial body, the amount of specific binding varied with the time and temperature of the reaction. The data of Scatchard analysis indicated that the number of the human EGF-RⅢ expressed in the bacteria was about 738 sites/cell, and its dissociation constant was about 3.0×10<sup>-11</sup> mol/L. The sites of the bacteria to which EGF bound were discovered mainly on its membrane by immunoelectronmicroscopy.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Yutian,HU Jialu,GAO Lei,CHEN Sumin,YANG Shengli,GONG Yi,FAN Daiming and ZHANG Xueyong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Yutian,HU Jialu,GAO Lei,CHEN Sumin,YANG Shengli,GONG Yi,FAN Daiming and ZHANG Xueyong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970621]]></guid><cfi:id>107</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A Gene Encoding Era-binding Protein Exists in <i>E.coli</i> Genome]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970622]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A λ ZAP expression library of <i>E.coli</i> genomic DNA has been constructed. Screening the library with the Era protein probe labeled by digoxigenin, a plaque specially bound with Era has been isolated from 4×10<sup>4</sup> plaques. It is confirmed that an Era-binding protein gene exists in <i>E.coli</i> genomic DNA. Compared with the data in GenBank, the 5′ end 800 bp of inserted DNA is located in the section 267 of <i>E.coli</i> genomic DNA.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Nanchun,CHEN Sumin,GAO Lei,HAO Xiaomeng,GAO Hui,JIN Jing and MA Xiaofeng]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Nanchun,CHEN Sumin,GAO Lei,HAO Xiaomeng,GAO Hui,JIN Jing and MA Xiaofeng</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970622]]></guid><cfi:id>106</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Purification and Stability Observation of Sensory Nerve-specific Protein in Rabbit]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970521]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A 29 ku protein, the sensory nerve-specific protein was isolated and purified from rabbit spinal ganglion and its fibers by anion exchange chromatography using DEAE-Sephacel and gel filtration HPLC. The purity was extiomatd to be over 80% by UV scanning. Western blot demonstrated that it immunoreacts with anti-rabbit the 29 ku protein monoclonal antibody. The stability also has been observed.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[PU Xiaoping,WANG Jiazheng,ZHANG Jie,GU Xiaosong and FAN Ming]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>PU Xiaoping,WANG Jiazheng,ZHANG Jie,GU Xiaosong and FAN Ming</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970521]]></guid><cfi:id>105</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Activity of Superoxide Dismutase on Cleaving Supercoiled Double-Stranded DNA]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970222]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Several superoxide dismutases (SODs), such as porcine and bovine erythrocyte Cu/Zn-SODs and N.tabacum Mn-SOD, were found to exhibit the activity to cleave supercoiled DNA in vitro. They converted supercoiled DNA into nicked and further into linear form. They did not act on linear double-stranded DNA. Activity assays after they were inactivated by H<sub>2</sub>O<sub>2</sub> or guanidine and hydrolyzed by proteases suggested that these two activities of dismuting O<sup>·</sup><sub>2</sub> and cleaving supercoiled-DNA involved in different sites in SODs.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LING Jun,RUAN Kangcheng and LIU Wangyi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LING Jun,RUAN Kangcheng and LIU Wangyi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970222]]></guid><cfi:id>104</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Partial Amino Acid Sequence of N-terminal of Thrombin-like Enzyme From <i>Agkistrodon acutus</i>]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970223]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A thrombin-like enzyme was purified from the venom of the snake <i>Agkistrodon acutus</i>. It was shown to be a single band both in SDS-PAGE and IEF. Its molecular weight is about 38 ku and isoelectric point is near 4.0. Also, its 15 amino acid sequence of N-terminal was obtained. It is VIGGVECDINEHRFL. It has high homology with thrombin-like enzymes from other snake venoms.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[DU Xiaoyan,ZHU Hong,JIANG Kexian,YU Henian and ZHOU Yuancong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DU Xiaoyan,ZHU Hong,JIANG Kexian,YU Henian and ZHOU Yuancong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19970223]]></guid><cfi:id>103</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning and Sequencing of Human Lipopolysacchride Binding Protein Gene]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980520]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Human lipopolysaccharide binding protein (LBP) gene was cloned from a human liver cDNA library by PCR. Sequencing result showed that the amino acid sequence coded by this gene is identical to that of the latest reported human LBP.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LONG Jian-yin,LIU Jian-qiang,XUE Yan-ning and WANG Hui-xin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LONG Jian-yin,LIU Jian-qiang,XUE Yan-ning and WANG Hui-xin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980520]]></guid><cfi:id>102</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning and Sequencing of Human CD14 Gene]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980422]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Human CD14 gene was cloned from genomic DNA of PMA-stimulated HL-60 cells by PCR. Sequencing result showed that it is identical to the reported human CD14 gene except four bases, among which two new mutations were identified.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LONG Jian-yin,XUE Yan-ning,SUN Lei and WANG Hui-xin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LONG Jian-yin,XUE Yan-ning,SUN Lei and WANG Hui-xin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980422]]></guid><cfi:id>101</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Atomic Force Microscopy Study of the Manipulation of Virus]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980221]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Manipulation of macromolecules is becoming an interesting research subject both in physics and biology recently. Linear phage virus has been aligned in one direction on atomic flat surfaces by a special method named “molecular combing”. Atomic force microscopy was used to check the results. The related mechanism has been discussed.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[HU Jun,ZHANG Zhi-hong,OUYANG Zhen-qian,CHEN Shen-fu and LI Min-qian]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HU Jun,ZHANG Zhi-hong,OUYANG Zhen-qian,CHEN Shen-fu and LI Min-qian</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980221]]></guid><cfi:id>100</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A Homeobox Gene Emx is Amplified in Human Placenta Chorionic Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980121]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Genomic DNA of human placenta chorionic cells and leukocytes were hybridized with Emx probe which is a cDNA fragment including homeobox from quail. The results showed Emx gene dose in human placenta chorioic cells was six-fold more than in leukocytes and indicated Emx gene amplified in human placenta chorioic cells.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Yi-pin,MA Xiao-jun,HUANG Jia-xue,GAO Hong,ZHANG Xi-yuan and Z.XUE]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Yi-pin,MA Xiao-jun,HUANG Jia-xue,GAO Hong,ZHANG Xi-yuan and Z.XUE</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19980121]]></guid><cfi:id>99</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Femtomolar Analysis of Sialic Acids in Glycoproteins by Capillary Electrophoresis Precolumn Derivatization]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19990124]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A new method was described which allowed the analysis of sialic acids in glycoproteins at femtomole. Sialic acids released from recombinant human erythropoietin(rhu-EPO), human urine trypsin inhibitor(h-UTI) and bovine α<sub>1</sub>-acid glycoprotein(α<sub>1</sub>-AGP) by acid hydrolysis, were derivatized with 2-aminoacridone(AMAC), and then separated by capillary electrophoresis, separately. The quantities of sialic acids in the first two glycoproteins were consistent with the previous results while inconsistency was found in the bovine α<sub>1</sub>-AGP case. It was found that in bovine α<sub>1</sub>-AGP N-glycoloyneuraminic acid (Neu5Gc) was present in addition to Neu5Ac with a quantity comparable to that of Neu5Ac. Based on these data, the AMAC-derivatized sialic acids were unstable and could undergo a decarboxylation reaction at room temperature under light, but they were stable at －20℃in the dark for at least 12 h.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHE Fa-Yun,SHAO Xiao-Xia,WANG Ke-Yi and XIA Qi-Chang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHE Fa-Yun,SHAO Xiao-Xia,WANG Ke-Yi and XIA Qi-Chang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/19990124]]></guid><cfi:id>98</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Molecular Cloning and Functional Primary Study of a Novel Candidate Tumor Suppressor Gene Related with Nasopharyngeal Carcinoma]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20000325]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In order to further identify expressing difference of cDNA fragments isolated from cDNA representational difference analysis (cDNA RDA) in nasopharyngeal carcinoma(NPC) biopsies and to clone those deregulated genes related with NPC, reverse transcription polymerase chain reaction (RT-PCR) was used to identify the differentially expressing of cDNA fragment, among which AF152605 was found to be down-regulated in sporadic NPC samples (74%). As it were shown by Northern blot, AF152605 is highly expressed in heart,brain, skeletal muscle and placenta whose transcription size is 2.1 kb. Combining bio-informatics, the gene (GenBank accession number AF179285) named as NAG4, was cloned by using library screening, which locates at 6p22～6p23.3. Comparative analysis shows that the NAG4 gene has at least two exons and a “TATAA BOX” sequence lies at upstream of the first exon. And the NAG4 gene encodes a protein proposed of 508 amino acid with predicted molecular mass of 57.4 ku, Blast homology searches reveal that NAG4 protein, containing a bromodomain and several important phosphorylation sites, takes on high similarity to musculus bromodimain-containing protein BP75. Moreover, condon mutation of NAG4 gene was found in HeLa cell line. So it is further demonstrated that NAG4 gene is a good candidate of putative tumor suppressor genes associated with NPC, whose down-expression may be involved in the development of NPC.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YU Ying,XIE Yi,CAO Li,ZHANG Bi-Cheng,ZHOU Ming,ZHAN Feng-Huang and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YU Ying,XIE Yi,CAO Li,ZHANG Bi-Cheng,ZHOU Ming,ZHAN Feng-Huang and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20000325]]></guid><cfi:id>97</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Coding-region Single Nucleotide Polymorphisms in BRD7 Gene and Nasopharyngeal Carcinoma Susceptiblity]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20010430]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In order to evaluate the role of inherited variation in the BRD7 gene in human nasoparyngeal carcinoma. RT-PCR, SSCP and sequencing were used to identified multiple coding-region single nucleotide polymorphisms (cSNPs), three cSNPs in BRD7 were found in fifty-seven sporadic biopsy specimens and corresponding blood samples from the same NPC patients and two pedigrees of NPC family. One of those cSNPs is A538C transition, which creates a missense change of Asp162Ala in three of NPC patients analyzed and three of fifty healthy individuals. Adjacent to the bromodomain (504～609 nt), another SNP (C450T) behind the start condon (484nt) results in a G133Ter substitution in 87.7% NPC biopsies and corresponding blood samples, all affected family members in the pedigrees and eight of nine susceptible members, the third SNP is synonymous polymorphism (A737G) which is coupled interestingly with the C450T alteration. The latter two forms of SNPs are also observed in eleven of fifty control normal blood samples. This findings suggest that the presence of the two coupled SNPs in BRD7 might be one of important risk factors for the development and/or progression of NPC (<i>P</i>＜0.01), and the BRD7 gene might have two modes of translation and the terminational SNP at 450 nt in BRD7 gene results in the second alternatively truncated isoform.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YU Ying,ZHU SHI-Guo,XIANG Juan-Juan,LI Zhong-Hua,ZHANG Bi-Cheng,CAO Li and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YU Ying,ZHU SHI-Guo,XIANG Juan-Juan,LI Zhong-Hua,ZHANG Bi-Cheng,CAO Li and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20010430]]></guid><cfi:id>96</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Search for Differentially Expressed Proteins Involved in the Treatment of Human Nasopharyngeal Carcinoma Cells with NGX6 Using Two-dimensional Electrophoresis and Mass Spectrometry]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20010431]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The current study was designed to reveal the preliminary function of NGX6 to NPC cells. In search of mechanisms of NGX6 2-D PAGE was used to identify proteins that were overexpressed in HNE cells that were transfected with NGX6. After staining and image analysis, spots of interest were isolated and subjected to mass spectrometry. Seven proteins such as Fas,ZNF and MHC-ⅡAg were identified. The possible significance of these findings is discussed. NGX6 may exert its effect on NPC cells by many ways.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Jiang,TAN Chen,XIANG Qiu,ZHANG Xiao-Mei,MA Jian,LI Wei-Fang,WANG Jie-Ru,YANG Jian-Bo,LIANG Song-Ping and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Jiang,TAN Chen,XIANG Qiu,ZHANG Xiao-Mei,MA Jian,LI Wei-Fang,WANG Jie-Ru,YANG Jian-Bo,LIANG Song-Ping and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20010431]]></guid><cfi:id>95</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Preliminary Study of LRRC4 Protein: Bioinformatic Analysis, Fusion Expression in Eukaryote and Prokaryote]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020508]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In previous study, a novel gene, LRRC4, a member of leucine-rich repeat(LRR) superfamily was cloned. Expression analysis indicated that LRR may play an important role in the central nervous system. To investigate the function and the structure-function relationship of LRRC4, full length coding region was amplified and subcloned into pGEM T Easy vector. Further, the recombinant plasmid, pEGFP-C1/LRRC4, was constructed and transfected transiently into U251 cell. Under the fluorescence microscope, the green fluorescence produced by LRRC4 fusion protein was observed on the cytoplasmic membrane. Consistent to prediction by bioinformatics, this result indicated that product of LRRC4 is a membrane protein. In addition, the recombinant of LRRC4，pGEX-4T-2/LRRC4 and truncated LRRC4 recombinant, pGEX-4T-2/mLRRC4, were constructed and transformed into <i>E.coli</i> BL21. Induced by 0.5 mmol/L IPTG, The band corresponding to fusion protein were observed in SDS-PAGE as expected. Together with bioinformatic analysis of LRRC4 protein, these results establish the basis for functional study of LRRC4.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Jie-Ru,DONG Li,JIANG Ming,TAN Chen,LI Xiao-Ling,XIANG Juan-Juan,FAN Song-Qing,PENG Cong,TANG Ke and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Jie-Ru,DONG Li,JIANG Ming,TAN Chen,LI Xiao-Ling,XIANG Juan-Juan,FAN Song-Qing,PENG Cong,TANG Ke and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020508]]></guid><cfi:id>94</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cinphorin: a Novel Type Ⅱ Ribosome-inactivating Protein With Miniature Active A-chain]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020408]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Cinnamomin is a type Ⅱ ribosome-inactivating protein (RIP) isolated from the seed of camphor tree (<i>Cinnamomum camphora</i>). Recently, a small RIP named as cinphorin was isolated from the seed of camphor tree. The reduced cinphorin exhibited the RNA N-glycosidase activity and inhibitory activity to protein synthesis <i>in vitro</i> like the reduced cinnamomin did. Cinphorin B-chain exhibited the same N-terminal 10 amino acid sequence and molecular mass as the B-chain of cinnamomin. Its A-chain exhibited the same 10 N-terminal amino acid sequence and owned a C-terminal cysteine residue linked to the B-chain, but the molecular mass of cinphorin A-chain was only half of cinnamomin A-chain. RT-PCR and Northern blotting revealed that there was no corresponding mRNA of cinphorin. Cinphorin is probably produced from cinnamomin by protein splicing.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[HOU Fa-Jian,LIU Ren-Shui and LIU Wang-Yi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HOU Fa-Jian,LIU Ren-Shui and LIU Wang-Yi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020408]]></guid><cfi:id>93</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Effect of NAG7 Gene Transfection on the Growth of Nasopharyngeal Carcinoma Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020309]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In order to study the effect of NAG7 gene on NAG7 down-regulated nasopharyngeal carcinoma (NPC) cell line HNE1, the pcDNA3.1(+)/NAG7 mammalian expression recombination was constructed and transfected into HNE1 cells. G418 was used to obtain the neomycin-resistant transformants of which indicated the vector was present in the HNE1 cells. The expression of NAG7 gene was detected by RT-PCR and Northern blot. The cytobiologic characteriztions of the transfected HNE1 cells were probed by population double time (PDT), xenograft of nude mice and cell cycle analysis. The results showed that the PDT of G418-resistant HNE1 cells with expression of NAG7 was longer than that of vector transfected HNE1 cells and untranstected HNE1 cells, and the more NAG7 transfected cells went into phase G0-G1 compared with the two other cells. It also presented inhibited the tumor formation in mude mice. Thus, these data suggested that NAG7 gene play an important role in the cell growth of HNE1, and might be a good candidate of tumor suppressor gene correlated with NPC.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[TAN Chen,LI Jiang,WANG Jie-Ru,Peng Cong,XIE Yi,CAO Li,LI Xiao-Ling and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TAN Chen,LI Jiang,WANG Jie-Ru,Peng Cong,XIE Yi,CAO Li,LI Xiao-Ling and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020309]]></guid><cfi:id>92</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Expression of Gut-enriched Kruppel-like Factor in Esophageal Squamous Cancer]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020112]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Gut-enriched Kruppel-like factor (GKLF) is a newly identified eukaryotic zinc finger protein expressed extensively in the gastrointestinal tract, the expression of which is associated with growth arrest. GKLF expression in the tumor was compared to normal mucosa in esophageal squamous cancer patients, using semi-quantitative RT-PCR. Expression of GKLF mRNA was detected all of 17 cases of esophageal squamous cancer. Decreased expression of GKLF mRNA was observed in 14 of esophageal squamous cancer patients compared to normal esophageal tissues adjacent to tumor from the same patient. Serum deprivation induced overexpression of GKLF was observed in the primary culture of human fibroblast and this induction was decreased in an esophageal squamous cancer cell line EC9706. Sequencing of GKLF cDNA from EC9706 showed no mutations in the coding region. The results demonstrate that GKLF expression in esophageal squamous cancer is down-regulated.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Nan,LIU Zhi-Hua,DING Fang,WANG Xiu-Qin,ZHOU Chuan-Nong,WANG Ming-Rong and WU Min]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Nan,LIU Zhi-Hua,DING Fang,WANG Xiu-Qin,ZHOU Chuan-Nong,WANG Ming-Rong and WU Min</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20020112]]></guid><cfi:id>91</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Direct Observation on The Surface Structure Change of Purple Membrane Induced by High pH Using Atom Force Microscope]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20030506]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The direct information of the surface structure change of purple membrane under high pH was obtained. The UV-VIS spectra showed that BR was totally denatured and lost its retinal under the pH 12.6. It was found by atom force microscope that the crystalline lattice of purple membrane was broken down at this pH. The typical and non-typical “Island” structures emerged as the BR molecules assemble irregularly in purple membrane.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Chen De-Liang,Li Hui,Han Bao-Shan,Xu Bing and Hu Kun-Sheng]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Chen De-Liang,Li Hui,Han Bao-Shan,Xu Bing and Hu Kun-Sheng</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20030506]]></guid><cfi:id>90</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Direct Observation on Single Molecular Rotation of High Activity F<sub>1</sub>-ATPase]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20030207]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The high activity F<sub>1</sub>-ATPase (the mutant α-C193S, γ-S107C, a ten histidine (His) tag inserted immediately downstream of the β initiation codon, α<sub>3</sub>β<sub>3</sub>γ subcomplex) of thermophilic <i>Bacillus</i> PS3 was purified from <i>E.coli</i>. JM103 Δ(<i>uncB-uncD</i>)，in which the majority of F<sub>1</sub>-ATPase genes have been eliminated. It was found that the enzyme hydrolyzed ATP more efficiently than previous papers. During the F<sub>1</sub>-ATPase hydrolyzing ATP, the rotary rate of the fluorescent actin filament attached to γ subunit of F<sub>1</sub>-ATPase was about one times faster than that of previous papers in the similar conditions.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Xing-Sheng,CUI Yuan-Bo,ZHANG Ying-Hao,YUE Jia-Chang and JIANG Pei-Dong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Xing-Sheng,CUI Yuan-Bo,ZHANG Ying-Hao,YUE Jia-Chang and JIANG Pei-Dong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20030207]]></guid><cfi:id>89</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Aggregated tau Induces The Inactivation and Conformational Changes of Lactate Dehydrogenase]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040704]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Human neuronal tau aggregates by incubation at 37℃ (pH 7.2) and the aggregated tau is inactivated in promoting tubulin assembly. Furthermore, aggregated tau induces inactivation and conformational changes of rabbit muscle lactate dehydrogenase, although native tau can promote LDH activity. It suggests that tau aggregation may affect the energy metabolism in which LDH is involved.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[TIAN Rui,QU Mei-Hua,LIU Ying and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TIAN Rui,QU Mei-Hua,LIU Ying and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040704]]></guid><cfi:id>88</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[MC1R Is The Candidate Gene Regulating Melanin Synthesis in Chicken]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040604]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Melanocortin 1-receptor (MC1R) gene is a key gene in melanogenesis in mammal. Three single nucleotide polymorphisms (SNPs) were detected in MC1R gene exon using PCR-SSCP and DNA sequencing in chicken. Then these SNPs were analyzed in a CAU three-generation chicken population whose founder population are broiler and white-silk chickens. The result of these analysis indicated that the polymorphisms of the amplified fragment of primer pair 3 is due to a single point mutation G867A, and primer pair 5 is due to two other single point mutations C1292T and C1377G. Lastly, the relations between SNPs and chicken melanin traits were analyzed, the results showed that there was significant correlation （<i>P</i>＜0.05）between the G867A mutation and chicken skin color , between the C1292T mutation and chicken live body shank color and between the C1377G mutation and chicken meat color. The results of the study indicated that MC1R gene is the candidate gene that regulates melanin traits in chicken.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YANG Yong-Sheng,DENG Xue-Mei,LI Ning,FU Yan,ZHU Mu-Yuan and WU Chang-Xin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YANG Yong-Sheng,DENG Xue-Mei,LI Ning,FU Yan,ZHU Mu-Yuan and WU Chang-Xin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040604]]></guid><cfi:id>87</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Melanoma Cell Adhesion Molecule (MCAM/CD146) Is a Critical Molecule in Trophoblast Invasion]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040405]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Previous study has shown that melanoma cell adhesion molecule (MCAM/CD146) is highly expressed by invasive trophoblasts in normal pregnancy, but it is absent in pregnancy disorder pre-eclampsia in which the invasion ability of trophoblast is seriously impaired. The mechanism that CD146 affects the trophoblast invasion was investigated. Immunofluorescence staining revealed that CD146 was selectively expressed on invasive intermediate trophoblasts, but was not expressed on non-invasive cytotrophoblasts and syncytiotrophoblasts. Functional studies showed that the anti-CD146 antibody significantly inhibited the migration of trophoblasts and the activity of matrix metalloproteinases secreted by trophoblastic cells, which are two critical factors for trophoblast invasion. The results demonstrate that adhesion molecule CD146 plays a critical role in trophoblast invasion, which will provide a valuable molecular model for the study of trophoblast and tumor cell invasion.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LIU Qin,ZHAO Xin-Gang,ZHANG Ying,SHEN Yi,LIU Yi-Xun and YAN Xi-Yun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIU Qin,ZHAO Xin-Gang,ZHANG Ying,SHEN Yi,LIU Yi-Xun and YAN Xi-Yun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20040405]]></guid><cfi:id>86</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Inactivation Effect of Photocatalytic Titanium Apatite Filter on SARS Virus]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20041106]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Photocatalytic titanium apatite filter (PTAF) is a new material that has been reported to have an ability to absorb and inactivate bacteria. The inactivation effect of PTAF on serious acute respiratory syndrome coronary virus (SARS-CoV) was tested. The results showed that PTAF filter inactivated/decomposed SARS CoV up to 99.99％ after 6 h interaction under the condition of non-UV irradiation. However, under the condition of UV irradiation, PTAF and HAF both were able to inactivate/decompose SARS CoV completely. The study has provided the first evidences that PTAF could inactivate SARS-CoV virus, suggesting that the PTAF material will be applied for the prevention of SARS-CoV as well as other viruses.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[HAN Wei,ZHANG Pan-He,CAO Wu-Chun,YANG Dong-Ling,SHIGEHARU TAIRA,YOSHIO OKAMOTO,JUN-ICHIRO ARAI and YAN Xi-Yun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HAN Wei,ZHANG Pan-He,CAO Wu-Chun,YANG Dong-Ling,SHIGEHARU TAIRA,YOSHIO OKAMOTO,JUN-ICHIRO ARAI and YAN Xi-Yun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20041106]]></guid><cfi:id>85</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Defective Membrane Localization of Dominant Hearing Impairment Associated Connexin31 Mutants]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0058]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Connexins form gap junctions that mediate the transfer of ions, metabolites, and second messengers between contacting cells. Connexin31(Cx31) is an important member of connexin β family. Mutations in Cx31 are associated with erythrokeratoderma variabilis (EKV) ， hearing impairment and peripheral neuropathy. The pathological mechanism for Cx31 mutants in these diseases remains unknown. Using Site-directed mutagenesis (SDM) to construct two dominant hearing impairment associated Cx31 mutant expression plasmids, R180X-pEGFP-N1 and E183K- pEGFP-N1. A number of functional analysis were described to investigate the effect of two dominant hearing impairment-associated Cx31 mutants, R180X and E183K, on connexon trafficking. The majority of the mutant R180X and E183K were cytoplasmic, they can not traffic to normal intracellular localization and can not form functional gap junction channels. But not observed with wild-type Cx31.This may provide an insight into the pathological mechanism of Cx31 mutants.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[TAN Zhi-Ping,LIU Yu,CAI Fang,PAN Qian,HE Li-Qiang,HUANG Liang-Qun,DAI He-Ping,XIA Kun,XIA Jia-Hui and ZHANG Zhuo-Hua]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TAN Zhi-Ping,LIU Yu,CAI Fang,PAN Qian,HE Li-Qiang,HUANG Liang-Qun,DAI He-Ping,XIA Kun,XIA Jia-Hui and ZHANG Zhuo-Hua</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0058]]></guid><cfi:id>84</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Inactivating Calcium-activated Potassium Currents in Rat Dorsal Root Ganglia Neurons]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0125]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Large conductance voltage and Ca2+-activated K+ channels (BK channels) ， which are ubiquitously expressed among mammalian tissues, play a variety of physiological roles. The inactivating BK channels have not been extensively studied in primary tissues and rarely do they exhibit inactivation. An inactivating BK current (BKi) was identified in rat small dorsal root ganglia (DRG) neurons . The inactivating currents are sensitive to the specific BK channel blocker charybdotoxin (ChTX) and the effect of ChTX can be removed partially when washed with normal external solution. The inactivation of BKi can be removed by external treatment of papain.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Wei,WAN You,HAN Ji-Sheng,DING Jiu-Ping and XU Tao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Wei,WAN You,HAN Ji-Sheng,DING Jiu-Ping and XU Tao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0125]]></guid><cfi:id>83</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Defective Tumor Angiogenesis and Retarded Tumor Growth in Aquaporin-1 Knockout Mice]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0066]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Tumor angiogenesis is a mandatory step of tumor growth, invasion, and metastasis involving endothelial cell proliferation and migration from blood vessels in peritumoral tissues and formation of tubules. Water channel aquaporin-1 (AQP1) has been reported to express in microvessels of many different type of tumors, indicating the possible involvement of AQP1 in tumor angiogenesis. A melanoma-bearing model in AQP1-knockout mice was used to evaluate the role of AQP1 in tumor angiogenesis. The results demonstrated nearly 30% retarded growth of subcutaneously inoculated melanoma in AQP1 knockout mice compared to tumors in wildtype mice. Immunohistochemistry of melanoma sections revealed strong AQP1 protein labeling in endothelium of tumor blood vessels in wildtype mice and negative labeling of AQP1 in the counterpart structures in AQP1-knockout mice. On the same tumor sections stained by hematoxylin, melanoma cells form islands with microvessels in the center. It is easily seen that high-density and thin microvessels (142/mm<sup>2<sup>) locate in the center of tumor islands in wildtype mice, whereas sparse and enlarged vessels (47/mm<sup>2<sup>) are evident in tumor islands in AQP1 knockout mice coincident with larger necrotic area in outer layer of the islands. These results provide definitive evidence that lacking of water channel AQP1 results in defective tumor angiogenesis and retarded tumor growth that may be involved in insufficient blood supply and/or abnormal transendothelial fluid transport. The underlying molecular and cellular mechanisms are worth further investigation.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[FENG Xue-Chao,Gao Hong-Wen,HE Cheng-Yan and MA Tong-Hui]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>FENG Xue-Chao,Gao Hong-Wen,HE Cheng-Yan and MA Tong-Hui</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0066]]></guid><cfi:id>82</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Electrostatic Microcantilever Array Biosensor and Its Application in DNA Detection]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0137]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Microcantilever array biosensor shows peculiarities of high speed, trace detection and label-free in bioanalysis. A method to increase the detection sensitivity and to speed up analysis of microcantilever array biosensor is reported. The gold covered microcantilever array immobilized by DNA probes is applied as a microcantilever array biosensor with electrostatic field. Microcantilever arry is acted as anode in hybridization solution cell where DNA molecules are removed to and congregated around anode, so the DNA hybridization is enhanced. The data demonstrated: (1) the time of DNA hybridization on the cantilever system drived by direct electric field was no more than 3 min; (2) the detection sensitivity was improved from 30 μg/L to 300 ng/L level.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG Zhi-Xiang and LI Mian-Qian]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG Zhi-Xiang and LI Mian-Qian</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0137]]></guid><cfi:id>81</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Protein Preparation, Crystallization and Preliminary X-ray Crystallographic Analysis of Smu.260 From Streptococcus mutans ——— a Cariogenic Dental Pathogen]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0094]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<em>Smu</em>.260 encodes a putative protein of 200 residues in <em>Streptococcus mutans</em>, a primary pathogen for human dental caries. <em>Smu</em>.260 was cloned into expression vector pET28a and expressed in good amount from the <em>E.coli</em> strain BL21 (DE3). Smu.260 protein was purified to homogeneity in a two-step procedure of Ni<sup>2+</sup> chelating and size exclusion chromatography. The purified protein exists in two forms, a dimer form about 46 ku with yellow color and a tetramer form without apparent color. Crystals were obtained from the dimer protein by hanging-drop vapor-diffusion method. The crystals diffracted to about 2.3 Amstrong resolution and belong to orthorhombic space group P2<sub>1</sub>2<sub>1</sub>2<sub>1</sub> with cell dimensions of a=89.88 Amstrong, b=90.91 Amstrong, c=105.17 Amstrong. The asymmetric unit is expected to contain two dimers with solvent content of 53%.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG Xiao-Yan,MI Wei,ZHOU Yan-Feng,LIU Xiang-Yu,LI Lan-Fen,LIANG Yu-He,WEI Shi-Cheng and SU Xiao-Dong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG Xiao-Yan,MI Wei,ZHOU Yan-Feng,LIU Xiang-Yu,LI Lan-Fen,LIANG Yu-He,WEI Shi-Cheng and SU Xiao-Dong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2005-0094]]></guid><cfi:id>80</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Screening, Identification and Functional Research of The Human gap Junction Connexin 31 Interaction Proteins]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2004-0745]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Connexins form gap junctions that mediate the transfer of ions, metabolites, and second messengers between contacting cells. Connexin31 (Cx31) is an important member of connexin β family. Mutations in Cx31 are associated with erythrokeratodermia variabilis(EKV), hearing impairment and peripheral neuropathy. The pathological mechanism for Cx31 mutants in these diseases remains unknown. Assembly, intracellular transport, plaque assembly and stability and channel conductivity of Cx31 are finely regulated and likely involve proteins that interact with Cx31. However, little is known about the Cx31 interaction proteins. A proteomics approach was applied to screen Cx31 binding proteins using HT1080 cells stably expressing a myc-tagged Cx31. Immunoprecipitation followed by peptide sequence analysis identified association of actin and Cx31. Interaction between actin and Cx31 is further confirmed by coimmunoprecipitation and immuno-colocalization. Pharmacological disruption of actin polymerization inhibits the plasma membrane localization of Cx31. The results suggested the actin cytoskeleton may play an essential role in regulating Cx31 trafficking via direct association.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LIU Yu,TAN Zhi-Ping,PAN Qian,HE Li-Qiang,CAI Fang,WU Ling-Qian,LIANG De-Sheng,XIA Kun,XIA Jia-Hui and ZHANG Zhuo-Hua]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIU Yu,TAN Zhi-Ping,PAN Qian,HE Li-Qiang,CAI Fang,WU Ling-Qian,LIANG De-Sheng,XIA Kun,XIA Jia-Hui and ZHANG Zhuo-Hua</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2004-0745]]></guid><cfi:id>79</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Expression of Matrix Metalloproteinase-26 in Human Normal Placental Cytotrophoblast Cells as Well as Its Regulation by Activin A]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2004-0825]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The processes of implantation and placentation involve various cell events, such as degradation and remodeling of extracellular matrix, cellular proliferation, apoptosis, and differentiation. Evidence indicates that members of the matrix metalloproteinase (MMP) family play crucial roles in these processes. In the present study, the expression and localization of MMP-26/endometase/matrilysin-2 in human cytotrophoblast cells as well as its regulation by activin A were investigated by using methods of reverse transcriptase-polymerase chain reaction, immunohischemistry and fluorescence immunohistochemistry. The results showed that MMP-26 was strongly localized in villous trophoblast cells, and weakly in some of the villous mesenchyma. The mRNA level of MMP-26 in chorionic villi was high in early pregnancy, and was down-regulated from gestational week 10 on, reaching a very low level at week 26. However, its mRNA expression was significantly up-regulated in the term placenta. In the primary cultured cytotrophoblast cells, the mRNA expression of MMP-26 maintained a stable level during gestational week 6~12. Moreover, the expression of MMP-26 in the cytotrophoblast cells was stimulated by activin A in a dose-dependent manner. All the data indicated that MMP-26 may be involved in trophoblast invasion during early pregnancy and placenta detachment at the time of delivery. There may exist autocrine/paracrine regulation of MMP-26 expression in cytotrophoblast cells.]]></description>
<pubDate></pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[QIU Wei,ZHAO Liang,Bai Su-Xia,SANG QING-XIANG AMY and Wang Yan-Ling]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>QIU Wei,ZHAO Liang,Bai Su-Xia,SANG QING-XIANG AMY and Wang Yan-Ling</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/2004-0825]]></guid><cfi:id>78</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Characterization of a Novel AP2/EREBP Transcription Factor TSH1 Specifically Binding to GCC Elements]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060348]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[TSH1, a novel transcription factor in rice containing conserved AP2/EREBP domain, was screened from the EST database. The specific interaction of TSH1 and DNA elements was detected by two kinds of traditional methods, electronic mobility assay and yeast one-hybrid assay, which suggested that THS1 specifically binds to GCC element <i>in vitro</i> and <i>in vivo</i>. Furthermore, It was confirmed by atom force microscopy (AFM) that TSH1 binds to GCC element (core sequence GCCGCC) not DRE element (core sequence GCCGAC), and the single molecular force between TSH1 and GCC element was quantitatively measured. The molecular force of TSH1 with GCC element is (83.9 ± 2.2) pN. This interaction can be observably blocked by the dissociate TSH1 protein in the solution. These above results proved that TSH1 recognizes and binds to GCC with specifically interaction, which also demonstrate the high sensitivity of the AFM measurements for the single base substitution of the GCC core sequence greatly reduced the binding affinity. Comparing these methods for identification the binding of transcription factor with its DNA element, it was considered that AFM is expected to be a sensitive and reliable method that offers valuable information for the characterization of transcription factors.]]></description>
<pubDate>2006/7/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Feng,YU Jun-Ping,Fang Xiao-Hong and Zhang Gui-You]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Feng,YU Jun-Ping,Fang Xiao-Hong and Zhang Gui-You</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060348]]></guid><cfi:id>77</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Functional Characterization and Comparison of Four Splicing Alternatives of Mouse Liver A-to-I RNA Editing Enzyme ADAR1]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060442]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The posttranscriptional modification of messenger RNA precursors by base deamination can alter profoundly the function of the encoded proteins. Adenosine deaminases that act on RNA (ADARs) are capable of catalyzing the site-specific conversion of adenosine to inosine in pre-mRNA transcripts, thereby affecting coding potential of mature mRNAs. ADAR1 is a member of ADAR1 family and is abundantly expressed in the brain and ubiquitously present in most tissues of the mammals. Alternatively spliced forms of ADAR1 cDNA were cloned from the mouse liver and the localization of these splicing forms were examined under a fluorescent microscope by fusing them to EGFP. The cDNAs of these splicing forms were cloned into a baculovirus expression vector and the recombinant protein of these splicing forms were produced in insect cells and purified with Ni-NTA resin. The double-stranded RNA editing activity of the recombinant proteins were determined and compared. The results showed four major splicing forms of ADAR1 were naturally present in mouse liver and consisted of cDNAs of    3.5 kb, 3.6 kb, 1.8 kb and 2.0 kb in length, respectively. These three splicing forms were La, Lb, Sa and Sb forms and found to have two distinct translation initiator codons. Furthermore, the four splicing forms of ADAR1 protein were localized to either the cytoplasm or nucleus of NIH 3T3 cells as shown by fluorescent microscopy. The double-stranded RNA editing activity of the four splicing forms also differ significantly, with the Lb form possessing the highest editing activity. In summary, four major mouse ADAR1splicing forms are present naturally in the mouse liver with either cytoplasmic or nuclear localizations and widely varied editing activities, which indicate they might have different substrates and functions.]]></description>
<pubDate>2006/7/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Zhang De-Xin,ZHAO Peng-Tao,ZHAO Qing-Chuan,LUO Xiao-Xing,NIE Yong-Zhan,SU Ying-Jun,YANG Jing-Hua,R.RABINOVICI and FAN Dai-Ming]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Zhang De-Xin,ZHAO Peng-Tao,ZHAO Qing-Chuan,LUO Xiao-Xing,NIE Yong-Zhan,SU Ying-Jun,YANG Jing-Hua,R.RABINOVICI and FAN Dai-Ming</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060442]]></guid><cfi:id>76</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Effect of Matrix Metalloproteinase-26 on Cell Invasiveness in Human Choriocarcinomal Cell Line JEG-3]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060210]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Trophoblast invasion during implantation mimics the process of tumor metastasis in some aspects, however with a significant difference in that the former is strictly controlled. Several members of matrix metalloproteinases (MMPs) family have been shown to play crucial roles in regulating trophoblast cell invasion. MMP-26 is a newly identified MMP family member, and its functions in human trophoblast cells have yet to be elucidated. A well-accepted human trophoblast cell model———choriocarcinoma cell line (JEG-3) was used as <i>in vitro</i> model to investigate the involvement of MMP-26 in trophoblast cell invasion. Expressing pCR3.1 plasmid containing MMP-26 cDNA was transfected into JEG-3 cells, and a stable cell line with over-expressed MMP-26 was named as JEG-3/MMP-26. Transwell insert invasion assay showed that cell invasiveness in JEG-3/MMP-26 cells was significantly promoted. Data of RT-PCR and gelatin zymography demonstrated that the mRNA expression and zymogen secretion of MMP-9 were increased in these cells. Double immunofluorescent staining revealed co-localization of MMP-26 and MMP-9 proteins in JEG-3/MMP-26 cells. The data indicated that MMP-26 was involved in invasion-promoting regulation of human trophoblast cells, and it may function, at least in part, through coordination with other MMPs such as MMP-9.]]></description>
<pubDate>2006/6/14 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Wu Xiao-qiu,Sang Amy Qing-xiang,Fu Ya-yuan,Li Dian-jun,Li Yu-xia and Wang Yan-ling]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Wu Xiao-qiu,Sang Amy Qing-xiang,Fu Ya-yuan,Li Dian-jun,Li Yu-xia and Wang Yan-ling</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060210]]></guid><cfi:id>75</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Measurement of Hydrophobicity of Peptides in Electrospray Ionization Time-of-flight Mass Spectrometry]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060679]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Hydrophobicity is the association of non-polar groups or molecules in an aqueous environment which arises from the tendency of water to exclude non-polar molecules. Hydrophobic interaction is one of the most important non-bonded interactions which determine protein folding and ligand-receptor binding. To date, hydrophobicity usually has to be evaluated by means of calculation of LogP, because it is a tedious procedure to experimentally measure the hydrophobicity of molecules using techniques reported previously. As a matter of fact, the nature of hydrophobicity in chemistry refers to the physical property of a molecule that is repelled by water, which is clearly associated with the non-polar area in the molecules. The later can be correlated to signal intensity of the molecules in electrospray ionization mass spectrometry. Various dilute water solutions of tripeptides with increasing non-polar area were investigated in ESI time-of-flight mass spectrometry, and the ESI response of the tripeptides was linearly correlated to the non-polar areas in the molecules. Therefore, the hydrophobicity of peptides can be measured quantitatively in terms of ESI signal intensity. Thus hydrophobicity of the peptides was experimentally measured within a few minutes, and data showed a good agreement with previous results obtained in high performance liquid chromatography.]]></description>
<pubDate>2006/10/18 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Zhou Yue-Ming,Wang Wei-Ping,LIANG Hua-Zheng,ZHANG Xie,Chen Huan-Wen and CHEN Lan-Hui]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Zhou Yue-Ming,Wang Wei-Ping,LIANG Hua-Zheng,ZHANG Xie,Chen Huan-Wen and CHEN Lan-Hui</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20060679]]></guid><cfi:id>74</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Nav1.5 Na<sup>+</sup> Channels in Human Brain Are Encoded by New Variants of Nav1.5/SCN5A]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070408]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Tetrodotoxin-resistant Nav1.5 Na<sup>+</sup> channel has been considered as the cardiac sodium channel. Na<sup>+</sup> currents with tetrodotoxin resistance (TTX-R) and Nav1.5/SCN5A mRNA have been observed in neurons, but the cDNA encoding the TTX-R Nav1.5 Na<sup>+</sup> channels in human central nervous system (CNS) has not been identified. Nav1.5/SCN5A cDNA was first cloned from human brain cortex by using RT-PCR method. Two variants of  Nav1.5/SCN5A were found and tentatively named hB1 and hB2.Full sequence of cDNA encoding the α-subunit of TTX-R Nav1.5 Na<sup>+</sup> channel in human brain cortex was 6 201 nucleotides long and was designated hB1. The longest open reading frame of hB1 (accession number EF629346 ) encodes 2 016 amino acid residues. Sequence analysis has indicated that hB1 is highly homologus with human cardiac Nav1.5/SCN5A with >98% amino acid identity. There are 28 different amino acids between them, with 7 of which locating in the region encoded by exon6A or exon6. Alternative splicing of exon18 was not found in the gene cloning of human brain Nav1.5/SCN5A, which was different from human heart Nav1.5/SCN5A, but a novel alternative splicing lacking exon24 was first found. The two variants were detected in similar ratio in brain, but they were proved to relate to age development in heart tissue. The exon24 of human Nav1.5/SCN5A has 54 nucleotides, encoding 30 amino acid residues, and are located in human chromosome 3P21. This alternative splicing was also found in other tissues other than heart and brain. The expression pattern of the two variants in different tissues was different when detected by competitive PCR method and it was also changing with age development. Furthermore,Nav1.5/SCN5A mRNA was detected in 16 different tissue types of Wistar rats (P80) by reverse polymerase chain reaction (RT-PCR). These results suggest that Nav1.5 Na<sup>+</sup> channels in human brain are encoded by new variants of Nav1.5/SCN5A and its mRAN is more widely expressed than previously thought. The study is useful for making further investigation in the functional analysis of Nav1.5 Na<sup>+</sup> channels in different tissues.]]></description>
<pubDate>2007/9/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[OU Shao-Wu,ZONG Zhi-Hong,WANG Jun and WANG Yun-Jie]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>OU Shao-Wu,ZONG Zhi-Hong,WANG Jun and WANG Yun-Jie</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070408]]></guid><cfi:id>73</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning and Distribution Analysis of Nav1.5 Sodium Channel in Rat Brain]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070336]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[To clarify the gene and molecule characters of the tetrodotoxin-resistant (TTX-R) voltage -gate sodium channel and the distribution in different lobe of brain in different developmental stage, reverse transcriptase- polymerase chain reaction (RT-PCR) was used to clone the full sequence of Nav1.5 sodium channel (designated as rN1) α subunit in rat brains and the distribution was compared in different lobe of brain in different developmental stage. The open reading frame(ORF) of rN1 encodes 2016 amino acid residues and sequence analysis indicated that rN1 is highly homologous with 96.53% amino acids identity to rat cardiac Nav1.5 sodium channel (rH1) and 96.13% amino acids identity to human neuroblastoma Nav1.5 sodium channel (hNbR1). It has all the structural features of a voltage-gated sodium channel and the presence of a cysteine residue (C373) in the pore loop region of domain Ⅰ suggests that this channel is TTX resistant. A new exon (exon7) that distinct from rN1 was found in DⅠ-S3～S4. In addition, an alternative splicing isoforms that deleted 53 amino acids(exon20) was found in the loop between DⅡ～Ⅲ in rN1(designated as rN1-2). Distribution result demonstrated that rN1 expressed discrepancy in different ages and lobe in brain. The expression level of rN1 was gradually more stable in adult than neonatal. These results suggest that Nav1.5 has a newly identified exon for alternative splicing and is more widely expressed than previously thought.]]></description>
<pubDate>2007/8/13 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[REN Cheng-Tao,OU Shao-Wu,WANG Yun-Jie,LIN Yi and ZONG Zhi-Hong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>REN Cheng-Tao,OU Shao-Wu,WANG Yun-Jie,LIN Yi and ZONG Zhi-Hong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070336]]></guid><cfi:id>72</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Necrosis Pathotype Induced on <i>Nicotiana glutinosa</i> by Infection of CMV-CB7 Related to RNA2]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070292]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Full length cDNAs of <i>Cucumber mosaic virus</i> (CMV) CB7 strain, causing necrosis on <i>Nicotiana glutinosa</i>, were obtained by RT-PCR, using viral genomic RNAs as templates. cDNAs of CMV-CB7 genomic RNAs were cloned and sequenced and results indicated that RNA1, 2 and 3 was 3 356 nt, 3 045 nt and 2 218 nt, respectively (accordingly Accession Number EF216866, DQ785470 and EF216867). Infectious RNA transcripts from cDNA clones of CMV-CB7 were inoculated onto <i>N. glutinosa</i> and the seedlings of host plants displayed necrosis symptom, whist that of CMV-Fny induced typical mosaic symptoms. Through pseudorecombination between CMV-CB7 and CMV-Fny genomic RNAs, the genetic determinant of necrosis phenotype was mapped to RNA2. Chimeric infectious clones consisting of partial sequences of RNA2 derived from CMV-CB7 and CMV-Fny, respectively, were obtained by Overlapping PCR. Pathogenic analysis with those chimeric RNA2 revealed that 2b gene or 3′UTR of CMV-CB7 RNA2 was responsible for the necrotic pathotype. Northern blotting analysis reflected that both necrotic and non-necrotic viruses accumulated to similar levels of genomic RNAs in host plants. Therefore, necrotic phenotype induced on <i>N. glutinosa</i> was not related to the level of accumulation of CMV genomic RNAs.]]></description>
<pubDate>2007/7/2 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LIAO Qian-Sheng,DU Zhi-You,ZHANG Hua-Rong,ZHU Li-Ping,WU Peng and CHEN Ji-Shuang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIAO Qian-Sheng,DU Zhi-You,ZHANG Hua-Rong,ZHU Li-Ping,WU Peng and CHEN Ji-Shuang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070292]]></guid><cfi:id>71</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Investigation of Inhibition of Wnt/β-catenin Pathway in Breast Cancer Cells Mediated by Dkk-1 Released From Human Mesenchymal Stem Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070174]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Growing evidences show that mesenchymal stem cells (MSCs) home to tumorgenesis and inhibit tumor cells, however, the molecular mechanisms underlying are unclear. The human mesenchymal stem cells (hMSCs) derived from human fetal bone marrow in 4 months were established without immortalization, designated BMMS-03 cells. In order to clarify the molecular mechanism underlying, the effect of conditioned media from hMSCs on human breast cancer MCF-7 cells was examined. The results showed that conditioned media from BMMS-03 cells were able to decrease the colony-forming units and proliferation of MCF-7 cells by colony-forming assay and MTT assay. Western blot analysis revealed that β-catenin and its target gene c-Myc, Bcl-2, PCNA and survivin were downregulated in MCF-7 cells treated with conditioned media from BMMS-03 cells. In addition, the treatment significantly reduced β-catenin nuclear assembly in MCF-7 cells by immunoflorescence staining. The finding demonstrated that the expression level of Dkk-1 in hMSCs was much higher than that in MCF-7 cells. Moreover, treatment with the antibody of rabbit against Dkk-1 abolished the inhibitory effects of conditioned media from BMMS-03 on the tumor cells. Conditioned media from BMMS-03 cells transiently transfected with pcDNA3.1(-)-Dkk-1 produced stronger downregulation of β-catenin and c-Myc expression in MCF-7 cells. The transfection with pcDNA3.1(-)-Dkk-1 in MCF-7 cells resulted in the downregulation of  β-catenin and c-Myc as well．The data suggest that hMSCs are able to decrease the malignant phenotype of tumor cells <i>in vitro</i>. Taken together, hMSCs may suppress tumor growth <i>via</i> Wnt/β-catenin pathway, in which Dkk-1 released from the hMSCs is responsible for the depression.]]></description>
<pubDate>2007/5/30 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[QIAO Ling,XU Zhi-Li,TAN Xu,YE Li-Hong and ZHANG Xiao-Dong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>QIAO Ling,XU Zhi-Li,TAN Xu,YE Li-Hong and ZHANG Xiao-Dong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070174]]></guid><cfi:id>70</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[MIF Regulates TNF Alpha Receptor Type Ⅱ Expression in RAW264.7 Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070233]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Macrophage migration inhibitory factor (MIF) plays an important role in the regulation of the innate and adaptive immunity and is implicated in inflammation, sepsis and autoimmune disease. Previous works have shown that MIF could induce the expression of many cytokines, such as TNF-α, IL-1β, IL-6 and IL-8 in macrophage. It was reported here that MIF up-regulates the type Ⅱ TNF-α receptor (p75 TNFR) expression at mRNA level in RAW264.7 cell line. When RAW264.7 cells were treated with MIF inhibitor, antibody neutralizing MIF activities or the siRNA specific to MIF receptor CD74, the baseline TNFRⅡ mRNA level was reduced.  Using inhibitors specific to Erk, JNK, p38, Src or PKA, it was demonstrated that MIF regulation of TNFRⅡ mRNA expression is mediated by Src and JNK.  The up-regulation of the TNF-α type Ⅱ receptor by MIF suggests a mechanism of amplifying inflammatory signals while avoiding side effects of TNF-α, such as apoptosis or cytotoxicity during macrophage activation.]]></description>
<pubDate>2007/5/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[王启宇,王惟,乔晓杭 and 唐捷]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>王启宇,王惟,乔晓杭 and 唐捷</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070233]]></guid><cfi:id>69</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Screening and Identification of Interaction Partner of Cytoplasmic Domain of L1]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070133]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[L1 cell adhesion molecular is a type Ⅰ membrane glycoprotein of immunoglobulin superfamily. L1 is expressed mainly in nervous system and plays important roles in nervous system development, learning and memory. L1 cytoplasmic domain (L1CD) is important for L1 function by mediating signaling. To investigate the molecular mechanisms of signaling mediated by L1CD, yeast two-hybrid assay was carried out to screen the human brain cDNA library using L1CD as the bait. After sequence analysis and BLAST, several candidates were identified. One candidate is PAX6 transcription factor. L1CD and PAX6 cDNA were cloned in expression vectors and cotransfected into COS-7 cells. The interaction between L1CD and PAX6 was verified by co-immunoprecipitation assay. These preliminary results suggest that L1CD may be involved in transcription regulation.]]></description>
<pubDate>2007/4/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Zhang Ling and Huang xinhan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Zhang Ling and Huang xinhan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070133]]></guid><cfi:id>68</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning, Distribution and Analysis of The New Exon Encoding Nav1.5 Channel in Brain]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20061044]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Among the tetrodotoxin-resistant(TTX-R) α-subunits, Nav1.5 mRNA showed the strongest expression in the heart, according with its consideration as the cardiac Na<sup>+</sup> channel. Compared to its mRNA transcription in the heart, the Nav1.5/SCN5A gene was also expressed in high levels in the brain, especially limbic regions of the brain. Exon6A of Nav1.5/SCN5A gene was first found in cloning of Nav1.5 channel in human neuroblastoma cells. It was found that it is exon6A that encodes Nav1.5 channels in human and rat brain while it is exon6 that encodes Nav1.5 channels in other tissues in the cloning of Nav1.5 channel in these tissues, Both exon6A and exon6 have 92 base pairs, which encodes 30 amino acid residues, and are located in human chromosome 3. But these two resulting products differ by 7 amino acid residues. There is only one different base pair between the enon6As encoding Nav1.5 channels in human and rat brain, but their encoding amino acid residues are identical. The expressions of exon6A in different part of the brain are different and the similar result was found in the expressions of exon6 among different tissues of rat when detected by using RT-PCR method. The study is useful for making further investigation in the functional analysis of Nav1.5 channels in different tissues.]]></description>
<pubDate>2007/2/28 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Jun,ZONG Zhi-Hong,OU Shao-Wu,WANG Yun-Jie,REN Cheng-Tao,LIN Yi and MENG Xiao-Na]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Jun,ZONG Zhi-Hong,OU Shao-Wu,WANG Yun-Jie,REN Cheng-Tao,LIN Yi and MENG Xiao-Na</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20061044]]></guid><cfi:id>67</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Promotion of Invasion and Metastasis in Human Breast Carcinoma Hs578T/Dox by Caveolin-1]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20061012]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[To investigate the effect of caveolin-1 on invasion and metastasis of human breast carcinoma Hs578T doxorubicin-resistanted cells, Hs578T/Dox+cav-1 was as experiment group which up-regulated caveolin-1 by introducing the pCI-neo caveolin-1 gene, and  Hs578T/Dox+vector introduced the pCI-neo vector was as controlled group. It was revealed that caveolin-1 in Hs578T/Dox cells is an important factor for mediating filopodia formation, which may enhance the invasive of cells. Hs578T/Dox+cav-1 cell formed long and abundant pseudopodia and only few filopodia were detectable in Hs578T/Dox+vector cells. It was shown that adhesive capability of Hs578T/Dox cells enhanced with up-regulated expression of caveolin-1 protein(<i>P</i>＜0.01). Introducing the caveolin-1 gene into Hs578T/Dox cells enhanced their migration and invasive capability, as revealed by an <i>in vitro</i> chamber invasion assay(<i>P</i>＜0.01). Apoptosis index of Hs578T/Dox+cav-1 group resulting from loss of cell-matrix interactions decreased comparing Hs578T/Dox+vector group(<i>P</i>＜0.01). Caveolin-1 inhibited anoikis of Hs578T/Dox cells and that allowed survival of cancer cells during systemic circulation, thereby facilitating secondary tumor formation in distant organs. The efficacy <i>in vivo</i> of caveolin-1 was tested using cells xenografted into nude mice. Each mouse in both fifteen-mice groups were hypodermically injected with equivalent doses of 5×10<sup>5</sup> cells from Hs578T/Dox+cav-1 or Hs578T/Dox+vector. Tumors in Hs578T/Dox+cav-1 group were all formed after injection followed for 4 weeks, while no one in Hs578T/Dox+vector group. Lung metastasis was found in one mouse injected Hs578T/Dox+cav-1 cells. In conclusion, up-regulated caveolin-1 level in Hs578T doxorubicin-resistanted cells markedly elevates their capacity to tumor invasion and metastasis.]]></description>
<pubDate>2007/1/15 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHENG Ya-Min,LI Fei,QI Bao-Ju,WU Ping,SUN Hai-Chen,LIU Shuang and CHEN Jian-Wen]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHENG Ya-Min,LI Fei,QI Bao-Ju,WU Ping,SUN Hai-Chen,LIU Shuang and CHEN Jian-Wen</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20061012]]></guid><cfi:id>66</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Increased Expression of TGF-β Inducible Early Gene (TIEG1) in Keloid Scarrin]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070491]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The transforming growth factor (TGF)-beta/Smad signaling pathway is thought to play a major role in keloid formation. This study showed that the expression of inhibitory Smad7 was significantly down regulated in keloid compared with normal scar (<i>P</i> < 0.05) and normal skin (<i>P</i> < 0.05), however, no significant difference of Smad2 , 3 and the phosphorylation of Smad2,3. But the mechanism of reduced expression of Smad7 is unclear. Sp1 binding sites were found in Smad7 promotor by bioinformatics system analysis, then, the expression of TIEG1 mRNA and proteins in keloids, in normal skin and in normal scars tissues and fibroblasts were investigated. Dermal fibroblasts were obtained from biopsies of keloids, normal scars and normal skin. Fibroblasts were cultured in vitro. The expression of TIEG1 mRNA was analysed by RT-PCR and protein expression was determined by Western blot analysis. The results demonstrated increased mRNA and protein expressions of TIEG1 in keloid tissue and fibroblasts as compared to normal scar tissues and fibroblasts (<i>P</i> < 0.05) and normal skin tissues and fibroblasts (<i>P</i> < 0.05). It suggested that TIEG1 might play a significant role to the decreased expression of the inhibitory Smad7 in keloid. Further investigation is necessary to illuminate the mechanism of TIEG1 regulating Smad7.]]></description>
<pubDate>2007/10/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[TANG Bing,ZHU Jia-Yuan,ZHU Bin,LIU Yang,LI Xin-Qiang and BI Liang-Kuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TANG Bing,ZHU Jia-Yuan,ZHU Bin,LIU Yang,LI Xin-Qiang and BI Liang-Kuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070491]]></guid><cfi:id>65</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Screen and Identification of The Protein-protein Interactors in The Host Cell With The SARS Coronavirus Nucleocapsid Protein]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080180]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[15 SARS-CoV N Protein Interacting Protein (NPIP) were selected  from host cells using Yeast Two-hybrid system (Y2H). These are Angiogenin, acyglycerol kinase, cytochrome oxydase subunit I, CXC chemokine ligand 16, epidermal growth factor receptor pathway substrate 15, glutathione S-transferase kappa 1,integrin beta 1, jun oncogene, NIMA (never in mitosis gene a)-related kinase 10, protein tyrosine kinase 2 beta,homo sapiens SH3KBP1 binding protein 1 and ubiquitin specific peptidase 53. With the aid of immunological co-precipitation (CO-IP), it was confirmed that chemokine CXCL16 was the interactor with SARS-CoV N protein in host cells.]]></description>
<pubDate>2008/8/1 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHANG Wei-Shan,ZHAI Jing,SONG Wen-Gang and LIU Yong-Qing]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHANG Wei-Shan,ZHAI Jing,SONG Wen-Gang and LIU Yong-Qing</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080180]]></guid><cfi:id>64</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Genomic Screen for Expression Pattern in Adult <i>Drosophila</i> Brains <i>In vivo</i> by Enhancer Trap Method and Establishment of Expression Database]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080286]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[“Enhancer trap” is an important technique to build and explore <i>Drosophila</i> brain gene expression pattern and its database. Large genome-wide screen for specific expression pattern in adult <i>Drosophila</i> brains by enhancer trap method provides fly tools for further understanding neural basis of learning and memory. Enhancer trap method was utilized to generate <i>Drosophila</i> P[Gal4] mutant library. Each mutant in library was crossed with GFP reporter flies (<i>UAS</i>-<i>eGFP</i>); heads of the adult off-springs were dissected to obtain the whole brain which were examined under the epifluorescence microscope and expression pattern of each mutant were further analyzed. JavaScript was utilized to establish an expression pattern library. A total of 2 677 mutant lines of <i>Drosophila</i> were obtained by P-element induced mutagenesis and subjected to expression pattern analysis. Most of mutated genes express in adult fly. 368 mutated genes specific express in the mushroom body, which was reported to involve in <i>Drosophila</i> olfactory learning and memory, and some others specific express in other neuron circuitries. <i>Drosophila</i> mutant libraries and genome-wide expression pattern database was built by enhancer trap method, which as a tool will be utilized to understand the function of genes and particular neural circuitries in <i>Drosophila</i> in the future.]]></description>
<pubDate>2008/6/16 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LIU Xiao-Jun,YUAN Xiao-Jing,SUN Kan,SHUAI Yi-Chun,SONG Qing-Xuan,WANG Lei,SHAO Li-Sha,ZHAO Xin-Yu,LU Yi-Sheng,LU Yu-Bing,WANG Lian-Zhang and ZHONG Yi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIU Xiao-Jun,YUAN Xiao-Jing,SUN Kan,SHUAI Yi-Chun,SONG Qing-Xuan,WANG Lei,SHAO Li-Sha,ZHAO Xin-Yu,LU Yi-Sheng,LU Yu-Bing,WANG Lian-Zhang and ZHONG Yi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080286]]></guid><cfi:id>63</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Molecular Mechanism Study on Different Isoforms of ING1 Family Inhibiting HeLa Cells Proliferation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080057]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[ING1 family is a candidate for tumor suppressor, which has three splicing isoforms named p47ING1a, p33ING1b, and p24ING1c. Study of the effect of different isoforms of ING1 on HeLa cells proliferation and its molecular mechanism would help further identifying the functional relationship of ING1 isoforms, and finding important genes regulated by ING1. Cell growth curve and cell cycle analysis were used to observe the effect of ING1a, ING1b, and ING1c on HeLa cells growth, and the result indicated that they could all inhibit HeLa cells growth by arresting cell cycle at G0/G1 phase. PCR method was used to construct the PHD domain deletions of ING1a and ING1b. ING1a, ING1b, ING1c and the PHD domain deletions 1a△C and 1b△C were then overexpressed in HeLa cells. p16<sup>INK4a</sup>, PTEN/p27<sup>Kip1</sup> and p53/p21<sup>Waf1</sup> protein levels were detected by Western blot. The result showed that ING1a, ING1b, ING1c, and 1a△C except for 1b△C induced p16<sup>INK4a</sup> protein expression, in which ING1c had the most powerful effect. Luciferase assay identified that overexpression of pcDNA3.1(+)-1a△C facilitated p16<sup>INK4a</sup> transcription through enhancing p16<sup>INK4a</sup> promoter activity, while pcDNA3.1(+)-1b△C repressed the p16<sup>INK4a</sup> promoter activity . In a word, it was found for the first time that except for the p53/p21<sup>Waf1</sup> pathway, three splicing isoforms of ING1 family could also inhibit HeLa cells proliferation though upregulation of p16<sup>INK4a</sup> and PTEN, and the PHD domain deletion of ING1a enhanced p16<sup>INK4a</sup> transcription. These findings provide new clews to further study on the mechanisms of ING1 family suppressing cancer cells growth.]]></description>
<pubDate>2008/5/23 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Na,ZHANG Ying-Tao,XUE Li-Xiang and TONG Tan-Jun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Na,ZHANG Ying-Tao,XUE Li-Xiang and TONG Tan-Jun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080057]]></guid><cfi:id>62</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Brain Glucose Metabolic Changes in Patients With Chronic Pain Due to Brachial Plexus Avulsion: a Positron Emission Tomography Study]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080168]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Chronic pain due to brachial plexus avulsion (BPA) is a kind of refractory neuropathic pain, yet there is a lack of knowledge regarding underlying brain activity. To further identify brain regions involved in chronic pain due to BPA, fluorine-18 fluorodeoxyglucose (<sup>18</sup>F-FDG) positron emission tomography (PET) was used to observe  brain glucose metabolic changes in those patients. Five patients with chronic pain due to left-BPA, whose pain reduced more than 75% after dorsal root entry zoneotomy (DREZotomy) were selected. The visual analog scale (VAS) , Hamilton depression scale, Hamilton anxiety scale and <sup>18</sup>F-FDG PET of brain were recorded before and 14 days after DREZotomy respectively. Statistical parametric mapping 2 (SPM2) was applied for data analysis. Comparing with PET during pain before DREZotomy, PET after DREZotomy showed significant glucose metabolism decreases in bilateral caudate, orbitofrontal cortex (OFC) (BA11), contralateral subgenual cingulate (BA25) and ipsilateral dorsolateral prefrontal cortex (DLPFC) (BA46/47), and significant glucose metabolism increases in contralateral thalamus, pulvinar and ipsilateral parietal lobe (BA7). The results suggested that the brain areas involved in emotion, attention and internal modulation of pain play an important role in the modulation of chronic pain due to BPA.]]></description>
<pubDate>2008/4/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Fu-Yong,TAO Wei,CHENG Xin,ZHOU Ke,SHAN Bao-Ci,YUAN Xiu-Li,HU Yong-Sheng,ZHANG Xiao-Hua and LI Yong-Jie]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Fu-Yong,TAO Wei,CHENG Xin,ZHOU Ke,SHAN Bao-Ci,YUAN Xiu-Li,HU Yong-Sheng,ZHANG Xiao-Hua and LI Yong-Jie</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080168]]></guid><cfi:id>61</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Formaldehyde-mediated Chronic Damage May Be Related to Sporadic Neurodegeneration]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080116]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Formaldehyde is directly toxic to cells and its intermediate metabolite formic acid leads to acidosis in microenvironment <i>in vivo</i>. According to recent literatures, endogenous formaldehyde production is related to several metabolic pathways such as amine oxidation (catalyzed by semicarbazide-sensitive amine oxidase, SSAO), methylation and demethylation. Under oxidation stress and energy metabolic imbalance, formaldehyde markedly increases in human circulation. Here, the authors found that formaldehyde is released from the reaction of malondialdehyde with a protein (BSA) in which protein side chains such as amino groups are chemically modified. Moreover, formaldehyde is also produced from the sphingomyelin solution in the presence of hydrogen peroxide as the myelin peroxidation occurs. Formaldehyde at low concentration induces neuronal Tau aggregation, resulting in formation of globular like aggregates which are toxic to SH-SY5Y cells, HEK-293 cells and hippocampus neurons in the primary culture. According to Chen <i>et al</i>. (2006), endogenous aldehydes are related to beta-amyloid misfolding, oligomerization and fibrillogenesis. Furthermore, formaldehyde is able to react with some neurotransmitters and thus impairs their structures and functions. Under physiological conditions, the human blood formaldehyde is dynamically kept approximately (0.087±0.004) mmol/L. Notably, this concentration is close to the half-lethal dose of formaldehyde (0.10～0.12 mmol/L) to neural cells in the <i>in vitro</i> cell culture such as SH-SY5Y cells. Furthermore, cell growth can be partially affected and inhibited in the presence of formaldehyde at (0.087± 0.004) mmol/L during the <i>in vitro</i> culture. This suggests that human body needs a strong degradation system to remove endogenous formaldehyde. As shown in clinical trials, the formaldehyde level in urine of Alzheimer's patients was markedly higher than the control subjects. The urine formaldehyde level was shown to be related to the cognitive impairment. Therefore, the level of blood (brain) formaldehyde is supposed to be changeable and increased under aging, leading to a higher risk chance to impair human brain, especially under stressing. The formaldehyde chronic damage to neural cells (grey mater) and neural fibers (white mater) may be one of the most important pathological mechanisms for sporadic neurodegeneration for instance Alzheimer's disease, because hypofunction in scavengering endogenous formaldehyde occurs as aging.]]></description>
<pubDate>2008/4/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Fang-Xu,LU Jing,XU Ya-Jie,TONG Zhi-Qian,NIE Chun-Lai and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Fang-Xu,LU Jing,XU Ya-Jie,TONG Zhi-Qian,NIE Chun-Lai and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20080116]]></guid><cfi:id>60</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[NOK Activates STAT3 Signaling by a JAK2-Dependent Mechanism]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070762]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Novel oncogene with kinase-domain (NOK) can activate multiple mitogenic signaling pathways including the janus kinases (JAK) and signal transducer and activator of transcription proteins (STAT). It was showed that NOK specifically and physically interacted with STAT3 in human embryo kidney 293T (HEK293T) cells. In addition, NOK could directly interact with most of the STAT3 subdomains except coiled-coil and C-terminal domains. Removing ectodomain and transmembrane domain of NOK markedly enhanced its intermolecular interaction with STAT3. Also, NOK could co-immunoprecipitate with JAK2 <i>in vivo</i>. Importantly, co-expression of NOK and JAK2 produced a synergistic effect on NOK-mediated STAT3 activation, while inactivating the kinase domain of JAK2 completely prevented this synergistic effect. Overall, the results indicated that NOK might complex with both STAT3 and JAK2 and activate STAT3 signaling by a JAK2-dependent mechanism.]]></description>
<pubDate>2008/2/18 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Ying-Hua,RONG Yu,CHANG Zhi-Jie and LIU Li]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Ying-Hua,RONG Yu,CHANG Zhi-Jie and LIU Li</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070762]]></guid><cfi:id>59</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[NOK Interacts With Akt and Enhances Its Activation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070737]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[NOK is a newly identified receptor protein-tyrosine kinase (PRTK) molecule that can promote tumorigenesis and metastasis. Previous data showed that NOK could activate the phosphatidylinositol 3'-kinase (PI3K) pathway in stable BaF3 cells. But how does NOK activate PI3K in cells remains unknown. It was showed that NOK physically interacted with the PI3K downstream effector Akt and enhanced its activation in human embryo kidney 293T (HEK293T) cells. Deletion mapping indicated that protein kinase B (Akt) was able to directly contact with the kinase domain of NOK. Inactivating the Akt kinase domain significantly reduced the intermolecular interaction between NOK and Akt, while constitutively active mutant of Akt apparently had a stronger interaction with NOK. NOK did not have an additive effect on insulin-mediated Akt activation. Overall, the results indicate that NOK might complex with Akt and directly activate PI3K/Akt signaling pathway.]]></description>
<pubDate>2007/12/19 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Ying-Hua,CHANG Zhi-Jie and LIU Li]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Ying-Hua,CHANG Zhi-Jie and LIU Li</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20070737]]></guid><cfi:id>58</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A study of  homologous recombination in foot-and-mouth disease virus in China]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090232]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Foot-and-mouth disease virus (FMDV) is a positive-sense RNA virus which has caused severe damage to world-wide livestock industry. The extensive genetic and antigenic diversity observed in the evolution of FMDV is generally the obstacle for controlling the disease. The homologous recombination, as a significant force driving the evolution of virus, has also effect on the epidemiological trait of FMDV. However，the role of homologous recombination in the diversification of FMDV in China has not investigated. So it is necessary to study the homologous recombination underlying the evolution of FMDV to control FMD. Based on a sound evolutionary framework, molecular evolutionary analysis was used to identify the putative recombinants. All complete FMDV genomes from China were respectively retrieved from GenBank. Homologous recombination was identified using Simplot program. Phylogenetic relations were analyzed to determine the recombination events among these FMDV isolates by using MEGA 4. The isolates O/NY00, O/China/1/99Tibet, O/Tibet/CHA/99, O/OMIII and O/ES/2001 among 16 FMDVs were identified as putative recombinants by analyzing the FMDV genomic sequences extracted from GenBank. The recombination events frequently happen between serological type Asia1 and O which are endemic FMDV circulating in China, suggesting frequent cross infection of FMDV in China. This situation further makes controlling FMDV in China more difficult. Moreover, serotypic conversion of FMDV between Asia1 and O was detected to be due to homologous recombination. These results provided clues for understanding the antigenic and genetic diversification in FMDV, and shed lights on the potential vaccination and treatment of FMD.]]></description>
<pubDate>2009/5/25 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Zhi-Yin,HE Cheng-Qiang,LIU Ying-Ying,FENG Qian,TENG Jun-Lin and CHEN Jian-Guo]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Zhi-Yin,HE Cheng-Qiang,LIU Ying-Ying,FENG Qian,TENG Jun-Lin and CHEN Jian-Guo</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090232]]></guid><cfi:id>57</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[RNA Silencing Suppressor p19 Regulates The Expressions of Cell Cycle Related Genes]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090009]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Besides its function as a pathogenicity determinant, the <i>Tombusvirus</i> P19 also serves as a suppressor of RNA interference (RNAi) by sequestering intracellular small RNAs such as the small interfering RNAs (siRNAs) and microRNAs (miRNAs). However, the effect of P19 on mammalian cells has not been evaluated before. A human embryonic kidney 293 cell line that stably expressed p19 (HEK293-p19) was generated. Flow cytometric analysis revealed that over-expression of P19 caused a significant accumulation of G2/M phase cells. Cell proliferation assays demonstrated a reduced DNA replication and cell growth in HEK293-p19 cells. Moreover, p19 altered the expression profiles of a number of cell cycle regulators in HEK293 cells, such as upregulation of cyclin A1, CDK2, CDK4, CDK6, p18, cyclin D2, p19INK4d and E2F1, and downregulation of p15, cyclin A2, cyclin B1 and cyclin E1. Thus, the data strongly indicate that p19 might influence multiple G2/M regulators to cause G2/M arrest.]]></description>
<pubDate>2009/4/2 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LIU Li,LI Jian,XU Yu-Ping,QIAO Wen-Tao,CHEN Qi-Min and GENG Yun-Qi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LIU Li,LI Jian,XU Yu-Ping,QIAO Wen-Tao,CHEN Qi-Min and GENG Yun-Qi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090009]]></guid><cfi:id>56</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<i>Sec-10</i> Knockout Increases The Neuroactive-drug Responses Without Affecting Function of The Postsynaptic Ionotropic Receptors in Neuromuscular Junctions]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090100]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Exocyst complex is known to function in the exocytosis network, however, the molecular mechanism is unclear yet. Using UV/trimethylpsoralen mutagenesis, the <i>sec-10</i> (one component of the exocyst complex) knockout mutant of <i>C. elegans</i> was obtained for the first time. The drug sensitive assays revealed clearly that the <i>sec-10</i> gene affected the neural signal transmission, however, the electrophysiological assay showed the function of the ionotropic receptors in the neuromuscular junctions (NMJs) were unaltered compared with the wild type (WT). Thus it was assumed that the <i>sec-10</i> gene might not influence the known ionotropic receptors in the NMJs, but some other pathways instead.]]></description>
<pubDate>2009/4/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG Lei,LI Jiang-Li,GAO Shang-Bang,WU Zheng-Xing,ZHANG Rong-Ying and XU Tao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG Lei,LI Jiang-Li,GAO Shang-Bang,WU Zheng-Xing,ZHANG Rong-Ying and XU Tao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090100]]></guid><cfi:id>55</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[p-SAGE: Parametric Statistical Analysis of Gene Sets]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090325]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Tumor genesis and development often result from deregulation of important biological pathways at the gene expression level. Although there has been much work focused on searching gene sets using gene expression data or other prior information, proper statistical testing of the gene sets is still an open question. Most studies have expanded the testing method of a single gene into the gene sets. Parametric statistical analysis of gene sets ( p-SAGE ) was presented for determining the significant gene sets or pathways associated with a phenotype of interest. The method was applied to brain tumor experiments to identify many gene sets. Some of the newly discovered gene sets were related to signal transduction and immunity. This simple and effective method gives useful biologically meaningful results.]]></description>
<pubDate>2009/9/1 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[HUANG Bo,LI Wen-Ting,LI Wen,XIA Xue-Feng and SUN Zhi-Rong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HUANG Bo,LI Wen-Ting,LI Wen,XIA Xue-Feng and SUN Zhi-Rong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090325]]></guid><cfi:id>54</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Overexpression and Effect on Apoptosis of the 150-ku Oxygen-regulated Protein (ORP150) in Human Hepatocellular Carcinoma]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090265]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In previous study, the 150-ku oxygen-regulated protein (ORP150) was identified as a candidate glycoprotein related to hepatocellular carcinoma.  In order to further validate the expression level of ORP150 in hepatocellular carcinoma, protein expression was determined by Western blot and cell immunochemistry, and messenger RNA (mRNA) expression was detected by quantitative real-time polymerase chain reaction.  The effect of ORP150 on apoptosis and invasive potential of hepatocellular carcinoma cells was evaluated using the small interference RNA (siRNA) technique.  Both the protein and mRNA expression levels of ORP150 were significantly upregulated in hepatocellular carcinoma cell lines compared with a non-tumor human liver cell line.  After transfection with the specific siRNA of ORP150, significantly greater apoptosis of hepatocellular carcinoma cells was induced compared with untransfected cells.  However, no significant effect on invasive potential was found. Overexpression of ORP150 was associated with hepatocellular carcinoma, and ORP150 might promote the proliferation of hepatocellular carcinoma cells by inhibiting apoptosis. ORP150 could be a potential therapeutic target for hepatocellular carcinoma.]]></description>
<pubDate>2009/9/1 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHOU Hai-Jun,HEI Zhen-Yu,SHI Jiong,GUO Kun,SUN Bing-Sheng,WU Jin-Cai,ZHAO Yue,FU Li-Yun,DAI Chun,GAO Dong-Mei,SUN Rui-Xia,ZHAO Yan,CHEN Jie,WANG Lu,QIN Lun-Xiu and LIU Yin-Kun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHOU Hai-Jun,HEI Zhen-Yu,SHI Jiong,GUO Kun,SUN Bing-Sheng,WU Jin-Cai,ZHAO Yue,FU Li-Yun,DAI Chun,GAO Dong-Mei,SUN Rui-Xia,ZHAO Yan,CHEN Jie,WANG Lu,QIN Lun-Xiu and LIU Yin-Kun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20090265]]></guid><cfi:id>53</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Generation and Characterization of Blood Vessel Specific EGFP Transgenic Zebrafish <i>via Tol2</i> Transposon Mediated Enhancer Trap Screen]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100301]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Cardiovasculature forms during early stages of embryonic development and enables other organs to develop, maintain and regenerate. Imbalanced growth of blood vessels can give rise to numerous pathological disorders. However, the genes involved in blood vessel development remain largely elusive. Zebrafish (<i>Danio rerio</i>) is an ideal vertebrate model organism for the study of developmental processes, especially for that of cardiovascular formation. 26 transgenic fish lines with blood vessel-specific EGFP expression were identified <i>via</i> a large scale enhancer trap screen mediated by <i>Tol2</i> transposon in zebrafish. The EGFP expression in some of these lines shows different and unique patterns in different part of blood vessels. The genomic sequences flanking the <i>Tol2</i> insertion sites have been successfully cloned from 22 lines <i>via</i> linker-mediated PCR, among which 17 sequences could be mapped to a unique location within current zebrafish genome assembly. Expression of 8 flanking genes from 9 transgenic lines was confirmed to recapitulate the expression of EGFP reporter gene in their corresponding lines <i>via</i> RNA whole mount <i>in situ</i> hybridization (ISH). Three of these genes, <i>hhex, ets1a</i> and <i>dusp5</i> are known to be important for vasculargenesis. Since <i>hhex</i> and <i>ets1a</i> are also expressed in hematopoietic precursors, these transgenic zebrafish should be very useful for the study of both hematopoiesis and vasculargenesis. The rest of these genes, namely <i>zvsg1, micall2a, arl8b</i> (<i>1</i> of <i>2</i>), <i>zgc:73355</i> and <i>hecw2</i> (<i>1</i> of <i>2</i>), are either novel or functionally unknown in zebrafish. Further investigation of these fish lines and corresponding genes will give important insights of blood vessel developmental mechanisms including hemangioblast formation and differentiation, as well as genes and enhancer elements important for cardiovascular system. In addition, these transgenic fish lines could also make invaluable contributions to small molecule screen for drug discovery.]]></description>
<pubDate>2010/7/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[XUE Yu-Lin,XIAO An,WEN Lu,JIA Yue,GAO Yue,ZHU Zuo-Yan,LIN Shuo and ZHANG Bo]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>XUE Yu-Lin,XIAO An,WEN Lu,JIA Yue,GAO Yue,ZHU Zuo-Yan,LIN Shuo and ZHANG Bo</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100301]]></guid><cfi:id>52</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Expression Pattern of Selected Cell Adhesion Molecules in Mammary Duct Repopulating Cells Sorted From The Mouse Mammary Anlagen]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100120]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Mammary stem cells (MaSCs) is an ideal model for studies of organogenesis, cell proliferation, differentiation, survival and apoptosis. Recent researches showed that many adult stem cell surface markers belonged to cell adhesion molecule (CAM) family. Therefore, analysis of relationship between mammary stem/progenitor cells and the expression pattern of CAM have directive meanings for identifying embryonic mammary stem/progenitor cells and understanding their properties. Here, cells in E14 mouse mammary anlagen were purified using the adult mouse mammary epithelial stem cell (MaESC) markers of CD24 and CD49f. It was  found that CD24 and CD49f double-positive cells contain two distinct cell populations: CD24<sup>hi</sup>CD49f<sup>+</sup> and CD24<sup>med</sup>CD49f<sup>+</sup>, and their percentages in total mammary anlagen cells were 16% and 47%, respectively. In the following monolayer culture and <i>in vivo</i> transplantation tests, it was found that the CD24<sup>med</sup>CD49f<sup>+</sup> cells could attach plate and regenerate mammary ductal units; correspondingly, CD24<sup>hi</sup>CD49f<sup>+</sup> cells did not possess of these capabilities. These results indicate that the two mammary anlagen cell populations represent different cell types, and CD24<sup>med</sup>CD49f<sup>+</sup> population may contain the self-renewal mammary anlagen stem/progenitor cells. Afterwards, the differences in the expressions of 19 mammary-related CAM transcripts in the two cell populations were validated by quantitative real-time PCR analysis. The data show that the CAM gene expressions of mammary repopulating-CD24<sup>med</sup>CD49f<sup>+ cells are dramatically different from that of CD24<sup>hi</sup>CD49f<sup>+</sup> cell population. The expressions of several adult stem cell markers in CD24<sup>med</sup>CD49f<sup>+</sup> cell population are remarkable higher than those in CD24<sup>hi</sup>CD49f<sup>+</sup> cell population.]]></description>
<pubDate>2010/4/28 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SONG Jia-Zhe,XUE Kai,LI Song and LI Ning]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SONG Jia-Zhe,XUE Kai,LI Song and LI Ning</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100120]]></guid><cfi:id>51</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Pore-like aggregates of Tau protein induced by formaldehyde]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100375]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Though the hypothesis of "aspecific amyloid ion channels" has been proposed by Lin, <i>et al</i> (University of California, Santa Barbara) to explain the mechanism of metabolic dysfunction and cell death during protein conformational diseases, the "pore-like" aggregates of misfolded neural Tau have not been observed. Revulsants involved in the formation of "pore-like" aggregates have not been found yet. According to the hypothesis "chronic impairment resulted from abnormally-increased endogenous formaldehyde is one of the important risk factors related to sporadic senile dementia", formaldehyde has been utilized to incubate with Tau protein resulting in amyloid-like deposits with marked cytotoxicity. Under the experimental conditions, 0.5% formaldehyde-treated Tau could form "pore-like" aggregates. These results may deliver a novel approach to study the mechanism of cellular metabolic disturbance, even cell death, which is induced by formaldehyde-treated neural Tau.]]></description>
<pubDate>2010/10/26 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Sajjad Haider Naqvi,WANG Wei-Shan,MIAO Jun-Ye and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Sajjad Haider Naqvi,WANG Wei-Shan,MIAO Jun-Ye and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100375]]></guid><cfi:id>50</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[ERp44 mediates gene transcription <i>via</i> inositol 1, 4, 5-trisphosphate receptors in HeLa cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110179]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Increase in nuclear calcium concentration has several biological effects which include controlling calcium-activated gene transcription. Using extracellular ATP to induce intracellular calcium transient as a model, Western blotting, immunofluorescence, real-time PCR as well as Ca<sup>2+</sup> image studies were carried out. It was found that inositol 1, 4, 5-trisphosphate receptors (IP<sub>3</sub>Rs) and endoplasmic reticulum protein 44 (ERp44) co-localized on the nuclear envelope and endoplasmic reticulum (ER). Extracellular ATP induced nuclear calcium transient <i>via</i> IP<sub>3</sub>Rs and subsequently increased the cAMP response element binding protein (CREB) phosphorylation and the expression of c-Myc. However, all these were inhibited by 2-aminoethoxydiphenyl borate (2-APB), an IP<sub>3</sub>Rs inhibitor, and by over-expression of ERp44.  These results suggest that ERp44 inhibits gene transcription <i>via</i> IP<sub>3</sub>Rs in HeLa cells.]]></description>
<pubDate>2011/6/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[PAN Cong-Yan,ZHOU Rong-Bin,CHEN Zheng,CHEN Ying-Xiao,WU Yan-Yun,MIAO Lin,YIN Wen-Xuan and JI Guang-Ju]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>PAN Cong-Yan,ZHOU Rong-Bin,CHEN Zheng,CHEN Ying-Xiao,WU Yan-Yun,MIAO Lin,YIN Wen-Xuan and JI Guang-Ju</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110179]]></guid><cfi:id>49</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Broad-spectrum Neutralizing Monoclonal Antibodies Against H5N1 Avian Influenza A Viruses and Primary Research on The Mechanism]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110090]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Avian influenza is a highly contagious disease of birds caused by A influenza viruses. The circulation in humans by the highly pathogenic H5N1 avian flu in the past few years have caused most pandemics and have heightened fear that the next influenza pandemic is due. Antibodies could be used as an efficient anti-virus agent in clinical therapy. The full-length HA of the A/Jiangsu/1/2007(H5N1) about 1.7 kb was amplified, subcloned to the pFastBac vector and recombinant bacmid DNA was selected. The recombinant HA was expressed and purified HA about 70 ku was used as the antigen to immunize Balb/c mice. The whole H5N1 virus was used to select 5 mono-antibodies (mAbs)，and all of them were tested using microneutralization assays. 8G10D7, one of the antibodies, had broad neutralizing effect against clade 2 and clade 9 H5N1 avian influenza A viruses, and the <i>IC</i><sub>50</sub> was from 1∶256 to 1∶64. When detected with 8G10D7, all 4 viruses showed 70 ku and 43 ku protein band, which confirms that the binding site of the scFv antibodies were located at the HA1 domain. The nucleuses of MDCK cells infected by 4 viruses were colored purple, and red around the nucleus. 8G10D7 showed HI activity to the 4 viruses, the HI has a positive correlation with neutralization concentration <i>IC</i><sub>50</sub>, which also further confirms that the binding site of the scFv antibodies were located at the HA1 domain. When the mAb 8G10D7 was used for the study of prophylaxis and therapeutic effect on influenza A viruses infection in an embryonated chicken eggs model. It had a complete 100% protection effect on the H5N1 viruses in avian host in the prophylactic and therapeutic groups. The 100% preventive protection effect could be reached when challenged with H5N1 avian influenza A viruse in human host in the prophylactic groups, and there is also a 87.5% protection effect with H5N1 viruses in human host in the therapeutic groups. Thereby, the study suggests that the mAb 8G10D7 could be used in therapies to counter the H5N1 influenza A virus, and the epitope could be the key point for the design and implementation of vaccines.]]></description>
<pubDate>2011/5/20 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG  Xiao,ZENG Xiao-Yan,LIU Zhe,JIN Qiu,XU Yan,FENG Zhen-Qing and JIAO Yong-Jun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG  Xiao,ZENG Xiao-Yan,LIU Zhe,JIN Qiu,XU Yan,FENG Zhen-Qing and JIAO Yong-Jun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110090]]></guid><cfi:id>48</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA["Induced Fit-Lock and Key" Model in Enzymic Reactions]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110052]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[As described in enzymology, "induced fit" and "lock and key" models are used to explain the enzymic specificity of substrate. Previously, authors have studied the substrate specificity of <i>Eisenia fetida</i> proteaseⅠ(<i>Ef</i>P-Ⅰ), showing that the interaction between this protease and its substrates underwent an "induced fit" followed by "lock and key" model. It needs further investigating whether this model is suitable for other enzymes. Here, the reactions of substrate-induced <i>Eisenia fetida</i> proteaseⅡ(<i>Ef</i>P-Ⅱ), subtilisin (Sub) and lactate dehydrogenase (LDH) with their substrates were shown. <i>Ef</i>P-Ⅱ and Sub could not recognize chromozym U (CU) (<i>P</i> < 0.05) after incubated with chromozym TH (CTH) although the two proteases are natively able to react with both CTH and CU. The reaction followed an "induced fit-lock and key" pattern. In contrast, the two proteases were still able to react with CTH even though they have been incubated with CU. But neither earthworm protease nor subtilisin could recognize CU after CU and CTH treatment in turn, still suggesting that the reactions followed an "induced fit and then lock and key" procedure. Furthermore, the activity of LDH with lactate significantly decreased (<i>P</i> < 0.05) after the enzyme had been incubated with pyruvate. The activity on the conversion of pyruvate into lactate was not significantly affected by a prior incubation with lactate. This suggests that the pyruvate-induced complementary conformation of LDH is more stable than lactate-induced conformation.]]></description>
<pubDate>2011/4/13 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG Zi-Jian,PAN Rong,ZHOU Yuan and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG Zi-Jian,PAN Rong,ZHOU Yuan and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110052]]></guid><cfi:id>47</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Genetic Fate Mapping Reveals The Differentiation Potential of Tbx18<sup>+</sup> Cardiac Progenitors Into Cardiomyocyte Lineages in The Mouse Heart]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100616]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The study of cardiac progenitor cells (CPCs) is important for understanding the pathogenesis of congenital heart diseases and treating cardiovascular diseases. The mammalian heart is derived from distinct sets of CPCs. T-box transcription factor Tbx18 is expressed in the developing epicardium of the heart and play key roles in heart developing. In order to monitor and elucidate the differentiation potential of Tbx18<sup>+</sup> CPCs in tissues and living cells, Tbx18 genetic fate-mapping model, Tbx18-Cre/Rosa26R-EYFP and Tbx18-Cre/Rosa26R-LacZ double-heterozygous mice, were founded by Cre-LoxP system. These double-heterozygous mice were useful in monitoring the fate of Tbx18<sup>+</sup> cells by Cre expression, and tracing the lineage of the cells in embryos and adult mice. YFP<sup>+</sup> cells can be easily isolated from heart of Tbx18-Cre/Rosa26R-EYFP double-heterozygous mice by fluorescence activated cell sorter(FACS) and be monitored under an inverted confocal microscope. X-gal staining of genetic fate-mapping model revealed that atria, ventricular septum, ventricular wall, coronary vascular and atrioventricular valves can be generated from Tbx18 lineages. Here it was showed that Tbx18<sup>+</sup> CPCs can differentiate into anticardiac troponin T(cTNT ) positive cardiomyocytes and anti-smooth muscle myosin heavy chain11 positive smooth muscle cells <i>in vivo</i> by immunofluorescence. The heart is a complex organ composed of a diverse set of muscle and non-muscle cells. It was speculated that Tbx18 may play an important role in regulating the signal pathway of progenitor cells differentiating into myogenic cell lineages. These results identify Tbx18 as a marker of cardiac progenitors cells by Tbx18 genetic fate mapping mice, and lay the foundation for researching the differentiation potential of cardiac progenitors into cardiomyocyte lineages in the field of cardiac regeneration and repair.]]></description>
<pubDate>2011/1/13 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[DU Jian-Lin,ZHANG Jin,PU Di,GAO Er-Zhi,YANG Jing-Tao,GAO Ling-Zhi,XIA Shuang,DENG Song-Bai and SHE Qiang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DU Jian-Lin,ZHANG Jin,PU Di,GAO Er-Zhi,YANG Jing-Tao,GAO Ling-Zhi,XIA Shuang,DENG Song-Bai and SHE Qiang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20100616]]></guid><cfi:id>46</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Formaldehyde-mediated Hyperphosphorylation Disturbs The Interaction Between Tau Protein and DNA]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110451]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Hyperphosphorylation of Tau protein and related neuron death is one of the most important characteristics of Alzheimer's disease. Our laboratory has shown that Tau protein is able to bind and protect DNA. It is still unknown whether phosphorylation affects the binding of Tau to DNA. Therefore, it is of importance to investigate the effect of phosphorylation on the interaction of Tau with DNA in cells. In this work, we treated N2a cells with formaldehyde and found that Tau protein was hyperphosphorylated in the cells under   the experimental conditions. Phosphorylation was remarkably observed at both T181 and S396 of Tau protein in the cells in the presence of formaldehyde compared with those in the absence of formaldehyde. Cytoimmunofluorescence hardly showed that most of the nuclear phosphorylated Tau protein was co-localized with DNA, while Tau protein was partially co-localized with DNA in the absence of formaldehyde as control. Electrophoretic mobility shift assay (EMSA) showed that phosphorylated Tau catalyzed by GSK-3β reduced the interaction between Tau protein and DNA <i>in vitro</i>. These findings reveal that hyperphosphorylation declines Tau protein to protect DNA, and may thereafter lead to damage of DNA and even cell death, giving a novel viewpoint to the pathology of Alzheimer's disease.]]></description>
<pubDate>2011/12/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LU Jing,MIAO Jun-Ye,PAN Rong and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LU Jing,MIAO Jun-Ye,PAN Rong and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20110451]]></guid><cfi:id>45</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Three Dimensional Structure of <i>Pseudomonas aeruginosa</i> Tsi2：a Novel Species-specific Antitoxin-like Protein With Coiled Coil Conformation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120126]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Utilizing the typeⅥ secretion system (T6SS), <i>Pseudomonas aeruginosa</i> secretes the effector protein Tse2, a toxin to other competitive bacteria. It is a newly identified molecular mechanism for <i>P. aeruginosa</i> to win a survival advantage. To avoid being poisoned itself, <i>P. aeruginosa</i> synthesizes the specific immunity protein, Tsi2 to inhibit the toxin. Sequence analysis shows that Tsi2 is a novel antitoxin-like protein which is specific for <i>P. aeruginosa</i>. Using the SAD method, we have successfully resolved the crystal structure of Tsi2 at 1.8&Aring; resolution. Our crystallographic studies reveal that Tsi2 adopts a novel coiled coil conformation which is not found in the antitoxins family previously. Meanwhile, Tsi2 is a well-assembled protein instead of an unfolded protein as an antitoxin in the toxin-free state. Tsi2 functions as a stable dimer and assembles as a unique  "clamp" structure through extensive hydrophobic interactions. Two grooves on the dimerization interface combining with one helix of two symmetric molecules respectively imply the potential region interacting with Tse2. This research not only offers comprehensive insights into the molecular essence of Tsi2 as an antitoxin, but also reveals its structural basis of antitoxin activity. Furthermore, the apo Tsi2 structure provides a good framework for further researches on the structure and function of the complex Tse2-Tsi2.]]></description>
<pubDate>2012/5/18 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Wei,DING Jing-Jin and WANG Da-Cheng]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Wei,DING Jing-Jin and WANG Da-Cheng</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120126]]></guid><cfi:id>44</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Crystallization of Mutations at SiteⅢ of Dvl2-DIX and Co-crystallization of Dvl2-DIX(G65A) With Ccd1-DIX]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120216]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Dvl (Dishevelled) is a key effector molecule of the Wnt signaling pathway. The DIX domain of Dvl (Dvl-DIX) can homo-oligomerize into cytoplasmic puncta via the intra-filament SiteⅠ, SiteⅡ and the inter- filament SiteⅢ, and form hetero-complex with the DIX domain of Ccd1 (Ccd1-DIX) through SiteⅠ and SiteⅡ. Since all efforts to solve the wildtype Dvl2-DIX structure were unsuccessful, we carried out crystallization trials with the SiteⅢ mutants of Dvl2-DIX that display impaired homo-oligomerization and Wnt activity. Crystals of Dvl2-DIX(G65A) protein were obtained, but the diffraction data encountered an unexpected lattice-translocation defect. These SiteⅢ mutations of Dvl2-DIX retained the ability to hetero-interact with Ccd1-DIX, and we thus successfully generated various complexes between Dvl2-DIX mutants and wildtype Ccd1-DIX. After extensive trials, crystals of the Dvl2-DIX(G65A)-Ccd1-DIX complex were produced, but of poor quality and unsuitable for diffraction studies. Optimization is under way.]]></description>
<pubDate>2012/5/31 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[DAN Qiong-Jie,LIU Yi-Tong,WU Jia-Wei and WANG Zhi-Xin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DAN Qiong-Jie,LIU Yi-Tong,WU Jia-Wei and WANG Zhi-Xin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120216]]></guid><cfi:id>43</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[sTn is a Novel Biomarker for TypeⅠ Endometrial Carcinoma]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120185]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Sialyl-Tn (sTn) is a tumor-associated carbohydrate antigen overexpressed in many carcinomas. But whether it is expressed in neoplastic human endometrium is controversial. Here we screened 111 clinical samples including 82 endometrial cancers, 16 atypical hyperplastic and 13 normal endometria, by immunohistochemistry using a novel anti-sTn antibody, namely 3P9. Our results showed that the expression of sTn in the endometrial carcinoma was significantly higher (76%) than that in normal tissues (31%) (<i>P</i> < 0.01) and in atypical hyperplasia (44%) (<i>P</i> < 0.05). Importantly, we found that sTn expression in typeⅠ carcinoma (80%) was obviously higher than that in typeⅡ(45%) (<i>P</i> < 0.05). These results suggested that sTn may be a biomarker for endometrial carcinoma, especially for typeⅠcarcinoma. Moreover, we observed that sTn expression was increased with the decline of tumor histological grade (<i>P</i> < 0.05), indicating that sTn was associated with a favorable prognosis in endometrial carcinoma.]]></description>
<pubDate>2012/5/18 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[AN Yun-He,ZHANG Hao-Feng,SUN Min,ZHANG Jun,CHEN Xiu-Qin,CHEN Dong,LU Di,FENG Jing,YANG Dong-Ling,SONG Li-Na and YAN Xi-Yun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>AN Yun-He,ZHANG Hao-Feng,SUN Min,ZHANG Jun,CHEN Xiu-Qin,CHEN Dong,LU Di,FENG Jing,YANG Dong-Ling,SONG Li-Na and YAN Xi-Yun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120185]]></guid><cfi:id>42</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Transcallosal Pathway of Whisker Information Between Rat Primary Somatosensory Cortices]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120103]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[It has been suggested that rodent primary somatosensory cortex (SⅠ) can be activated by ipsilateral whisker stimulation, while SⅠ only receives the ascending input from contralateral whiskers. Previous anatomical research revealed two transcallosal pathways transferring whisker information between bilateral cortices: perigranular zone (PGZ) pathway and dysgranular zone (DZ) pathway. But which pathway plays more important role in transferring whisker information remains unknown. We used voltage-sensitive dye (VSD) imaging to visualize the SⅠ activation by stimulating whiskers. We found that the contralateral whisker stimulation first activates the barrel (granular zone, GZ), then the activity forms a propagating wave and spread to the DZ outside the sub-barrel field cortex (BFC). In contrast, ipsilateral whisker stimulation first activates the DZ outside the BFC. The evoked activity in the DZ forms a propagating wave and spreads into the BFC in SⅠ. Inactivating opposite cortex blocks this ipsilateral whisker activation. Electrical stimulus to opposite cortex also first evokes DZ in the imaging cortex. Our results suggested that whisker stimulation first activated the barrel and then DZ in the opposite SⅠ. After a delay of transcallosal transfer, the DZ of the other hemisphere (ipsilateral to the whisker being stimulated) was activated. The callosal fibers connecting the DZs on the two hemispheries play a major role in the SⅠ activation by the ipsilateral whisker stimulation.]]></description>
<pubDate>2012/4/23 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Zhi-Jie,GAO Xin,LI Bing and WU Jian-Young]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Zhi-Jie,GAO Xin,LI Bing and WU Jian-Young</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120103]]></guid><cfi:id>41</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[IL-8 Regulates The Epithelial-mesenchymal Transition (EMT) of Renal Cancer Through PKC/ERK Signaling Pathway]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120298]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The epithelial-mesenchymal transition (EMT) is an essential component in tumor metastasis. However, the molecular mechanism of EMT in renal cancer is unclear. IL-8 is an important chemokine in tumor microenvironment. Studies have shown that renal cancer cells can secrete IL-8，whether it could induce EMT in renal cancer cells is unknown. Here we found that IL-8 could induce EMT in renal cancer cells. Upon the stimulation of IL-8，the expression of E-cadherin was up-regulated，while the expression of N-cadherin was down-regulated; IL-8 promoted the invasion of renal cancer cells, but there was no obvious impact on cell proliferation. In addition, IL-8 could activate ERK through PKC. Therefore, we believe that IL-8 may promote renal cancer EMT through PKC / ERK signaling pathway, which may be one of the important mechanisms of renal cancer metastasis.]]></description>
<pubDate>2012/9/14 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[BI Liang-Kuan,LIN Tian-Xin,XU Ke-Wei,HAN Jin-Li,HUANG Hai,ZHANG Cai-Xia,DONG Wen,LIU Hao and HUANG Jian]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>BI Liang-Kuan,LIN Tian-Xin,XU Ke-Wei,HAN Jin-Li,HUANG Hai,ZHANG Cai-Xia,DONG Wen,LIU Hao and HUANG Jian</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120298]]></guid><cfi:id>40</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Abnormally High Level of Uric D-Ribose for Type-2 Diabetics]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130341]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In 1815, the French chemist Michel Eug?ne Chevreul (1786-1889) discovered that the sweetness in the urine of diabetics comes from grape sugar or D-glucose. Diabetes mellitus (DM) is considered as a group of metabolic diseases characterized by hyperglycemia (high concentration of blood D-glucose) resulting from defects in insulin secretion, insulin action, or both. On the other hand, D-ribose as an energetic enhancer was found to decrease the concentration of blood D-glucose, and thus "Oral administration of D-ribose in diabetes mellitus" was ever described by Steinberg and colleagues (1970). As described previously in this laboratory, D-ribose rapidly glycates proteins, such as BSA, neuronal Tau and α-synuclein, producing advanced glycation end products (AGEs) with severe cytotoxicity, leading to dysfunction and cell death, <i>in vitro</i> and <i>in vivo</i>. Intraperitoneal injection of D-ribose into mice significantly increases their glycated serum protein and blood AGEs though the concentration of D-glucose became slightly decreased, suggesting that D-ribose is much easier to produce AGEs than D-glucose <i>in vivo</i>. Here, using 4-(3-Methyl-5-oxo-2-pyrazolin-1-yl) benzoic acid (MOPBA) coupled with HPLC, we determined the concentration of uric D-ribose of type 2 diabetic patients (<i>n</i>=30) and the age-matched healthy controls (<i>n</i>=30). The results show that the yield of the derivative of MOPBA-ribose is linearly correlated with the concentration of D-ribose (<i>r</i><sup>2</sup>=0.999) with a recovery of 99%. The isolated fractions of D-ribose and D-glucose from urine of type 2 diabetic patients through HPLC were analyzed by mass spectrometry, and the results showed that the fractions contained 569.19 u compound (C<sub>27</sub>H<sub>29</sub>N<sub>4</sub>O<sub>10</sub>, D-ribose), and 599.20 u compound (C<sub>28</sub>H<sub>31</sub>N<sub>4</sub>O<sub>11</sub>, D-glucose) respectively. The concentration of uric D-ribose of Type 2 diabetics (male (134.28±35.09) μmol/L, female (97.33±23.68) μmol/L) was significantly (<i>P</i> < 0.001) higher than that of the age-matched healthy control (male (35.99±5.64) μmol/L, female (33.72±6.27) μmol/L). Under the experimental conditions, the uric D-glucose level of the patients was also markedly (<i>P</i> < 0.001) higher than the control. Further analyses showed a marked increase in the level of uric D-ribose from either male (<i>P</i> < 0.001) or female (<i>P</i> < 0.001), but a significant difference of the uric levels between male and female could not be observed (<i>P</i> > 0.05). The high levels of uric D-ribose and D-glucose of the patients suggest that type 2 diabetic patients are not only suffered from D-glucose metabolism disorders, but also from D-ribose metabolism disorders.]]></description>
<pubDate>2013/9/16 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SU Tao,XIN Liang,HE Ying-Ge,WEI Yan,SONG Yi-Xiang,LI Wei-Wei,WANG Xue-Mei and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SU Tao,XIN Liang,HE Ying-Ge,WEI Yan,SONG Yi-Xiang,LI Wei-Wei,WANG Xue-Mei and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130341]]></guid><cfi:id>39</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[GSNOR：a Novel Regulator of Inflammation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130131]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Regulation of inflammatory cytokines is a critical stage in inflammation, an important factor in autoimmune disease and cancer. Nitric oxide (NO) is known to be an important regulator of inflammatory cytokines, however, most existing studies focus on the role of NO synthesis in the regulation of inflammatory cytokines, and little is known about the role of NO metabolism. Since S-nitrosoglutathione reductase (GSNOR) is a key protein in the control of NO metabolism, investigating its role in inflammation will be important for understanding the role of NO metabolism. Here we found that GSNOR transcription and protein expression is downregulated by lipopolysaccharide (LPS) in RAW264.7 cells, an inflammatory cell model. Inhibitors of MEK1/2, p38 and PI3K significantly attenuate the decrease in GSNOR transcription. Furthermore, inhibition of the enzyme activity of GSNOR promoted expression of LPS-induced inflammatory cytokines IL-1β, IL-6 and TNF-α, whereas overexpression of GSNOR had the opposite effect. The anti-inflammatory drug trichostatin A (TSA) rescued the downregulation of GSNOR expression by LPS. Furthermore, inhibition of GSNOR impaired the anti-inflammatory effect of TSA by increasing the expression of IL-6 and TNF-α. In conclusion, our work reveals a new mechanism used by macrophage cells to enhance the inflammatory response by simultaneously upregulating inducible  nitric oxide synthase(iNOS) and downregulating GSNOR, thus expanding our understanding of NO metabolism in inflammatory responses. This study shows that GSNOR is a novel regulator of inflammation and may be a potential target for the regulation of NO-mediated inflammation.]]></description>
<pubDate>2013/8/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Kai-Yuan,ZHANG Yu-Ying,SU Wen-Ting and CHEN Chang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Kai-Yuan,ZHANG Yu-Ying,SU Wen-Ting and CHEN Chang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130131]]></guid><cfi:id>38</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Effect of Formaldehyde on Cell Cycle Is in a Concentration-dependent Manner]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130079]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[A certain concentration of formaldehyde can cause protein misfolding, cell death and biological dysfunction. Though it has been reported that formaldehyde has cytotoxicity, how formaldehyde affects cell cycle of neural cells and the molecular mechanism still needs to be clarified. In this study, neuroblastoma cell line SH-SY5Y was utilized to incubate with formaldehyde and the effect of formaldehyde on cell cycle was in formaldehyde concentration-dependent manner. No significant changes in cell cycle could be detected when [FA]≤0.1 mmol/L (cells were incubated for 48 h), while the percentages of cells in S phase and G2/M phase were markedly increased with the elevation of formaldehyde concentration (0.1 mmol/L <[FA]≤0.2 mmol/L). In the medium with 0.3 mmol/L formaldehyde, 46.28% of cells were in S phase while only 16.05% of them were in G2/M phase, that is, cell proliferation was obviously inhibited under the conditions. When cells were synchronized at G2/M phase, formaldehyde (0.1～0.3 mmol/L) could markedly increase the number of cells in S phase, though, to some extent, the number of cells in G2/M phase decreased. When cells were synchronized at S phase,  0.1 mmol/L formaldehyde could decrease the number of cells in G2/M phase, while 0.3 mmol/L formaldehyde could markedly decrease the number of cells in G2/M phase and significantly increase that in S phase. In the presence of formaldehyde, primary neurons of SD rat exhibited similar changes in cell cycle as that in SH-SY5Y cells. Furthermore, early and late apoptosis was markedly observed when 0.1 mmol/L≤[FA]≤0.2 mmol/L, while DNA were obviously damaged and most cells were apoptosis and some of them underwent necrosis when [FA]≥0.3 mmol/L. In sum, formaldehyde at a low concentration (0.1 mmol/L≤[FA]≤0.2 mmol/L) mainly suppresses DNA synthesis in S phase via hypermethylation of global DNA, while formaldehyde at a higher concentration ([FA]≥ 0.3 mmol/L) causes DNA damage, both of them lead to the aberrant effects on cell cycle.]]></description>
<pubDate>2013/7/24 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[MIAO Jun-Ye,LU Jing,ZHANG ZI-JIAN,TONG Zhi-Qian and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MIAO Jun-Ye,LU Jing,ZHANG ZI-JIAN,TONG Zhi-Qian and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130079]]></guid><cfi:id>37</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Role of The Anterior-Temporal Lobe in The Perceptual Organization: a Neuropsychological Study]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130063]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Proximity and similarity organization are two extremely important kinds of perceptual organization. In this study, a patient with anterior-temporal lobe damage CXY took part in our proximity and similarity experiments. In this study, compound stimuli that a global figure made up of local figures were used to investigate the interference of global and local in the proximity and similarity perceptual organization. In the global-local experiment, we found that, normal subjects showed stronger global interference than local interference in the proximity perceptual organization. Such effect, however, disappeared in CXY, suggesting there was an obstacle in his automatic processing of the proximity organization; in similarity organization, there was no difference between CXY and normal subjects. In the uniform connectedness experiment, we also found the obstacle in CXY's automatic processing of the proximity organization. These results indicated that the anterior-temporal lobe plays an important role in proximity organization, global organization and uniform connectedness.]]></description>
<pubDate>2013/5/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SUN Di,WANG Bo and ZHOU Tian-Gang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SUN Di,WANG Bo and ZHOU Tian-Gang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130063]]></guid><cfi:id>36</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[E3 Ligase RNF148 Ubiquitinates and Down-regulates TSPAN15]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130053]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Ubiquitination plays very important roles in regulating protein degradation and transportation. Many RING finger proteins act as E3 ligase in these processes. A new typeⅠ transmembrane protein with unknown function, named RNF148 was studied. A RFP -IRES- TSPANs-EGFP/pCI vector was constructed to screen the substrate of RNF148. By using FACS, co-IP and confocal test, RNF148 was identified to interact with TSPAN15 which belongs to a tetraspanin family. RNF148 could down-regulate TSPAN15 by its E3 ligase activity. The RING domain of RNF148 was a key structure of its ubiquitin-ligase activity and was required for the poly-ubiquitination of TSPAN15. The mutation of Lys-21 and Lys-278 to arginine in the cytosolic fragment of TSPAN15 led to low ubiquitination density compared with the wild-type. RNF148-mediated ubiquitination promoted proteasomal degradation and downregulation of TSPAN15 <i>via</i> Lys-29 linkages. RNF148 also ubiquitinated TSPAN15 <i>via</i> generating Lys-63 polymerize ubiquitin molecules. These findings demonstrate for the first time that RNF148 is a RING finger ubiquitin E3 ligase and TSPAN15 is one of its substrates.]]></description>
<pubDate>2013/4/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SUO Ta-Lin and TANG Jie]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SUO Ta-Lin and TANG Jie</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130053]]></guid><cfi:id>35</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Post-response Inhibition on Medial Geniculate Neurons in Sleep]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120568]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The medial geniculate body (MGB, the auditory thalamus) receives strong corticofugal modulation that includes facilitation and inhibition.  Auditory stimuli evoke an onset response that in many neurons followed by a lasting post response inhibition in MGB neurons. In the present study, we investigated the post response inhibition of MGB neurons in sleeping rats.  Chronically implanted electrodes were used to record the neuronal activities of the MGB, as well as, the electroencephalogram (EEG) and the electromyography (EMG) from the rats in different stages of sleep.  Both ON and ON-OFF neurons in the MGB showed prolonged post-response inhibition of over 　50 ms. The post-response inhibition showed a shorter duration in rapid eye movement (REM) sleep than that in non-rapid eye movement (NREM) sleep. After the auditory sector of the thalamic reticular nucleus (TRN) was reversibly inactivated by local application of lidocaine, the post-response inhibition of MGB neurons disappeared or decreased. Based on these results, we concluded that the TRN was involved in the post response inhibition of the MGB in sleep. The TRN applied stronger inhibition to the MGB neurons during non-REM sleep than during REM sleep.]]></description>
<pubDate>2013/3/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[MENG Xian-Kai,SUN Wen-Jian,XU Xin-Xiu,ZHANG Zi-Cong and HE Ju-Fang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MENG Xian-Kai,SUN Wen-Jian,XU Xin-Xiu,ZHANG Zi-Cong and HE Ju-Fang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120568]]></guid><cfi:id>34</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Effect of Attentional Task and Task Difficulty on Microsaccades in Macaques]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140122]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Microsaccades are the largest and fastest of the fixational eye movements during attempted visual fixation. They can overcome visual fading that is due to neural adaptation and play an important role in the process of visual perception and cognition. We designed experiments to explore the difference of the microsaccades on the fixation tasks and attention tasks based on the correlation between microsaccades and visual perception. Comparing microsaccadic parameters in the different difficulty levels in fixation tasks, we found that amplitude, velocity and frequency of macaques' microsaccades are decreased with increasing task difficulty. On the other side, we don't get the same results on the two macaques on comparing the different visual tasks. It represents the different kind of visual tasks maybe lead to the different visual means. This conclusion will provide the basis for the further study on the mechanism of microsaccades.]]></description>
<pubDate>2014/9/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YE Jing-Ying,XUE Lin-Yan,HUANG Dan,YANG Yue-Jiao and CHEN Yao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YE Jing-Ying,XUE Lin-Yan,HUANG Dan,YANG Yue-Jiao and CHEN Yao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140122]]></guid><cfi:id>33</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Implicit Perception of "Holes" Under Continuous Flash Suppression]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130463]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The Global First theory considers the global properties of objects could be described as topological invariants, with the earliest detection and highest priority in visual processing. The theory is supported by accumulating evidence in conscious vision, but remains unclear in implicit perception, the perception in the absence of awareness, whose mechanism and application have been studied a lot in cognition research for years. In the present study we probed into the processing of global properties in implicit perception by means of a variant of binocular rivalry called continuous flash suppression, in which our target stimuli were suppressed by dynamic mosaic noise patterns in order to achieve subconscious vision. The number of holes, a crucial topological invariant of an object, is the target of this study. In Exp1, the disk, the S and the O shape were used as target stimuli, the shapes might change or not after being suppressed, subjects reported the breakthrough of suppressed figures by keypress, we measured the suppression time of the figures, and found stimuli of topological changes(changes of numbers of holes in stimuli) took significantly less time to get into dominance, comparing with those of non-topological changes or unchanged. In Exp2, disks with different amount of holes or similar arcs were used as target stimuli, subjects were required to perform a 2AFC task after a 3s display in which the suppressed figures might be presented in the upper or lower visual field, the detection accuracy were compared, which indicated that the topological changes have a higher chance to be detected during suppression. The result strongly supported Global First in implicit perception, and revealed the high priority of topological properties in human visual processing, meanwhile it suggested the possible subcortical visual processing of topological properties.]]></description>
<pubDate>2014/6/18 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Ya-Qi,ZHOU Tian-Gang and CHEN Lin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Ya-Qi,ZHOU Tian-Gang and CHEN Lin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130463]]></guid><cfi:id>32</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[FKBP12.6 Regulates The Secretion of Adrenal Chromaffin Cell in Mice]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140066]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[FK506 binding protein 12.6 (FKBP12.6), a protein that binds to and regulates the ryanodine receptor type 2 (RyR2) Ca<sup>2+</sup> release channels, may act as an important regulator of catecholamine secretion. In the present study, the role of FKBP12.6 in the control of chromaffin cell exocytosis has been investigated using FKBP12.6-null mice. The results showed that FKBP12.6 was expressed in mouse chromaffin cells; deletion of FKBP12.6 did not change the depolarization induced Ca<sup>2 </sup>  current and exocytosis. However, deletion of FKBP12.6 resulted in an enhanced caffeine-induced global Ca<sup>2 </sup>  transient and larger caffeine-induced exocytosis in chromaffin cells of mice. These results indicate that FKBP12.6 is involved in catecholamine secretion through regulation of Ca<sup>2 </sup>  release channel in mouse chromaffin cells.]]></description>
<pubDate>2014/5/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YUAN Qi,GUO Ning,GU Lei,WANG Jun,WANG Li,ZHOU Zhuan and JI Guang-Ju]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YUAN Qi,GUO Ning,GU Lei,WANG Jun,WANG Li,ZHOU Zhuan and JI Guang-Ju</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140066]]></guid><cfi:id>31</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Reduction of The Crowding Effect by Topological Difference Between Target and Flankers]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130464]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The crowding effect refers to the fact that observers' ability to recognize an object in the periphery deteriorates when the target object is flanked by other items, especially if the target and flankers are similar. Here, a reduction of the crowding effect was caused by a topological difference between target and flankers. In three experiments using a number of different stimulus patterns (<i>e.g.</i>, triangles and arrows; digits and letters and geometrical shapes), results showed that the crowding effect was significantly reduced when the target and the flankers were topologically different. Control experiments showed that such a reduction of the crowding effect was not due to differences in subjective similarity, or differences in geometrical features such as area and shape. This finding suggests that topological properties play an important role in perceptual grouping which influences the crowding effect.]]></description>
<pubDate>2014/2/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Rui-Jie,WANG Bo and ZHUO Yan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Rui-Jie,WANG Bo and ZHUO Yan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20130464]]></guid><cfi:id>30</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Cloning and Functional Characterization of a Novel Long Non-coding RNA Gene Associated With Hepatocellular Carcinoma]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120613]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Recently, we sequenced the transcriptomes of a hepatocellular carcinoma biopsy and a normal liver tissue using the RNA-Sequencing (RNA-Seq) strategy based on the Next Generation Sequencing (NGS) technique, and identified several adjacent high RNA-Seq signal peaks on chromosome 11q13.1 in the hepatocellular carcinoma biopsy, while not in the normal control tissue. In this chromosome region, there is no characterized genes have been identified, implying that these RNA-Seq peaks may represent one or more novel genes. Further study was confirmed that these RNA-Seq peaks were transcribed by one novel gene. Through cloning the full length of this novel gene, we found that this novel gene transcribed many splicing isoforms, and the longest isoform is 3 562 bp. Then we deposited twelve representative RNA isoforms into the GenBank database of the National Center for Biotechnology Information (NCBI), and created the GenBank IDs from KC136297 to KC136308 for these isoforms. None significant open reading fragment (ORF) was found in any transcripts of this novel gene, implying that this gene may encodes long non-coding RNAs (lncRNAs). To further elucidate the potential transcriptional regulation mechanism of this lncRNA gene, we predicted the promoter from the upstream sequence of the lncRNA gene using bioinformatic tools, and found that there is one potential promoter in -719 to -469 bp from the transcript start site of the lncRNA gene, and there are seven Sp1, one STAT5 and one EGR1 transcription factor binding sites in the promoter region. The molecular mechanisms of the lncRNA gene in carcinogenesis and progression of hepatocellular carcinoma are worthful for further investigation.]]></description>
<pubDate>2014/2/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[TANG Ke,WEI Fang,BO Hao,HUANG Hong-Bin,ZHANG Wen-Ling,GONG Zhao-Jian,LI Xia-Yu,SONG Ya-Li,LIAO Qian Jin,PENG Shu-Ping,XIANG Juan-Juan,ZHOU Ming,MA Jian,LI Xiao-Ling,XIONG Wei,LI Yong,ZENG Zhao-Yang and LI Gui-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TANG Ke,WEI Fang,BO Hao,HUANG Hong-Bin,ZHANG Wen-Ling,GONG Zhao-Jian,LI Xia-Yu,SONG Ya-Li,LIAO Qian Jin,PENG Shu-Ping,XIANG Juan-Juan,ZHOU Ming,MA Jian,LI Xiao-Ling,XIONG Wei,LI Yong,ZENG Zhao-Yang and LI Gui-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20120613]]></guid><cfi:id>29</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Research of <i>Caenorhabditis elegans</i> New piRNAs]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140072]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[PIWI-interacting RNAs(piRNA) are endogenous small RNAs(sRNA), which play roles in resisting exogenous gene invasion and transposon mobility. More than 16 000 piRNAs are found in <i>Caenorhabditis elegans</i>, and the piRNA loci share a conserved upstream sequence. New piRNAs can be predicted based on its conserved upstream sequence. <i>C. elegans</i> are synchronized and small RNAs from wild type and <i>prg-1</i> strains at L4 developmental period are sequenced through illumina technology. Basing on piRNA conserved uptream sequence, we find 967 new piRNAs expressed at L4 period, and the expressions of new piRNAs disappear in <i>prg-1</i> mutant. Most of new piRNAs are mapped into two piRNA clusters of Chromosome Ⅳ, and have an overwhelming bias for a 5' uracil. Compared to the published co-immunoprecipitation data from adult worms, over 100 new piRNAs can interact with PRG-1. However, some non-21nt long sRNAs, which also share the same loci with piRNAs, are also found in wide type worms. These non-21nt long sRNA may be co-products of piRNA precursors. Together, these results indicate that our sRNA sequencing identified many new piRNAs in <i>C. elegans</i>.]]></description>
<pubDate>2014/12/19 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CUI Dong-Ya,WANG Jia-Jia,SUN Xu-Bin,ZHANG Peng,HE Shun-Min and huangdawei]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CUI Dong-Ya,WANG Jia-Jia,SUN Xu-Bin,ZHANG Peng,HE Shun-Min and huangdawei</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140072]]></guid><cfi:id>28</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Ca2+ Sensor for Asynchronous Vesicle Release Has High-affinity to Sr2  and Mediates Spontaneous Release at The Calyx of Held Synapses]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140138]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The kinetics of Ca<sup>2+</sup> triggered synaptic vesicle fusion contains synchronous and asynchronous components. At the Calyx of Held synapse, synaptotagmin-2 has been identified as the Ca<sup>2 </sup> sensor protein for synchronous vesicle release while the Ca<sup>2 </sup> sensor for asynchronous vesicle release remains unknown. Sr<sup>2 </sup> is a divalent cation similar in size to Ca<sup>2 </sup> and often substituted for Ca<sup>2 </sup> as a tool in studying asynchronous vesicle release. However, the mechanism of Sr<sup>2 </sup>  triggering vesicle release is still under debate. We studied the spontaneous and evoked vesicle release at the wild type and synaptotagmin-2 knock-out calyceal synapses in the existence of extracellular Sr<sup>2 </sup> and found synaptotagmin-2 only mediates the Sr<sup>2 </sup>  triggered synchronous vesicle release but not the asynchronous and spontaneous release; the unknown divalent sensor for asynchronous vesicle release has high-affinity to Sr<sup>2 </sup>  and mediates the spontaneous vesicle release. Our study provided a new insight into exploring the divalent sensor in triggering asynchronous synaptic vesicle release.]]></description>
<pubDate>2014/11/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[GUO Jian-Li,TIAN Hao and SUN Jian-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>GUO Jian-Li,TIAN Hao and SUN Jian-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140138]]></guid><cfi:id>27</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Mild Prenatal Stress Exposure Contributed to Behavioral Changes Induced by Postnatal Injections and Blocked 	The Effects of Olanzapine]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20150086]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Exposure of pregnant females to strong prenatal stress generally induces psychotic-like behavioral impairments in their offspring. In contrast to strong stress exposure, mild prenatal stress exposure (MPSE) has been reported to increase the vulnerability of the nervous system to adverse environmental stimuli. However, the impacts of MPSE on treatment with antipsychotic medication have not been well investigated. In addition, although commonly utilized in animal experiments, the potential influences of injections per se on animal behavior have not been evaluated. Here, we investigated how MPSE, postnatal injections and olanzapine (OLZ) treatment might interact to affect the behavior of rats. Pregnant female rats were exposed to mild stress or left undisturbed during the last week of gestation. Their offspring were divided into three sub-groups and subjected to injections with saline or OLZ (2 mg/kg) on postnatal days (PDs) 7, 9 and 11 or were left undisturbed without injection. Social and olfactory discrimination tests were performed during adolescent (PD 35) and adult (PD 60) periods. Total exploratory time and the degree of preference in the discrimination tests were measured. We found that postnatal injections changed the degree of preference in adolescent prenatally stressed rats but had no effect on the degree of preference in the non-stressed rats. OLZ treatment increased the social exploratory time in the non-stressed rats during the adolescent and adult periods. However, these enhancing effects were diminished in the prenatally stressed rats. Our results indicate that MPSE could contribute to the behavioral changes induced by adverse stimuli such as postnatal injections and could reduce the treatment effects of antipsychotic medication.]]></description>
<pubDate>2015/6/24 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SHAN Liang, LIU Tian-E, ZHAO Xu-Dong and MA Yuan-Ye]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SHAN Liang, LIU Tian-E, ZHAO Xu-Dong and MA Yuan-Ye</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20150086]]></guid><cfi:id>26</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Evidence of The Presence of Bacteria Highly Resistant to β-Lactam Antibiotics in Taklimakan Desert and Biochemical Characterization of <i>Paramesorhizobium deserti</i> gen. nov., sp. nov.]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140261]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[During the surveying of indigenous bacterial diversity in Taklimakan Desert of Xinjiang of China, we obtained 10 isolates, which possess a capacity to grow on 0.1×Tryptic Soy Broth agar supplemented with 1000 mg/L ampicillin. These bacteria display extensive resistances to different β-lactam antibiotics. All of these isolates belong to <i>Proteobacteria</i>. Five of them were identified as the human opportunistic pathogen <i>Stenotrophomonas matltophila</i>. Four strains were closely related to <i>Mesorhizobium amorphae</i>. It is interesting to see that one isolate A-3-E<sup>T</sup> showed low 16S rRNA gene sequence similarity (< 96.8%) to those of the recognized species. The results of polyphasic taxonomy showed the strain represents a novel species of the new genus, for which the name <i>Paramesorhizobium desertii</i> gen. nov., sp. nov. is proposed. Moreover, it was found that high concentrations of β-lactam antibiotics are not able to inhibit the growth of strain A-3-E<sup>T</sup>. The novel bacterium grows well in the media containing 1000 mg/L of cefazolin or    250 mg/L of cefotaxime. The strain also resists 17 of the 28 tested antibiotics. We just presented a case that the Taklimakan Desert is a natural reservoir of novel β-Lactam antibiotic resistant bacteria.]]></description>
<pubDate>2015/1/19 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LUO Xue-Song, PAN Yun-Fan, SHI Jing-Jing, DAI Jun, HOU Sha, FANG Cheng-Xiang and PENG Fang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LUO Xue-Song, PAN Yun-Fan, SHI Jing-Jing, DAI Jun, HOU Sha, FANG Cheng-Xiang and PENG Fang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20140261]]></guid><cfi:id>25</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[c-MYC-Regulated miRNA-92b Inhibits Expression of The E3 Ligase FBXW7 in Colorectal Cancer]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160128]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Colorectal cancer (CRC) is the third leading cause of cancer-related death worldwide. Many microRNAs (miRNAs) have been reported to be abnormally expressed in CRC. Recent studies have identified miR-92b as a potential oncogene in several types of cancer. However, the role of miR-92b in CRC has not been clarified. This study aimed to elucidate the role of miR-92b in CRC progression. Relative quantitative PCR revealed that miR-92b expression was significantly increased in human CRC tissues compared to the adjacent tissues. Overexpression of miR-92b in the colorectal cancer cell line SW620 substantially increased cell viability <i>in vitro</i> and xenograft tumor growth <i>in vivo</i>. Also, miR-92b was identified as a secreted miRNA, which can be detected in both cultured medium and the peripheral blood of xenograft mice. Furthermore, we demonstrated that c-MYC, which was also elevated in CRC tissues, promoted the transcription of miR-92b by regulating its promoter activity. Luciferase assay and Western blot analysis revealed that FBXW7 was a novel target of miR-92b and can be negatively regulated by c-MYC. As FBXW7 is a major E3 ligase of c-MYC, our data suggested a potential positive regulatory feedback loop among c-MYC, miR-92b and FBXW7 in CRC. Collectively, we partly provided evidence on how miR-92b is regulated and the potential implications of miR-92b in CRC diagnosis.]]></description>
<pubDate>2016/7/19 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YIN Xiao-Fei, WU Shuai, YANG Yuan-Qin, FANG Xian-Long, XU Hai-Neng, LIU Xin-Yuan, ZHENG Shu and ZHANG Kang-Jian]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YIN Xiao-Fei, WU Shuai, YANG Yuan-Qin, FANG Xian-Long, XU Hai-Neng, LIU Xin-Yuan, ZHENG Shu and ZHANG Kang-Jian</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160128]]></guid><cfi:id>24</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Distinct Binding and Enzymatic Activities of Two Ribosome-dependent NTPases YchF and YihA]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160119]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[P-loop NTPases (GTPase and ATPase) are widely employed in both prokaryotes and eukaryotes to regulate various cellular processes. YchF and YihA are two highly conserved NTPases in bacteria, but their cellular roles remain elusive. Previous data revealed that the ribosome or ribosomal subunits are binding partners of these two NTPases. Here, we examined the binding preferences of <i>Escherichia coli</i> YchF and YihA to the 30S, 50S and 70S ribosomes in the presence of different nucleotides, and assayed whether these binding preferences were associated with the stimulation of their NTPase activities. Our data show that YchF and YihA display a strong preference for the 70S and 50S, respectively. While the 70S ribosome, but not the 50S or 30S, promotes both the ATPase and GTPase activities of YchF, YihA responds to both the 50S and 70S, with the moderate GTPase stimulation (～8.8 fold) seen in the presence of the 70S ribosome.]]></description>
<pubDate>2016/6/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[KONG Meng-Yuan, YAN Kai-Ge, MA Cheng-Ying and GAO Ning]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>KONG Meng-Yuan, YAN Kai-Ge, MA Cheng-Ying and GAO Ning</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160119]]></guid><cfi:id>23</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Heat Shock Protein gp96 3′UTR Functions as A ceRNA in Promoting DOHH Expression <i>via</i> miR-642a]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160086]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Heat shock protein gp96 is overexpressed in many kinds of tumors including hepatic tumors, and its overexpression is significantly correlated with tumor malignant degree and poor prognosis in patients. The mechanisms of heat shock protein gp96 in the development of tumors need to be further investigated. The effects of gp96 3′UTR as a ceRNA (competing endogenous RNA) on miR-642a and DOHH expression was studied through bioinformatics prediction, luciferase reporter assay, Western blotting, real-time PCR, RNA interference. MiR-642a specifically targets gp96 3′UTR. The wild type but not the mutant gp96 3′UTR in miR-642a binding site could sequester and downregulate miR-642a levels, which led to increased expression of the miR-642a target DOHH. Further studies showed that regulation of DOHH expression by gp96 3′UTR was miR-642a dependent. It was also found that DOHH does not affect the expression of gp96. Heat shock protein gp96 promotes DOHH expression via its 3′UTR as a ceRNA, providing new insights into the role of gp96 on the development of hepatic tumors and other tumors.]]></description>
<pubDate>2016/10/24 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SHENG Chun-Hai, SUN Lu, CHU Xiao-Yu, LI Chang-Fei and MENG Song-Dong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SHENG Chun-Hai, SUN Lu, CHU Xiao-Yu, LI Chang-Fei and MENG Song-Dong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20160086]]></guid><cfi:id>22</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Effect of Oxidative Stress on Accommodation and Transportation of Formaldehyde by Lysosome]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20170050]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Dysmetabolism of endogenous formaldehyde is regarded as one of the risk factors for the onset and progression of Alzheimer’s disease. Excess extracellular and intracellular formaldehyde induce neuron death, involving the impairment of cognitive ability. As previously reported, lysosome dysfunction plays an important role in neurodegenerative diseases and intracellular formaldehyde locates in the lysosome. Utilizing formaldehyde fluorescent probe, abnormally increase of the lysosomal formaldehyde was detected in the blood endothelial cell line (bEnd.3) and neuroblastoma N2a cells (N2a) from mouse brain under oxidative stress. Brain formaldehyde was significantly (<i>P</i> < 0.01) elevated in the chronic cerebral hypoperfusion rats compared with those with SHAM. LeuLeuOMe was used to induce the permeabilization of lysosome membrane in bEnd.3. After LeuLeuOMe tretment, higher intracellular and lower extracellular formaldehyde were measured by microplate reader and high performance liquid chromatography (HPLC) respectively. In other words, lysosome not only accommodates endogenous formaldehyde, but also transports the compound out of cells. Abnormal lysosome function causes dysmetabolism of formaldehyde, which is correlated with age-related cognitive impairment.]]></description>
<pubDate>2017/6/20 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Xi-Xi, SU Tao, HE Ying-Ge and HE Rong-Qiao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Xi-Xi, SU Tao, HE Ying-Ge and HE Rong-Qiao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20170050]]></guid><cfi:id>21</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Abnormal Attentive Tracking in Children With Intermittent Exotropia]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20170102]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Intermittent exotropia is a common pediatric ocular disease, which is also a hot research area in ophthalmology. In this study, we tested the tracking ability of children with intermittent exotropia using multiple object tracking (MOT) paradigm, and compared with amblyopic children and normal children. The experimental results showed that the tracking capacity of children whether with intermittent exotropia or amblyopia was significantly decreased as compared with normal children, and children with intermittent exotropia suffers the same degree of damage with children with amblyopia. It is the first report of the abnormal attentive ability of children with intermittent exotropia, which may be beneficial to future research of pathogenesis and early diagnosis of the disease.]]></description>
<pubDate>2017/5/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHOU Li-Qin, ZUO Zhen-Tao, WANG Jing, FU Tao and CHEN Lin]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHOU Li-Qin, ZUO Zhen-Tao, WANG Jing, FU Tao and CHEN Lin</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20170102]]></guid><cfi:id>20</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Hybridization Chain Reaction-based Assay for The Detection of Influenza A Virus]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180083]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Rapid point-of-care (POC) detection of influenza A virus is critical for timely and effective flu prevention and control. In this study, we developed a hybridization chain reaction (HCR)-based assay, through coupling HCR reaction with fluorescence quenching by graphene oxide (GO), for the rapid detection of influenza A virus. The target is detected as it triggers HCR, which results in the extension of short DNA chains, protecting the 6-carboxy-fluorescein amidite (FAM) group from GO quenching. The results demonstrate that it could specifically recognize target nucleic acid fragment of influenza A virus from other pathogen, and even from single-base mismatched oligonucleotides. A good linear correlation between fluorescence intensity and the target concentrations ranging from 10 to 40 nmol/L was achieved, with a detection limit of 5 nmol/L. Its detection performance was verified on nasopharyngeal swab samples, which is the first clinical application of HCR-based influenza assay. This HCR-based method shows many advantages including the enzyme-free amplification of nucleic acids, simple reaction system and convenient protocols, suggesting its availability for POC detection.]]></description>
<pubDate>2018/6/20 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[SUN Ming-Xuan, ZHAO Rong-Tao, LI Yang, KONG Wen, YANG Yi, GUO Xu-Dong, LIU Wan-Ying, SONG Hong-Bin, ZHANG Zhi-Hong and HAO Rong-Zhang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>SUN Ming-Xuan, ZHAO Rong-Tao, LI Yang, KONG Wen, YANG Yi, GUO Xu-Dong, LIU Wan-Ying, SONG Hong-Bin, ZHANG Zhi-Hong and HAO Rong-Zhang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180083]]></guid><cfi:id>19</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Directed Graph of Human Brain’s Default Network: a DCM With 7T fMRI]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180075]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The default mode network (DMN) has been reported to be involved in a variety of important cognitive functions and received increasing attention in neuroscience recently. Its dysfunction is also reported to be associated with multiple psychiatric disorders. However, the causal information flow (effective connectivity) within the default mode network remains poorly understood. In this study, we explored the effective connectivity pattern between 4 key DMN brain areas based on a high resolution 7T resting state fMRI dataset using a cutting-edge spectral dynamic causal modelling technique. Results showed that there was a distinct effective connectivity pattern among the DMN nodes. We found medial prefrontal cortex(MPFC) and bilateral inferior parietal cortex(IPC) sent information to the posterior cingulate cortex(PCC), which suggested that the PCC might be a hub region that collected information from other DMN areas. Besides, a causal influence was found from bilateral IPC to MPFC, and from left IPC to right IPC. This work was the first 7T fMRI study that investigated effective connectivity pattern among DMN nodes, which may promote our understandings about the functions of DMN and benefit future research in DMN-related psychiatric disorders.]]></description>
<pubDate>2018/4/17 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[ZHANG Xian-Chang, XUE Rong and ZUO Zhen-Tao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHANG Xian-Chang, XUE Rong and ZUO Zhen-Tao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180075]]></guid><cfi:id>18</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Study of Membrane Protein TmrAB by Analytical Ultracentrifugation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180200]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Detergent is critical for membrane protein purification, impacting the state of oligomerization, crystallization conditions and other physicochemical properties. Analytical ultracentrifugation (AUC), by characterizing the sedimentation of membrane protein-detergent complex in centrifugal fields, is able to measure various hydrodynamic and thermodynamic properties, including sedimentation coefficient, molar mass, hydrodynamic radius, binding coefficient, thus defining the homogeneity and oligomerization state of membrane protein-detergent complex. This study focuses on an ABC transporter from thermophilic bacteria, TmrAB, and utilizes AUC coupled to size-exclusion chromatography and negative staining electron microscopy to determine its homogeneity, oligomerization, and stoichiometry of membrane protein and detergent molecules. The results indicate that TmrAB complex exists as homogeneous monomer of heterodimers of TmrA and TmrB, in the condition of 8× Critical Micelle Concentration (CMC) DDM, having a ratio of DDM/TmrAB equal to 116∶1. This study suggests, AUC is a reliable method to analyze the molecular mass of membrane protein.]]></description>
<pubDate>2018/10/22 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHU Wen-Dan, XU Yang, ZHOU Cui-Yan, LU Ya-Fei, YU Xiao-Xia, ZHANG Rui-Xuan and LI Wen-Qi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHU Wen-Dan, XU Yang, ZHOU Cui-Yan, LU Ya-Fei, YU Xiao-Xia, ZHANG Rui-Xuan and LI Wen-Qi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20180200]]></guid><cfi:id>17</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Nobiletin Rescues Cognitive Impairment  in Naturally Aging Mice]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20190108]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[With the aging of the world's population, the threat of age-related cognitive impairment is increasing. It is of great significance to study the mechanism of age-related cognitive impairment and find effective strategies to rescue it. Our previous studies have demonstrated that S-nitrosoglutathione reductase(GSNOR) was significantly increased in the hippocampus of aging mice and neuronal-specific GSNOR transgenic mice showed cognitive impairment in behavior tests. However, the mechanisms underlying this process remain unclear. Here, we found that CREB signaling was significantly decreased by GSNOR in cultured mice hippocampus neurons and GSNOR transgenic mice. Up regulation of the CREB signaling pathway by nobiletin rescued the cognitive impairment in GSNOR transgenic mice in Y-maze test. Nobiletin also showed protective effects on memory impairment in aging mice model. These results provide a new mechanism for the cognitive impairment in GSNOR transgenic mice and provide a new potential strategy to improve the cognitive function by nobiletin. GSNOR transgenic mice may be used as a screen model as age-related cognitive impairment.]]></description>
<pubDate>2019/7/1 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[YAO Qin,ZHANG Yu-Ying,WU Kai-Yuan,CHU Bo-Yu and CHEN Chang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YAO Qin,ZHANG Yu-Ying,WU Kai-Yuan,CHU Bo-Yu and CHEN Chang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20190108]]></guid><cfi:id>16</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[C-type Lectin Protein mosGCTL-2 From <i>Aedes aegypti</i> is a Novel Factor for Dengue Virus Infection]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20190219]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[C-type lectins (CTLs) are a family of carbohydrate-binding proteins that share a common structural motif; they are quite conserved evolutionarily from arthropods to mammals and play an essential role in immune responses. <i>Aedes aegypti </i>is a pivotal vector for the dengue virus and expresses more than 30 types of C-type lectins, which are critical for both viral and bacterial infections. A recent study indicates that mosGCTL-3 interacts with a dengue virus-2 envelope protein (DENV-2 E protein) in<i> vivo</i> and <i>in vitro</i> thereby enhancing the infection of <i>A. aegypti</i>. Here, in this report we found another C-type lectin protein, mosGCTL-2 with important functions similar to mosGCTL-3. Results from the phylogenetic tree analysis suggested that there is sequence similarity between mosGCTL-2 and mosGCTL-3, with 43.56% of their amino acid sequences being identical. We constructed<i> Drosophila </i>S2 cell expression system to purify mosGCTL-2. <i>In vitro</i> experiments showed that mosGCTL-2 binds to the DENV-2 E protein through a calcium-dependent manner. The upregulation of mosGCTL-2 was noted in <i>A. aegypti</i> and was important for dengue virus 2 (DENV-2) infection<i> in vivo</i>. These findings suggest that mosGCTL-2 may be a pattern recognition receptor that performs an important function in the infection of<i> A. aegypti</i> by the dengue virus.]]></description>
<pubDate>2020/4/23 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Yu-Jie,LIU Shan,ZHANG Xi,LI Dong-Yang,WU Yu-Lan,SUN Jing-Chuan,XU Shao-Jian,REN Yan,WANG Tao,LIU Li and GONG Jun-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Yu-Jie,LIU Shan,ZHANG Xi,LI Dong-Yang,WU Yu-Lan,SUN Jing-Chuan,XU Shao-Jian,REN Yan,WANG Tao,LIU Li and GONG Jun-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20190219]]></guid><cfi:id>15</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Crystal Structure of The Catalytic Domain of Human Ubiquitin Ligase AREL1]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200008]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Ubiquitination is an important post-translational modification that controls nearly every facet of a cell’s life and death. Only ubiquitin ligases E3 can specifically recognize substrates during ubiquitination, so E3 plays a pivotal role in ubiquitination and degradation of substrate proteins. Human apoptosis-resistant E3 ubiquitin protein Ligase 1 (AREL1) belongs to the Homology to E6AP C-Terminus(HECT) ubiquitin ligase family, and it inhibits apoptosis through ubiquitinating mitochondrial proapoptotic proteins such as SMAC, HtrA2, and ARTS, which are degraded by the 26 S proteasome. Here, the crystal structure of the HECT domain of AREL1 (AREL1<sup>HECT</sup>) at 3.2 ? resolution is reported, and structural comparisons of AREL1<sup>HECT</sup> against different HECT E3 ligases are conducted. Size Exclusion Chromatography (SEC) and Small Angle X-ray Scattering (SAXS) indicate that there are diverse oligomeric states of AREL1<sup>HECT</sup> in solution, and the SAXS 3D model further suggests that AREL1<sup>HECT</sup> can dimerize in solution. These findings offer a structural basis for studying the complex of AREL1<sup>HECT</sup> and ubiquitin, and provide insights into molecular mechanisms of substrate ubiquitination by AREL1.]]></description>
<pubDate>2020/8/11 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Zhi-Hui,SHANG Guo-Hui,TANG Chen-Jun,TIAN Zi-Zi,WU Wei and CHEN Zhong-Zhou]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Zhi-Hui,SHANG Guo-Hui,TANG Chen-Jun,TIAN Zi-Zi,WU Wei and CHEN Zhong-Zhou</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200008]]></guid><cfi:id>14</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Inhibition of mitochondrial complex II induces mitophagy and attenuates cell proliferation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200278]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Mitochondrial complex II, or succinate dehydrogenase (SDH), is regarded as a central regulator of respiratory adaptation and metabolic reprogramming in various stimuli and abnormalities. Four subunits of complex II are considered as tumor suppressors, whose mutations are associated with various type of cancer. However, little is known how complex II regulates cell proliferation. 2-Thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial complex II, and SDHB shRNA were used to abolish the activity of complex II in cell lines. Inhibition the activity of complex II by TTFA treatment or knockdown of SDHB could trigger mitochondrial fragmentation and subsequently mitophagy. We also found that inhibition of complex II also increased the glucose consumption and the lactate production which termed as Warburg effect. Despite of these, complex II dysfunction showed negative regulation to cell proliferation. Collectively, complex II is a potential target to induce mitophagy and inhibit cell proliferation.]]></description>
<pubDate>2021/3/4 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[MU Cheng-Long,HE Li-Qun,WANG Jia-Le,ZHAO Tian,ZHU Yu-Shan and CHEN Quan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MU Cheng-Long,HE Li-Qun,WANG Jia-Le,ZHAO Tian,ZHU Yu-Shan and CHEN Quan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200278]]></guid><cfi:id>13</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[RBM15 Promotes Intron or Exon Retention]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210028]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[RBM15 is an RNA binding protein that is known of involving in the m<sup>6</sup>A modification and the regulation of alternative splicing (AS). However, how RBM15 regulates AS is currently unclear. Here, using super-resolution microscopy, we found that RBM15 forms puncta structures that closely contact with or even embedded in the nuclear speckles. Nuclear speckles are enriched in splicing factors, which implies that RMB15 might be involved in RNA AS. To determine whether and how RBM15 regulates AS, we knocked down RBM15(RBM15-KD) using siRNA and performed RNA-seq for wildtype(WT) cells and RBM15-KD cells. We analyzed the RNA-seq of WT and RBM15-KD cells. We show that RBM15-KD cause 1 279 differential AS events in 1 111 transcripts. After comparing to public RBM15-CLIP data, we identify that 191 out of 1 111 transcripts are directly bound by RMB15, indicating that these 191 transcripts are probably direct targets of RBM15. Moreover, RBM15 promotes the retention of the adjacent regions proximal to its binding sites in 121 out of the 191 transcripts. This study reveals that how RBM15 regulates AS on a transcriptomic level.]]></description>
<pubDate>2021/6/24 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Ru,KE Yan,WEI Rong-Fei,WANG Xin-Yu and LI Dong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Ru,KE Yan,WEI Rong-Fei,WANG Xin-Yu and LI Dong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210028]]></guid><cfi:id>12</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Effect of Deuterium Oxide on <i>Bacillus</i> <i>atrophaeus</i> Spore Germination]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210056]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[This short communication is to report the inhibitory effect of deuterium oxide (D<sub>2</sub>O) on germination and culturability of bacterial spore. Germination was triggered by L-alanine under ambient condition and <i>in situ </i>monitored by Tb<sup>3+</sup>-dipicolinic acid assay, phase contrast microscopy and absorbance measurement. Germination kinetics were characterized by final germination level, germination half time, and germination speed. The culturability of germinated spores was evaluated by enumerating colony-forming units. Results revealed that D<sub>2</sub>O retarded the whole germination process and reduced the culturability but didn’t affect the final germination level. We postulate that D<sub>2</sub>O enhanced the stability of some spore-specific signaling proteins.]]></description>
<pubDate>2021/11/26 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHANG Jinhui and WU Wen Jie]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHANG Jinhui and WU Wen Jie</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210056]]></guid><cfi:id>11</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Whole Brain Imaging of Larval Zebrafish during Rheotaxis]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220354]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Rheotaxis, namely to orient and swim against the water flow, is a conserved behavior across most fish and amphibians. While the study of rheotaxis behavior has a relatively long history, and in recent years the behavioral algorithm of rheotaxis has been described, how distributed neural circuits integrate multisensory information, make decisions, and generate counterflow motor sequences remain largely unknown. Whole brain calcium imaging of larval zebrafish during rheotaxis would provide a unique opportunity to tackle this difficult problem.<b>Methods</b> To this end, we developed a microfluidic device that can precisely control the water flow and elicit rheotaxis behavior. By integrating the chip with a customized light field tracking microscope, we built a system to record whole brain neural activity in freely behaving larval zebrafish during rheotaxis.<b>Results</b> Larval zebrafish showed reliable rheotaxis behavior in the setup, represented by prominent positional holding and counterflow swimming bouts in water flow. In the meanwhile, we successfully recorded zebrafish whole brain neural activity, from which a few brain regions were identified whose calcium signals strongly correlated with rheotaxis behavior.<b>Conclusion</b> Our study, for the first time, demonstrates a method for imaging whole brain neural activity in larval zebrafish while the animal is performing rheotaxis. Future analysis and modelling of the neural activity and behavioral data will deepen our understanding of sensorimotor transformation in this important naturalistic behavior.]]></description>
<pubDate>2022/9/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Yu-Bin,ZHANG Ren-Chang,LI Da-Guang,QI Ke-Xin,CHAI Yu-Ming,SHEN Chen,SI Guang-Wei and WEN Quan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Yu-Bin,ZHANG Ren-Chang,LI Da-Guang,QI Ke-Xin,CHAI Yu-Ming,SHEN Chen,SI Guang-Wei and WEN Quan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220354]]></guid><cfi:id>10</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[DNA End Configurations Regulate RecJ Exonuclease Activity]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220131]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> DNA end resection is a common mechanism for the formation of 3"-ssDNA tails in homologous recombination (HR) and is mainly mediated by 5"-3" exonuclease. However, whether DNA end configurations directly regulate 5"-3" exonuclease activity remains unclear. In this study, we explored the regulation and mechanisms of DNA end configurations on RecJ, the only 5"-3" exonuclease of RecF recombination pathway in<i> Escherichia coli</i>.<b>Methods</b> To investigate the regulation of DNA 3"-end configurations on RecJ exonuclease, single-stranded DNAs (ssDNAs) containing different lengths of 3"-ssDNA overhangs (9 nt and 18 nt) and 3"-end modifications (phosphorylation and phosphorothioation) were used for exonuclease assays in the presence of Mg<sup>2+</sup>. To elucidate the mechanisms, RecJ was incubated with substrates containing different 3"-end configurations in the absence of Mg<sup>2+</sup> and analyzed by electrophoretic mobility shift assays (EMSA). Furthermore, the coordination of DNA 3" end configurations and two other RecJ regulatory factors, DNA 5"-end phosphorylation and single-stranded DNA binding protein (SSB), were determined by exonuclease assays and EMSA on substrates with different 3"-end configurations respectively.<b>Results</b> DNA 3"-end configurations inhibited the RecJ exonuclease activity, including DNA 3"-overhang length and 3"-end modifications (phosphorylation and phosphorothioation). 3"-End phosphorylation and phosphorothioation of DNA reshaped the RecJ-DNA binding patterns to inhibit RecJ exonuclease activity. DNA 5"-end phosphorylation overcame RecJ inhibition of 3"-end modifications and remodeled the RecJ-DNA binding patterns. In addition, SSB partially overcame the 3"-end modifications mediated inhibition by enhancing RecJ-DNA binding.<b>Conclusion</b> The RecJ exonuclease activity was regulated and orchestrated by the DNA configurations of 3" and 5" ends.]]></description>
<pubDate>2022/6/21 0:00:00</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[MA Lan-Zhi,XIE Yan,ZHANG Peng,CHEN Hou-Zao and LIU De-Pei]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MA Lan-Zhi,XIE Yan,ZHANG Peng,CHEN Hou-Zao and LIU De-Pei</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220131]]></guid><cfi:id>9</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[LBP1C Extracted From <i>Lycium barbarum </i>Delays Aging by Activating TFEB]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230219]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> This study aims to explore the effects and mechanisms of LBP1C extracted from <i>Lycium barbarum</i> on delaying the natural aging of human fibroblasts and nematodes, and provide scientific evidence and explanation for the anti-aging and skin whitening effects recorded in the “Ben Cao Gang Mu (Compendium of Materia Medica)”.<b>Methods</b> Human fibroblasts and <i>C. elegans</i> were used as natural aging models and treated with LBP1C. The expression levels of <i>P16</i>, <i>P21</i> and the number of SA-β-gal staining positive cell were used to indicate the cell senescence level. The levels of GATA4, indicators related to the senescence associated secretory phenotype (SASP), transcription factor EB (TFEB) targeting genes and autophagy marker protein LC3 were detected by qPCR or Western-blot. The level of nuclear transcription of TFEB, a key regulatory factor for lysosomal biogenesis and autophagy, was detected by immunofluorescence in fibroblasts. The effects of LBP1C on lipofuscin levels in fibroblasts and <i>C. elegans </i>were<i> </i>respectively detected by lipofuscin kit and fluorescence microscope. The motor ability of LBP1C to <i>C. elegans </i>was evaluated through body bends and pumping analysis.<b>Results</b> Human fibroblasts and <i>C. elegans</i> were used as natural aging models in this study. Aging related indicators (<i>P16</i>,<i> P21</i> expression levels and the number of SA-β-gal staining positive cell) in the LBP1C treatment group decreased markedly compared with the control group, which indicated that LBP1C delayed cell senescence. The proportion of TFEB nuclear translocation significantly increased in the LBP1C treated groups and activated autophagy. Detection of TFEB downstream genes showed that mRNAs of lysosomal enzymes, lysosomal membrane proteins and functionally related vesicular ATPases were all significantly upregulated in the LBP1C treatment groups. The increase in autophagy level autophagy reduced the level of SASP transcription factor GATA4, thereby reducing the levels of SASP related IL-1β and iNOS. Besides, the increase in autophagy level accelerated the degradation of lipofuscin, and reduced the accumulation of lipofuscin in cells and <i>C. elegans</i>. LBP1C reduced the accumulation of lipofuscin in cells and <i>C. elegans</i> and improved the motor ability of <i>C. elegans</i>, which suggested that LBP1C promotes healthy aging of <i>C. elegans</i>.<b>Conclusion</b> This study investigated the new function and mechanism of LBP1C extracted from <i>Lycium barbarum</i>, which delays cell senescence by promoting autophagy to achieve the effects of anti-aging and skin whitening. LBP1C increased autophagy level by activating TFEB, thereby reducing the accumulation of SASP and lipofuscin, delaying aging and promoting healthy aging. This study reveals the effects and mechanisms of <i>Lycium barbarum</i> in anti-aging and skin whitening aspects, and provides scientific and theoretical basis for further application research, which provides exciting translational opportunities ahead.]]></description>
<pubDate>2023/8/14 11:14:21</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WU Dong-Li,QIAO Xin-Hua,HAN Wen-Sheng,XIE Ting,SHI Chang,HUANG Yu-Yun-Fei,SUN Chuan-Xin,DING Kan and CHEN Chang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WU Dong-Li,QIAO Xin-Hua,HAN Wen-Sheng,XIE Ting,SHI Chang,HUANG Yu-Yun-Fei,SUN Chuan-Xin,DING Kan and CHEN Chang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230219]]></guid><cfi:id>8</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Mutations in Acetylcholine-gated Chloride Channel Receptors Affect Locomotion Kinematics and Motor State Transitions in <i>C. elegans</i>]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230146]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Acetylcholine is a highly conserved neurotransmitter that plays a crucial role in the regulation of animal motor behavior. Abnormalities in acetylcholine signaling can lead to various motor dysfunctions. However, the inhibitory regulatory mechanisms of acetylcholine in motor behavior are not fully understood. In this study, we used <i>Caenorhabditis elegans</i> as a model organism to investigate the regulatory effects of acetylcholine-gated chloride channel receptor subunits (ACC-1, ACC-2, ACC-3, ACC-4) on motor behavior.<b>Methods</b> We used a combination of locomotion tracking, molecular genetics, and optogenetics to analyze <i>C. elegans</i> locomotion in acetylcholine-gated chloride channel subunit deficient mutants.<b>Results</b> We found that mutations in these subunits affected the kinematics of forward, backward, and turning movements of nematodes. The body bending amplitude during forward movement was also modified. Optogenetic activation of RIB interneurons led to delayed termination of the reversal in these mutant strains.<b>Conclusion</b> These results suggest that the regulation of acetylcholine-gated chloride channel subunits is required for maintaining and modulating <i>C. elegans</i> motor states. They also suggest that these subunits may be involved in mediating the inhibitory regulation of RIB interneurons on backward movement in <i>C. elegans</i>. This study provides new insights into the regulatory mechanisms of acetylcholine-gated inhibitory receptors in motor behavior.]]></description>
<pubDate>2023/6/20 16:49:48</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[Mahiber Polat,XIONG Rong-Kang,HUO Jing and WEN Quan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Mahiber Polat,XIONG Rong-Kang,HUO Jing and WEN Quan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230146]]></guid><cfi:id>7</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The Quercetin-modulated Activity-dependent Inhibition of Endocytosis at a Central Synapse]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230191]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Quercetin, a flavonol compound widely distributed in fruits, vegetables, and medicinal plants, has been suggested to act as a neuroprotective agent. In the present study, we investigated the presynaptic effect of quercetin on synaptic transmission and plasticity.<b>Methods</b> Using whole-cell patch clamp and capacitance measurement technique, we recorded miniature excitatory postsynaptic currents (mEPSC), presynaptic calcium influx, vesicle release and recycling, and the replenishment of readily releasable pool (RRP). Additionally, we stimulated the axon with 5-200 Hz and recorded short-term depression (STD) in the postsynaptic neuron.<b>Results</b> We found that 100 μmol/L quercetin in the extracellular solution did not affect the mEPSC amplitude and frequency, indicating a presynaptic mechanism modulating synaptic transmission. At the presynaptic nerve terminals, 100 μmol/L quercetin did not induce notable changes in calcium influx or vesicle release, but significantly inhibited clathrin-dependent slow endocytosis following exocytosis. The inhibition of endocytosis led to a slowdown of vesicle mobilization during stimulation, a reduction in readily releasable pool replenishment after stimulation, and enhancement of short-term depression during high-frequency repetitive stimulation in the postsynaptic principal neurons.<b>Conclusion</b> These results provide new insights into quercetin-modulated neuronal signaling and suggest a protective effect that prevents excessive excitatory synaptic transmission in brain circuits.]]></description>
<pubDate>2023/6/20 16:50:07</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[LI Shun,GAO Yi-Ming,XU Yue,HU Jia-Qi,TANG Wen-Xu,SUN Xiao-Quan,XUE Lei and WANG Wan-Chun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Shun,GAO Yi-Ming,XU Yue,HU Jia-Qi,TANG Wen-Xu,SUN Xiao-Quan,XUE Lei and WANG Wan-Chun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20230191]]></guid><cfi:id>6</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[PRMT7 Regulates Adipogenic Differentiation of hBMSCs by Modulating IGF-1 Signaling]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20240099]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Protein arginine methyltransferases (PRMTs) play pivotal roles in numerous cellular biological processes. However, the precise regulatory effects of PRMTs on the fate determination of mesenchymal stromal/stem cells (MSCs) remain elusive. Our previous studies have shed light on the regulatory role and molecular mechanism of PRMT5 in MSC osteogenic differentiation. This study aims to clarify the role and corresponding regulatory mechanism of PRMT7 during the adipogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs).<b>Methods</b> (1) Human bone marrow-derived mesenchymal stem cells (hBMSCs) were cultured in a medium that induces adipogenesis. We used qRT-PCR and Western blot to monitor changes in PRMT7 expression during adipogenic differentiation. (2) We created a cell line with PRMT7 knocked down and assessed changes in PRMT7 expression and adipogenic capacity using Oil Red O staining, qRT-PCR and Western blot. (3) We implanted hBMSCs cell lines mixed with a collagen membrane subcutaneously into nude mice and performed Oil Red O staining to observe ectopic lipogenesis<i> in vivo</i>. (4) A cell line overexpressing PRMT7 was generated, and we examined changes in PRMT7 expression using qRT-PCR and Western blot. We also performed Oil Red O staining and quantitative analysis after inducing the cells in lipogenic medium. Additionally, we assessed changes in PPARγ expression. (5) We investigated changes in insulin-like growth factor 1 (IGF-1) expression in both PRMT7 knockdown and overexpressing cell lines using qRT-PCR and Western blot, to understand PRMT7’s regulatory effect on IGF-1 expression. siIGF-1 was transfected into the PRMT7 knockdown cell line to inhibit IGF-1 expression, and knockdown efficiency was confirmed. Then, we induced cells from the control and knockdown groups transfected with siIGF-1 in lipogenic medium and performed Oil Red O staining and quantitative analysis. Finally, we assessed PPARγ expression to explore IGF-1’s involvement in PRMT7’s regulation of adipogenic differentiation in hBMSCs.<b>Results</b> (1) During the adipogenesis process of hBMSCs, the expression level of PRMT7 was significantly reduced (<i>P</i><0.01). (2) The adipogenic differentiation ability of PRMT7 knockdown group was significantly stronger than that of control group (<i>P</i><0.001). (3) The ectopic adipogenic differentiation ability of PRMT7 knockdown group was significantly stronger than that of control group. (4) The adipogenic differentiation ability of the PRMT7 overexpression group was significantly weaker than that of the control group (<i>P</i><0.01). (5) The expression level of IGF-1 increased after PRMT7 knockdown (<i>P</i><0.000 1). The expression level of IGF-1 decreased after PRMT7 overexpression (<i>P</i><0.000 1), indicating that PRMT7 regulates the expression of IGF-1. After siIGF-1 transfection, the expression level of IGF-1 in all cell lines decreased significantly (<i>P</i><0.001). The ability of adipogenic differentiation of knockdown group transfected with siIGF-1 was significantly reduced (<i>P</i><0.01), indicating that IGF-1 affects the regulation of PRMT7 on adipogenic differentiation of hBMSCs.<b>Conclusion</b> In this investigation, our findings elucidate the inhibitory role of PRMT7 in the adipogenic differentiation of hBMSCs, as demonstrated through both <i>in vitro </i>cell-level experiments and<i> in vivo</i> subcutaneous transplantation experiments conducted in nude mice. Mechanistic exploration revealed that PRMT7’s regulatory effect on the adipogenic differentiation of hBMSCs operates <i>via</i> modulation of IGF-1 signaling pathway. These collective findings underscore PRMT7 as a potential therapeutic target for fatty metabolic disorders, thereby offering a novel avenue for leveraging PRMT7 and hBMSCs in the therapeutic landscape of relevant diseases.]]></description>
<pubDate>2024/7/30 17:10:40</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[GUO Qian,QING Jia,LU Da-Zhuang,WANG Xu,LI Yang,ZHANG Hui,ZHANG Ying-Fei,LIU Yun-Song,ZHOU Yong-Sheng and ZHANG Ping]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>GUO Qian,QING Jia,LU Da-Zhuang,WANG Xu,LI Yang,ZHANG Hui,ZHANG Ying-Fei,LIU Yun-Song,ZHOU Yong-Sheng and ZHANG Ping</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20240099]]></guid><cfi:id>5</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Therapeutic Study on The Inhibition of Neuroinflammation in Ischemic Stroke by Induced Regulatory T Cells]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250019]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Neuroinflammation plays a crucial role in both the onset and progression of ischemic stroke, exerting a significant impact on the recovery of the central nervous system. Excessive neuroinflammation can lead to secondary neuronal damage, further exacerbating brain injury and impairing functional recovery. As a result, effectively modulating and reducing neuroinflammation in the brain has become a key therapeutic strategy for improving outcomes in ischemic stroke patients. Among various approaches, targeting immune regulation to control inflammation has gained increasing attention. This study aims to investigate the role of<i> in vitro </i>induced regulatory T cells (Treg cells) in suppressing neuroinflammation after ischemic stroke, as well as their potential therapeutic effects. By exploring the mechanisms through which Tregs exert their immunomodulatory functions, this research is expected to provide new insights into stroke treatment strategies.<b>Methods</b> Naive CD4<sup>+</sup> T cells were isolated from mouse spleens using a negative selection method to ensure high purity, and then they were induced <i>in vitro </i>to differentiate into Treg cells by adding specific cytokines. The anti-inflammatory effects and therapeutic potential of Treg cells transplantation in a mouse model of ischemic stroke was evaluated. In the middle cerebral artery occlusion (MCAO) model, after Treg cells transplantation, their ability to successfully migrate to the infarcted brain region and their impact on neuroinflammation levels were examined. To further investigate the role of Treg cells in stroke recovery, the changes in cytokine expression and their effects on immune cell interactions was analyzed. Additionally, infarct size and behavioral scores were measured to assess the neuroprotective effects of Treg cells. By integrating multiple indicators, the comprehensive evaluation of potential benefits of Treg cells in the treatment of ischemic stroke was performed.<b>Results</b> Treg cells significantly regulated the expression levels of both pro-inflammatory and anti-inflammatory cytokines <i>in vitro</i> and<i> in vivo</i>, effectively balancing the immune response and suppressing excessive inflammation. Additionally, Treg cells inhibited the activation and activity of inflammatory cells, thereby reducing neuroinflammation. In the MCAO mouse model, Treg cells were observed to accumulate in the infarcted brain region, where they significantly reduced the infarct size, demonstrating their neuroprotective effects. Furthermore, Treg cell therapy notably improved behavioral scores, suggesting its role in promoting functional recovery, and increased the survival rate of ischemic stroke mice, highlighting its potential as a promising therapeutic strategy for stroke treatment.<b>Conclusion</b> <i>In vitro</i> induced Treg cells can effectively suppress neuroinflammation caused by ischemic stroke, demonstrating promising clinical application potential. By regulating the balance between pro-inflammatory and anti-inflammatory cytokines, Treg cells can inhibit immune responses in the nervous system, thereby reducing neuronal damage. Additionally, they can modulate the immune microenvironment, suppress the activation of inflammatory cells, and promote tissue repair. The therapeutic effects of Treg cells also include enhancing post-stroke recovery, improving behavioral outcomes, and increasing the survival rate of ischemic stroke mice. With their ability to suppress neuroinflammation, Treg cell therapy provides a novel and effective strategy for the treatment of ischemic stroke, offering broad application prospects in clinical immunotherapy and regenerative medicine.]]></description>
<pubDate>2025/2/28 16:13:08</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[KANG Tian-Fang,MA Ai-Qing,CHEN Li-Qi,GONG Han,OUYANG Jia-Cheng,PAN Fan,PAN Hong and CAI Lin-Tao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>KANG Tian-Fang,MA Ai-Qing,CHEN Li-Qi,GONG Han,OUYANG Jia-Cheng,PAN Fan,PAN Hong and CAI Lin-Tao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250019]]></guid><cfi:id>4</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Catalpol Promotes Differentiation of Neural Stem Cells into Oligodendrocyte <i>via</i> Caveolin-1-dependent Pathway in The 3D Microfluidic Chip]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250337]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Cerebral palsy (CP) is a prevalent neurodevelopmental disorder acquired during the perinatal period, with periventricular white matter injury (PWMI) serving as its primary pathological hallmark. PWMI is characterized by the loss of oligodendrocytes (OLs) and the disintegration of myelin sheaths, leading to impaired neural connectivity and motor dysfunction. Neural stem cells (NSCs) represent a promising regenerative source for replenishing lost OLs; however, conventional two-dimensional (2D) <i>in vitro</i> culture systems lack the three-dimensional (3D) physiological microenvironment. Microfluidic chip technology has emerged as a powerful tool to overcome this limitation by enabling precise spatial and temporal control over 3D microenvironmental conditions, including the establishment of stable concentration gradients of bioactive molecules. Catalpol, an iridoid glycoside derived from traditional medicinal plants, exhibits dual antioxidant and anti-apoptotic properties. Despite its therapeutic potential, the capacity of catalpol to drive NSC differentiation toward OLs under biomimetic 3D conditions, as well as the underlying molecular mechanisms, remains poorly understood. This study aims to develop a microfluidic-based 3D biomimetic platform to systematically investigate the concentration-dependent effects of catalpol on promoting NSCs-to-OLs differentiation and to elucidate the role of the caveolin-1 (Cav-1) signaling pathway in this process.<b>Methods</b> We developed a novel multiplexed microfluidic device featuring parallel microchannels with integrated gradient generators capable of establishing and maintaining precise linear concentration gradients (0-3 g/L catalpol) across 3D NSCs cultures. This platform facilitated the continuous perfusion culture of NSC-derived 3D spheroids, mimicking the dynamic <i>in vivo</i> microenvironment. Real-time cell viability was assessed using Calcein-AM/propidium iodide (PI) dual staining, with fluorescence imaging quantifying live/dead cell ratios. Oligodendrocyte differentiation was evaluated through quantitative reverse transcription polymerase chain reaction (qRT-PCR) for <i>MBP</i> and <i>SOX10</i> gene expression, complemented by immunofluorescence staining to visualize corresponding protein changes. To dissect the molecular mechanism, the Cav-1-specific pharmacological inhibitor methyl-β-cyclodextrin (MCD) was employed to perturb the pathway, and its effects on differentiation markers were analyzed.<b>Results</b> Catalpol demonstrated excellent biocompatibility, with cell viability exceeding 96% across the entire tested concentration range (0-3 g/L), confirming its non-cytotoxic nature. At the optimal concentration of 0-3 g/L, catalpol significantly upregulated both MBP and SOX10 expression (<i>P</i><0.05, <i>P</i><0.01), indicating robust promotion of oligodendroglial differentiation. Intriguingly,<i> Cav-1</i> mRNA expression was progressively downregulated during NSC differentiation into OLs. Further inhibition of Cav-1 with MCD further enhanced this effect, leading to a statistically significant increase in OL-specific gene expression (<i>P</i><0.05, <i>P</i><0.01), suggesting Cav-1 acts as a negative regulator of OLs differentiation.<b>Conclusion</b> This study established an integrated microfluidic gradient chip-3D NSC spheroid culture system, which combines the advantages of precise chemical gradient control with physiologically relevant 3D cell culture. The findings demonstrate that 3 g/L catalpol effectively suppresses Cav-1 signaling to drive NSC differentiation into functional OLs. This work not only provides novel insights into the Cav-1-dependent mechanisms of myelination but also delivers a scalable technological platform for future research on remyelination therapies, with potential applications in cerebral palsy and other white matter disorders. The platform’s modular design permits adaptation for screening other neurogenic compounds or investigating additional signaling pathways involved in OLs maturation.]]></description>
<pubDate>2025/11/5 11:41:42</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[WANG Ya-Chen,WANG Liang,SHEN Li-Ming and LIU Jing]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Ya-Chen,WANG Liang,SHEN Li-Ming and LIU Jing</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250337]]></guid><cfi:id>3</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[TGF-β1-engineered Biomimetic Platelet Nanoparticles for Targeted Therapy of Ischemic Stroke]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250541]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Post-ischemic acute inflammation and the subsequent persistent dysregulation of the immune microenvironment represent major pathological drivers that aggravate neuronal injury and severely restrict functional recovery following ischemic stroke. Although current reperfusion therapies partially restore blood flow, they fail to effectively modulate the secondary inflammatory cascade and oxidative stress, which remain critical barriers to neurological restoration. To address this challenge, this study aimed to engineer and systematically evaluate a biomimetic nanosystem composed of transforming growth factor-β1 (TGF-β1)-loaded platelet membrane-camouflaged lipid nanoparticles (PLP). This nanosystem was designed to achieve dual lesion-targeted delivery and immune microenvironment remodeling. By verifying its spatiotemporal accumulation, anti-inflammatory activity, and neuroprotective efficacy, we sought to establish an integrated therapeutic strategy that simultaneously enables lesion targeting, immune regulation, and functional recovery after ischemic injury.<b>Methods</b> The physicochemical properties of PLP, including hydrodynamic particle size, zeta potential, structural stability, and morphology, were characterized using dynamic light scattering, zeta potential analysis, and transmission electron microscopy. The preservation of platelet membrane-derived adhesion and immunoregulatory proteins was confirmed by SDS-PAGE through comparative analysis of protein band profiles between PLP and native platelet membranes. The <i>in vitro</i> biological activities of PLP were evaluated using two complementary cellular models. LPS-induced M1-polarized RAW264.7 macrophages were employed to assess inflammatory modulation, while oxygen glucose deprivation/reperfusion (OGD/R)-induced BV2 microglial cells and SH-SY5Y neuronal cells were utilized to investigate neuroinflammatory regulation and neuronal protection. For<i> in vivo </i>validation, a transient middle cerebral artery occlusion (tMCAO) mouse model was established to mimic ischemia-reperfusion injury. The spatiotemporal biodistribution and lesion-targeting capability of the PLP were monitored through live fluorescence imaging. Therapeutic efficacy was comprehensively evaluated by triphenyltetrazolium chloride (TTC) staining, glial fibrillary acidic protein (GFAP) immunofluorescence analysis, body weight monitoring, and neurological severity score (NSS) assessment.<b>Results</b> PLP nanoparticles displayed a uniform spherical morphology, nanoscale particle size distribution, and stable negative surface charge, indicating favorable colloidal stability and circulation potential. SDS-PAGE results confirmed the effective retention of key platelet membrane proteins associated with endothelial adhesion, immune evasion, and inflammatory regulation, demonstrating the successful biomimetic construction. Optimal therapeutic concentrations were determined in OGD/R-induced BV2 cells, where PLP exhibited excellent cytocompatibility and anti-inflammatory activity. <i>In vitro</i> experiments demonstrated that PLP significantly inhibited the polarization of RAW264.7 macrophages toward the pro-inflammatory M1 phenotype and markedly reduced neuronal apoptosis under ischemia-reperfusion conditions. <i>In vivo</i> fluorescence imaging revealed that PLP rapidly accumulated in the ischemic brain hemisphere and maintained prolonged retention for up to 7 d, suggesting enhanced lesion-specific targeting and sustained drug release. Compared with control group, PLP treatment significantly reduced cerebral infarct volume, attenuated reactive astrogliosis, improved weight recovery, and accelerated neurological functional restoration, as reflected by significantly improved NSS scores.<b>Conclusion</b> This study establishes a multifunctional biomimetic nanoplatform that integrates platelet membrane-mediated active targeting with the anti-inflammatory, antioxidative, and neuroprotective properties of TGF-β1. The PLP system enables rapid lesion homing and long-term retention while synergistically regulating the post-stroke inflammatory microenvironment by suppressing pro-inflammatory immune activation, reducing neuronal apoptosis, and limiting excessive astrocyte reactivity. Importantly, this study proposes a conceptually therapeutic paradigm that combines targeted delivery with immune microenvironment remodeling to achieve comprehensive neurovascular protection. These findings provide strong experimental evidence supporting the translational potential of biomimetic nanotherapeutics as next-generation precision interventions for ischemic stroke.]]></description>
<pubDate>2026/2/7 8:22:53</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[CHEN Li-Qi,KANG Tian-Fang,HUANG Guo-Jun,YIN Ting,MA Ai-Qing,CAI Lin-Tao and PAN Hong]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Li-Qi,KANG Tian-Fang,HUANG Guo-Jun,YIN Ting,MA Ai-Qing,CAI Lin-Tao and PAN Hong</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250541]]></guid><cfi:id>2</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Polypeptide-based Nanocarriers for Oral Targeted Delivery of CAR Genes to Pancreatic Cancer]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250508]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Pancreatic ductal adenocarcinoma (PDAC) exhibits a limited response to current treatments due to its dense fibrotic stroma and highly immunosuppressive tumor microenvironment. In recent years, advancements in cellular immunotherapy, particularly chimeric antigen receptor macrophage (CAR-M) therapy, have offered new hope for pancreatic cancer treatment. Although CAR-M therapy demonstrates dual potential in directly killing tumor cells and remodeling the immune microenvironment, it still faces challenges such as complex <i>in vitro</i> preparation processes and low <i>in vivo</i> targeting and delivery efficiency. Therefore, developing strategies for efficient and targeted <i>in vivo</i> delivery of CAR genes has become crucial for overcoming current therapeutic limitations. This study aims to develop an orally administrable nano-gene delivery system for the targeted delivery of CAR genes to pancreatic tumor sites.<b>Methods</b> Core nano-gene particles (PNP/pCAR) were constructed by loading plasmid DNA encoding CAR (pCAR) with cationic polypeptides (PNP). Subsequently, PNP/pCAR was surface-modified with β-glucan to prepare the targeted nanoparticles (βGlus-PNP/pCAR). The loading efficiency of PNP for pCAR was quantitatively assessed by gel retardation assay. The particle size, Zeta potential, morphology, and storage stability of PNP/pCAR were characterized using a Malvern particle size analyzer and transmission electron microscopy. At the cellular level, RAW 264.7 macrophages were selected. The cytotoxicity of PNP/pCAR was evaluated using the CCK-8 assay. The cellular uptake efficiency and lysosomal escape ability of the nanoparticles were assessed <i>via</i> flow cytometry and confocal microscopy. Transfection efficiency was quantitatively evaluated by detecting the expression of the reporter gene GFP using flow cytometry. At the <i>in vivo</i> level, an orthotopic pancreatic cancer mouse model was established. Cy7-labeled βGlus-PNP/pCAR nanoparticles were administered orally, and the fluorescence distribution in mice was dynamically monitored at 1, 2, 4, 8, and 16 h post-administration using a small animal <i>in vivo</i> imaging system. Forty-eight hours after oral gavage, the mice were euthanized, and pancreatic tumor tissues were collected for further analysis of intratumoral fluorescence signals using the imaging system. Additionally, βGlus-PNP/pCAR-GFP nanoparticles loaded with the reporter gene (GFP) were administered orally. Forty-eight hours post-administration, pancreatic tumor tissues were harvested to prepare frozen sections, and GFP expression was observed and analyzed under a fluorescence microscope.<b>Results</b> The PNP carrier exhibited a high loading capacity for pCAR. The successfully prepared PNP/pCAR nanoparticles were regular spheres with a hydrodynamic diameter of approximately (120±10) nm and a Zeta potential of about +(6±1) mV. They maintained good structural stability after incubation in PBS buffer for 7 d. Cell experiments demonstrated that PNP/pCAR exhibited no significant cytotoxicity in RAW 264.7 cells while being efficiently internalized and effectively escaping lysosomal degradation. The transfection positive rate of PNP/pCAR-GFP in RAW 264.7 cells reached (25±3)%, surpassing that of Lipofectamine 2000-loaded pCAR-GFP (Lipo/pCAR-GFP), which was (20±1)%. <i>In vivo</i> experiments revealed that, compared to unmodified PNP/pCAR, βGlus-PNP/pCAR exhibited stronger <i>in situ</i> pancreatic tumor targeting ability after oral administration. Furthermore, oral administration of βGlus-PNP/pCAR-GFP resulted in significant GFP protein expression detectable within pancreatic tumor tissues.<b>Conclusion</b> This study successfully constructed and validated an orally administrable, pancreatic cancer-targeting polypeptide-based nano-gene delivery system. It provides an important technological foundation in delivery systems and experimental basis for the subsequent development of <i>in situ</i> CAR-M-based therapeutic strategies for pancreatic cancer.]]></description>
<pubDate>2026/1/14 10:00:02</pubDate>
<category><![CDATA[Rapid  Communications]]></category>
<author><![CDATA[XIN Feng,REN Jian,LI Zhao-Zhen,FANG Quan,LIANG Rui-Jing,LIU Lan-Lan and CAI Lin-Tao]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>XIN Feng,REN Jian,LI Zhao-Zhen,FANG Quan,LIANG Rui-Jing,LIU Lan-Lan and CAI Lin-Tao</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250508]]></guid><cfi:id>1</cfi:id><cfi:read>true</cfi:read></item>
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