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  • Endo-beta-N-acetylglucosaminidase (ENGase) is widely distributed in various organisms. The first reported ENGase activity was detected in Diplococcus pneumoniae in 1971. The protein (Endo D) was purified and its peptide sequence was determined in 1974. Three ENGases (Endo F1-F3) were discovered in Flavobacterium meningosepticum from 1982 to 1993. After that, the activity was detected from different species of bacteria, yeast, fungal, plant, mice, human, etc. Multiple ENGases were detected in some species, such as Arabidopsis thaliana and Trichoderma atroviride. The first preliminary crystallographic analysis of ENGase was conducted in 1994. But to date, only a few ENGases structures have been obtained, and the structure of human ENGase is still missing. The currently identified ENGases were distributed in the GH18 or GH85 families in Carbohydrate-Active enZyme (CAZy) database. GH18 ENGase only has hydrolytic activity, but GH85 ENGase has both hydrolytic and transglycosylation activity. Although ENGases of the two families have similar (β/α)8-TIM barrel structures, the active sites are slightly different. ENGase is an effective tool for glycan detection and glycan editing. Biochemically, ENGase can specifically hydrolyze β-1,4 glycosidic bond between the two N-acetylglucosamines (GlcNAc) on core pentasaccharide presented on glycopeptides and/or glycoproteins. Different ENGases may have different substrate specificity. The hydrolysis products are oligosaccharide chains and a GlcNAc or glycopeptides or glycoproteins with a GlcNAc. Conditionally, it can use the two products to produce a new glycopeptides or glycoprotein. Although ENGase is a common presentation in cell, its biological function remains unclear. Accumulated evidences demonstrated that ENGase is a none essential gene for living and a key regulator for differentiation. No ENGase gene was detected in the genomes of Saccharomyces cerevisiae and three other yeast species. Its expression was extremely low in lung. As glycoproteins are not produced by prokaryotic cells, a role for nutrition and/or microbial-host interaction was predicted for bacterium produced enzymes. In the embryonic lethality phenotype of the Ngly1-deficient mice can be partially rescued by Engase knockout, suggesting down regulation of Engase might be a solution for stress induced adaptation. Potential impacts of ENGase regulation on health and disease were presented. Rabeprazole, a drug used for stomach pain as a proton inhibitor, was identified as an inhibitor for ENGase. ENGases have been applied in vitro to produce antibodies with a designated glycan. The two step reactions were achieved by a pair of ENGase dominated for hydrolysis of substrate glycoprotein and synthesis of new glycoprotein with a free glycan of designed structure, respectively. In addition, ENGase was also been used in cell surface glycan editing. New application scenarios and new detection methods for glycobiological engineering are quickly opened up by the two functions of ENGase, especially in antibody remodeling and antibody drug conjugates. The discovery, distribution, structure property, enzymatic characteristics and recent researches in topical model organisms of ENGase were reviewed in this paper. Possible biological functions and mechanisms of ENGase, including differentiation, digestion of glycoproteins for nutrition and stress responding were hypothesised. In addition, the role of ENGase in glycan editing and synthetic biology was discussed. We hope this paper may provide insights for ENGase research and lay a solid foundation for applied and translational glycomics.
    Citation
    LU Xin-Rong, TONG Yong-Liang, KONG Wei-Li, ZOU Lin, SHEN Dan-Feng, Lü Shao-Xian, LIU Rui-Jie, ZHANG Shao-Xing, ZHANG Yu-Xin, HOU Lin-Lin, SUN Gui-Qin, CHEN Li.Endo-beta-N-acetylglucosaminidase: Possible Functions and Mechanisms[J].,2024,51(5):985-999.Export: BibTex EndNote
  • Neuronal network is the structural basis for the execution of higher cognitive functions in the brain. Research has shown that learning, memory, and neurodegenerative diseases are closely related to neuronal network plasticity. Therefore, uncovering the mechanisms that regulate and modify neuronal network plasticity is of great significance for understanding information processing in the nervous system and for the treatment of diseases. Currently, neuronal networks cultured on microelectrode array (MEA) provide an ideal model for investigating learning and memory mechanisms in vitro. Additionally, studying such models offers a unique perspective for the prevention and treatment of neurodegenerative diseases. In this review, we summarize relevant research on functional network construction based on recording the electrical signals of neuronal networks cultivated on MEA. We focus on two aspects: 2D neuronal networks and 3D brain organoid development, as well as the effects of open-loop and closed-loop electrical stimulation on neuronal network plasticity. Lastly, we provide an outlook on the future applications of studying neuronal network plasticity using in vitro cultured networks.
    Citation
    SHAO Qi, MENG Wei-Wei, LI Xiao-Hong, SHAO Wen-Wei.Plasticity of Cultured Neural Networks In Vitro[J].,2024,51(5):1000-1009.Export: BibTex EndNote
  • ZHANG Ya-Ning, ZHANG Yi-Fei
    2024, 51(5): 2024,51(5):1010-1022
    DOI: 10.16476/j.pibb.2023.0260
    As the vanguard of the innate immune system to recognize external environmental stimuli, macrophages can respond to subtle changes in the environment and achieve adaptive regulation of their own functions, playing a crucial role in maintaining homeostasis and resisting infection. Various mechanical stress stimuli including endogenous stress mediated by mechanical characteristics of extracellular matrix, and exogenous stress such as solid/liquid pressure, tension and fluid shear stress, exist in the physiological or pathological tissue microenvironment, which have important effects on the immune function of macrophages. The understanding of macrophage mechanobiology will contribute to the development of new immunotherapies targeting macrophages. This review focuses on the functional regulation of macrophages by mechanical stress, summarizes the research progress from the perspective of influencing cell adhesion, migration, phagocytosis and polarization, and summarizes the molecular mechanisms of macrophage mechanical sensing and transduction from the outside to the inside in three levels: cell membrane mechanical sensors, force signal transduction of cytoskeleton system, and YAP/TAZ-mediated gene expression regulation response to mechanical stress. In addition, the application prospects and future vision of macrophage mechanobiology research in tissue engineering, regenerative medicine, and tumor immunotherapy are discussed, providing strong support for a deeper understanding of the plasticity of macrophage function.
    Citation
    ZHANG Ya-Ning, ZHANG Yi-Fei.Regulation and Mechanism of Macrophage Function by Mechanical Force[J].,2024,51(5):1010-1022.Export: BibTex EndNote
  • Protein as the allergens could lead to allergy. In addition, a widespread class of allergens were known as glycans of N-glycoprotein. N-glycoprotein contained oligosaccharide linked by covalent bonds with protein. Recently,studies implicated that allergy was associated with glycans of heterologous N-glycoprotein found in food, inhalants, insect toxins, etc. The N-glycan structure of N-glycoprotein allergen has exerted an influence on the binding between allergens and IgE, while the recognition and presentation of allergens by antigen-presenting cells (APCs) were also affected. Some researches showed that N-glycan structure of allergen was remodeled by N-glycosidase, such as cFase I, gpcXylase, as binding of allergen and IgE partly decreased. Thus, allergic problems caused by N-glycoproteins could potentially be solved by modifying or altering the structure of N-glycoprotein allergens, addressing the root of the issue. Mechanism of N-glycans associated allergy could also be elaborated through glycosylation enzymes, alterations of host glycosylation. This article hopes to provide a separate insight for glycoimmunology perspective, and an alternative strategy for clinical prevention or therapy of allergic diseases.
    Citation
    ZHANG Yu-Xin, LIU Rui-Jie, ZHANG Shao-Xing, YUAN Shu-Ying, CHEN Yan-Wen, YE Yi-Lin, LIN Qian-Ge, LU Xin-Rong, TONG Yong-Liang, CHEN Li, SUN Gui-Qin.Allergy Associated With N-glycans on Glycoprotein Allergens[J].,2024,51(5):1023-1033.Export: BibTex EndNote
  • LEI Qian, DENG Yi-Hao, HE Hong-Yun
    2024, 51(5): 2024,51(5):1034-1042
    DOI: 10.16476/j.pibb.2023.0180
    Cerebral ischemic stroke is an acute cerebrovascular disease caused by cerebral vascular occlusion, and it is associated with high incidence, disability, and mortality rates. Studies have found that excessive or insufficient autophagy can lead to cellular damage. Autophagy consists of autophagosome formation and maturation, autophagosome-lysosome fusion, degradation and clearance of autophagic substrates within autolysosomes, and these processes collectively constitute autophagic flux. Research has revealed that cerebral ischemia can induce impaired fusion between autophagosomes and lysosomes, resulting in autophagic flux impairment. Intracellular membrane fusion is mediated by three core components: N-ethylmaleimide sensitive factor (NSF) ATPase, soluble NSF attachment protein (SNAP), and soluble NSF attachment protein receptors (SNAREs). SNAREs, after mediating fusion between autophagosomes and lysosomes, remain in an inactive complex state on the autolysosomal membrane, requiring NSF reactivation into monomers to perform subsequent rounds of membrane fusion-mediated functions. NSF is the sole ATPase capable of reactivating SNAREs. Recent studies have shown that cerebral ischemia significantly inhibits NSF ATPase activity, reducing its reactivation of SNAREs. This may be a pathological mechanism for impaired fusion between autophagosomes and lysosomes, leading to neuronal autophagic flux impairment. This article discusses the pathological mechanisms of NSF ATPase inactivation, including SNAREs dysregulation, impaired fusion between autophagosomes and lysosomes, and insufficient transport of proteolytic enzymes to lysosomes, and explores approaches to improve neuronal autophagic flux through NSF ATPase reactivation. It provides references for stroke treatment improvement and points out directions for further research.
    Citation
    LEI Qian, DENG Yi-Hao, HE Hong-Yun.Pathological Mechanism of Neuronal Autophagy Flow Disturbance Caused by NSF ATPase Inactivation After Cerebral Ischemia[J].,2024,51(5):1034-1042.Export: BibTex EndNote
  • ZHOU Yu, YU Hong-Bo, CAO Yuan, WANG Jun-Jie
    2024, 51(5): 2024,51(5):1043-1053
    DOI: 10.16476/j.pibb.2023.0277
    Cysteine dioxygenase 1 (CDO1) gene is a non-heme structured, iron-containing metalloenzyme involved in the conversion of cysteine to cysteine sulfinic acid to regulate cysteine accumulation in vivo. Elevated levels of cysteine have been shown to be cytotoxic and neurotoxic, and this is the first important step in the breakdown of cysteine metabolism in mammalian tissues. The human CDO1 gene is located on chromosome 5q23.2. Studies have shown that deletion or epigenetic silencing of this chromosomal region contributes to tumorigenesis. It is highly expressed in the liver and placenta, and weakly in the heart, brain and pancreas. CDO1 is a tumor suppressor gene (TSG) with a wide range of functions, which can be involved in various biological processes such as tumor cell proliferation, differentiation, apoptosis and iron death, thus affecting the tumor development. CDO1 is epigenetically regulated in human cancers, compared to normal tissues. The CDO1’s mRNA or protein expression levels were significantly down-regulated in tumor tissues, whereas promoter DNA methylation of the CDO1 gene usually accumulates with the progression of human cancers. Aberrant hypermethylation on the CDO1 promoter is a common event in tumor cells, which leads to transcriptional inactivation and silencing of the CDO1 gene. High frequency of methylation of CDO1 gene promoter methylation region in a variety of tumors including breast, oesophageal, lung, bladder, gastric and colorectal cancers. CDO1 gene promoter methylation levels reflect cancer progression and malignant tumorigenesis, which is a common molecular indicator explaining poor prognosis in human cancers. Treatment with 5-aza-2′-deoxycytidine (a drug that promotes demethylation) reactivated the CDO1 expression in most cancer cell lines, indicating that the transcriptional expression of CDO1 is closely correlated with its promoter methylation level, CDO1 gene promoter methylation and tumor progression have also received increasing attention from researchers. It was found that CDO1 gene promoter hypermethylation can be used as an early tumor marker for clinical aid diagnosis and helps to differentiate cancerous from benign diseases. It was also found that CDO1 promoter DNA methylation showed reliable tumor monitoring potential in human body fluids, and furthermore, the degree of CDO1 promoter methylation was strongly correlated with resistance to chemotherapy with tumor drugs, which would be helpful in evaluating the efficacy of chemotherapeutic drugs. Thus, CDO1, a common promoter methylation gene in human cancers, is closely associated with the development of a wide range of tumors and is one of the most promising candidate genes for assessing tumor-specific epigenetic changes. This article reviews the biological functions of CDO1 and its promoter DNA methylation in tumors, focusing on the mechanism of CDO1 DNA promoter methylation in tumors, with a view to providing theoretical guidance for the clinical diagnosis and treatment of tumors with CDO1 as a potential therapeutic target.
    Citation
    ZHOU Yu, YU Hong-Bo, CAO Yuan, WANG Jun-Jie.Application of CDO1 Gene Promoter Methylation in Tumors[J].,2024,51(5):1043-1053.Export: BibTex EndNote
  • LI Xiang, LI Ye
    2024, 51(5): 2024,51(5):1054-1066
    DOI: 10.16476/j.pibb.2023.0287
    Extracellular vesicles (EVs) are a kind of exsomes secreted by cells, which all cells release them as part of their normal physiology and during acquired abnormalities. EVs can be broadly divided into two categories by their sizes, small EVs (sEVs) and medium/large EVs (m/l EVs). As a kind of extracellular vesicle, sEVs are mostly discoid vesicles with diameters ranging from 40 nm to 200 nm. The medium/large EVs are elliptical with a diameter more than 200 nm. sEVs play a crucial role in intercellular communication and have emerged as important mediators in the development and progression of liver diseases. In this review, we discussed the current understanding of the role of sEVs, particularly sEV derived non-coding RNA in non-alcoholic fatty liver disease (NAFLD) and their potential as diagnostic and therapeutic targets. sEVs are small membrane-bound particles secreted by cells, which fuse with plasma membrane and release to extracellular matrix. Depending on the cell of origin, sEVs could contain many cell constituents, including various DNA, RNA, lipids, metabolites, and cytosolic and cell-surface proteins, biomolecules. In addition, many RNA and DNA molecules contained by sEVs, such as mRNA, microRNA (miRNA), long noncoding RNA (lncRNA) and mitochondrial DNA (mtDNA), can be transferred to recipient cells to effectively promote their biological response, physiological and pathological functions. Such sEVs-mediated responses can be disease promoting or restraining. The intrinsic properties of sEVs in regulating complex intracellular pathways has advanced their potential utility in the therapeutic control of many diseases. Recent studies reviewed here also indicate a functional, targeted, mechanism-driven accumulation of specific cellular components in sEVs, suggesting that they have a role in regulating intercellular communication. Many studies have also shown the involvement of sEVs’ noncoding RNAs (ncRNAs) in controlling cell activities and their crucial functions in regulating lipid metabolism. sEVs ncRNAs, including miRNAs, lncRNAs, and circular RNAs (circRNAs) regulate physiological functions and maintain lipid metabolism homeostasis. miRNA are small non-coding RNA molecules that regulate posttranscriptional gene expression by repressing messenger RNA-targets. These circulating miRNAs are easily accessible, disease-specific and sensitive to small changes, which makes them ideal biomarkers for diagnostic, prognostic, predictive or monitoring purposes. Specific miRNA signatures can be reflective of disease status and development or indicators of poor treatment response in liver diseases. And lncRNAs have been shown to regulate gene expression by interacting with transcription factors or chromatin-modifying enzymes, which regulate gene expression by binding to target mRNAs. Then circRNAs contributed to NAFLD progression by acting as miRNA sponges, functional protein sponges, or novel templates for protein translation. Finally, sEVs could be engineered to deliver diverse therapeutic payloads, including short interfering RNAs, antisense oligonucleotides and so on, with an ability to direct their delivery to a desired target. The potential of targeting sEVs with lncRNAs and microRNAs not only could be potential diagnostic biomarkers for NAFLD, but also have potential therapeutic effects on NAFLD, which might provide new ideas for the NAFLD treatment. In conclusion, this review provides an overview of the current understanding of the roles of sEVs ncRNAs in NAFLD, so we suggest that further research into sEVs could lead to new diagnostic tools and therapeutic strategies for NAFLD.
    Citation
    LI Xiang, LI Ye.The Roles of Small Extracellular Vesicles and Small Extracellular Vesicles-derived Non-coding RNA in Non-alcoholic Fatty Liver Disease[J].,2024,51(5):1054-1066.Export: BibTex EndNote
  • WU Sheng-Quan, YANG Meng, LIU Xin-Guang
    2024, 51(5): 2024,51(5):1067-1078
    DOI: 10.16476/j.pibb.2023.0305
    Chronic kidney disease (CKD) has become a significant global public health problem. It is defined as chronic renal structural and functional dysfunction caused by various reasons. The prevalence of obesity and diabetes has increased dramatically in developing countries, which substantially affected the patterns of CKD observed in these regions. It’s inevitable that the disease spectrum of CKD is converting to metabolic diseases. CKD is also considered an independent risk factor for renal aging and cardiovascular disease in the elderly, which usually progresses to end-stage renal disease (ESRD). Renal interstitial fibrosis is the pathological basis of ESRD and is a microscopic manifestation of renal aging. Conversely, renal aging is a risk factor for interstitial fibrosis. Although the healthy kidney has a relatively low lipid level, CKD-associated dyslipidemia has been extensively studied. Nevertheless, less is known about the contribution of lipid disorders to the development of renal senescence and interstitial fibrosis. Recent studies have demonstrated that lipid metabolism disorders occur in the progress of renal aging and interstitial fibrosis. Renal lipids accumulate once lipid uptake and synthesis exceed the balance with lipolysis, which is mainly characterized by increased levels of triglyceride (TG) and oxidized low-density lipoprotein, and decreased levels of high-density lipoprotein. Excessive lipid accumulation in the kidney not only induces lipotoxicity and endoplasmic reticulum stress but also increases intracellular and mitochondrial reactive oxygen species, which induce stress injury and senescence in renal tubular epithelial cells. Pro-inflammatory and pro-fibrotic cytokines in a senescence-associated secretory phenotype secreted by senescent renal tubular epithelial cells further accelerate their senescence as well as the occurrence of inflammation and pericyte loss, promoting secretion of extracellular matrix (ECM) and subsequent fibrosis in the tubulointerstitial compartment. In addition, podocyte hypertrophy also leads to glomerulosclerosis. Currently, most of the studies on inhibiting or even reversing renal interstitial fibrosis are still in the experimental stage. What’s more, effective drugs to slow down renal aging have not been reported. Many inflammatory and fibrotic factors are both components of the senescence-associated secretory phenotype (SASP), nevertheless, they are not sufficient to recognize cellular senescence. Given that indicators of senescence may vary from disease to disease and organ to organ, there is a need for more sensitive and specific senescence assays. Crucial enzymes and regulatory proteins of lipid metabolic pathways are expected to be potential targets for ameliorating renal aging and interstitial fibrosis. Lipid-lowering approach might represent another therapeutic in the management of kidney injury associated with metabolic dysfunction. Thus, clarifying the molecular regulatory mechanisms of lipid metabolism in kidney is extremely important for the delay of renal aging and the treatment of interstitial fibrosis. This review outlines the effects of lipid metabolism disorders on renal aging and renal fibrosis, analyses the role of lipid metabolism disorders in the development of renal diseases, and summarizes the potential targets and strategies for the prevention of renal aging and renal fibrosis based on lipid metabolism regulation, which will provide a reference for the discovery of new targets for the treatment of renal fibrosis.
    Citation
    WU Sheng-Quan, YANG Meng, LIU Xin-Guang.Role of Lipid Metabolism Disorders in Renal Ageing and Renal Fibrosis[J].,2024,51(5):1067-1078.Export: BibTex EndNote
  • Objective To investigate the expression of cyclin-dependent kinase 8 (CDK8) in esophageal squamous cell carcinoma (ESCC) and its effect on ESCC cells, and to explore its potential molecular mechanism.Methods The expression level of CDK8 mRNA was analyzed by UALCAN database, and then the expression level of CDK8 protein in tumor tissues of ESCC patients was detected by immunohistochemistry(IHC). Esophageal cancer cell lines Kyse-30 and Kyse-150 were stably transfected with lentivirus to knockdown and overexpression of CDK8. EdU proliferation assay, cell colony formation assay, cell cycle assay, cell scratch assay and invasion assay were used to explore the effect of CDK8 protein expression level on the phenotype of esophageal squamous cell carcinoma cells. Subsequently, the effect of CDK8 on the growth of esophageal cancer xenografts in vitro was observed by subcutaneous tumor formation assay in mice. Finally, the expression of proliferation and metastasis related proteins was detected by Western blot.Results CDK8 showed high transcription and protein expression levels in ESCC tissues compared with normal esophageal tissues. Knockdown of CDK8 expression significantly inhibited the proliferation, migration and invasion of ESCC cells. In addition, inhibition of CDK8 expression significantly affected the JAK2/STAT3 pathway and the expression of E-Cadherin/ N-Cadherin, while overexpression of CDK8 reversed these effects. Inhibition of STAT3 pathway reversed the promoting effect of CDK8 overexpression on ESCC cell phenotype.Conclusion CDK8 is a cancer-promoting factor of ESCC, which mediates the phosphorylation of JAK2/ STAT3 and epithelial-mesenchymal transition (EMT).
    Citation
    QU Hang-Shuai, TIAN Xiong, PAN Yi-Xiao, BAO Jia-Qian, YE Lu-Xia, Zheng Jing-Min.CDK8 Promotes Cell Proliferation, Migration and Invasion in Esophageal Squamous Cell Carcinoma Through JAK/ STAT3/EMT Pathway[J]..Export: BibTex EndNote
  • Objective The controllability changes of structural brain network were explored based on the control and brain network theory in young smokers, this may reveal that the controllability indicators can serve as a powerful factor to predict the sleep status in young smokers.Methods Fifty young smokers and 51 healthy controls from Inner Mongolia University of Science and Technology were enrolled. Diffusion tensor imaging (DTI) was used to construct structural brain network based on fractional anisotropy (FA) weight matrix. According to the control and brain network theory, the average controllability and the modal controllability were calculated. Two-sample t-test was used to compare the differences between the groups and Pearson correlation analysis to examine the correlation between significant average controllability and modal controllability with Fagerstr?m Test of Nicotine Dependence (FTND) in young smokers. The nodes with the controllability score in the top 10% were selected as the super-controllers. Finally, we used BP neural network to predict the Pittsburgh Sleep Quality Index (PSQI) in young smokers.Results The average controllability of the dorsolateral superior frontal gyrus, supplementary motor area, lenticular nucleus putamen, and lenticular nucleus pallidum in the young smokers’ group, and the modal controllability of the orbital inferior frontal gyrus, supplementary motor area, gyrus rectus, and posterior cingulate gyrus, were all significantly different from those of the healthy controls group (P<0.05). The average controllability of the right supplementary motor area (SMA. R) in the young smokers group was positively correlated with FTND (r=0.393 0, P=0.004 8), while modal controllability was negatively correlated with FTND (r=-0.330 1, P=0.019 2).Conclusion The controllability of the structural brain network in young smokers is abnormal. which may serve as an indicator to predict sleep condition. It may provide the imaging evidence for evaluating the cognitive function impairment in young smokers.
    Citation
    DING Jing-Jing, DONG Fang, WANG Hong-De, YUAN Kai, CHENG Yong-Xin, WANG Juan, MA Yu-Xin, XUE Ting, YU Da-Hua.Controllability Analysis of Structural Brain Networks in Young Smokers[J]..Export: BibTex EndNote
  • Objective Dust has steadily emerged as a frontier research in the field of forensic science because it is a material evidence with significant features and application potential that carries rich environmental DNA information. However, as a crucial foundational step in forensic applications, the collection and DNA extraction research of dust on object surfaces from the perspective of practical applications in forensic science are still in urgent need of development.Methods Dust was collected from object surfaces using a Copan Liquid Amies Elution Swab. DNA was extracted separately from the swab head, sediment, and supernatant within the sample collection tube to evaluate DNA content, thereby determining which components within the tube should be processed and lysed. Dust samples were collected according to five different sampling areas (25-400 cm2) and the DNA concentration was measured to determine the optimal sampling area. The extraction efficiency of three commercial DNA extraction kits for dust samples was compared. The size of the DNA fragments extracted from the dust was analyzed, as well as the presence of human DNA. Additionally, 16S rDNA amplicon sequencing was used to analyze the bacterial information in dust DNA from object surfaces. This process aimed to establish a quality control method for dust DNA extraction. Regarding the critical step of cell lysis in DNA extraction, the quantity of DNA extracted was compared and evaluated under different cell lysis methods and varying vortexing times. This was done to establish an appropriate cell lysis method for dust DNA extraction.Results The sediment and swab head in the dust sampling tube are the primary sources of DNA, and both should be included in subsequent extraction processes. The sampling area of dust is positively correlated with dust DNA concentration, and it is recommended that the sampling area be larger than 5×5 cm2. Using the DNeasy PowerSoil Pro kit can yield a higher amount of DNA. Additionally, there were no significant differences in the sizes of DNA fragments extracted by the three different DNA extraction kits. No human DNA was detected in the DNA extracted from the dust samples, while bacterial DNA was present in the dust from object surfaces. Furthermore, there were differences in microbial species composition between different sampling points. Additionally, using a biological sample homogenizer to grind and lyse for 4 min (2 min× 2 times) resulted in the highest concentration of dust DNA.Conclusion The extraction of dust DNA is influenced by the sampling area, extraction kits, and lysis methods. It is crucial to establish a comprehensive and suitable dust DNA extraction scheme. This not only lays the foundation for researching and extracting environmental DNA data from dust, but also provides a methodological reference for forensic case work involving environmental samples.
    Citation
    YANG Qi, PENG Jia-Jin, WANG Le, LU Qi, MEI Hong-Cheng, GE Wen-Dong, ZHANG Tao, JI An-Quan, YE Jian, KANG Ke-Lai.Optimization of Dust Collection and DNA Extraction Methods on Object Surfaces[J]..Export: BibTex EndNote
  • Parkinson"s disease (PD) is a neurodegenerative disorder characterized by muscle rigidity, resting tremor, and postural instability, which severely impair the quality of life in middle-aged and elderly individuals. PD"s pathogenesis is complex, involving oxidative stress, immune inflammation, and genetic factors. Despite extensive research, precise therapeutic targets for PD remain elusive, necessitating further investigation into its underlying mechanisms. Recent studies highlight the pivotal role of regional brain iron overload, oxidative stress, and lipid peroxidation in PD"s pathogenesis. Ferroptosis, a form of regulated cell death driven by iron dependency and lipid peroxidation, has emerged as a critical factor in PD pathology. This review examines the relationship between ferroptosis and PD and explores the potential of exercise as a therapeutic intervention to modulate ferroptosis and alleviate PD symptoms. Ferroptosis, distinct from other forms of cell death such as necrosis, autophagy, pyroptosis, and apoptosis, is characterized by mitochondrial shrinkage, reduced cristae, and membrane collapse, without nuclear fragmentation, DNA cleavage, or caspase activation. It is induced by the accumulation of intracellular Fe2+, which enhances lipid peroxidation and reactive oxygen species (ROS) generation, ultimately leading to cell death. Studies show disrupted iron metabolism in PD patients, with elevated iron levels in dopaminergic neurons of the substantia nigra correlating with disease severity. Iron chelation therapy has shown promise in alleviating PD symptoms by reducing brain iron levels, highlighting the significance of iron metabolism in PD pathogenesis. Lipid peroxidation, a hallmark of ferroptosis, involves the oxidation of polyunsaturated fatty acids (PUFAs) in cell membranes, compromising membrane integrity and increasing permeability. Elevated lipid peroxidation in the substantia nigra contributes to neuronal damage in PD. Enzymes such as ACSL4 and LPCAT3, crucial in PUFA metabolism, play significant roles in ferroptosis. Exercise has been shown to modulate these enzymes, potentially reducing lipid peroxidation and preventing ferroptosis in PD. Glutathione (GSH) metabolism is another crucial factor in ferroptosis regulation. GSH depletion impairs ROS detoxification, exacerbating oxidative stress and lipid peroxidation. PD patients exhibit reduced GSH levels in the substantia nigra, making dopaminergic neurons more vulnerable to oxidative damage. Exercise enhances GSH synthesis and activity, mitigating oxidative stress and ferroptosis in PD. α-synuclein aggregation, a hallmark of PD, is closely linked to iron metabolism and oxidative stress. Excessive α-synuclein binds to iron, promoting its aggregation and inducing ferroptosis. Exercise has been found to reduce α-synuclein accumulation and its pathological phosphorylation, potentially through the upregulation of neuroprotective proteins like DJ-1 and Irisin. These proteins enhance antioxidant defenses and facilitate α-synuclein degradation, providing a protective effect against PD progression. Additionally, glutamate excitotoxicity, driven by dysregulated glutamate metabolism and receptor activity, contributes to ferroptosis in PD. Exercise modulates glutamate levels and receptor expression, reducing excitotoxicity and iron-induced neuronal damage. In conclusion, emerging research suggests that exercise may inhibit ferroptosis through multiple mechanisms, including regulation of iron metabolism, enhancement of antioxidant defenses, reduction of α-synuclein aggregation, and modulation of glutamate metabolism. These findings highlight the potential of exercise as a non-pharmacological intervention in the prevention and treatment of PD. Further research is needed to elucidate precise mechanisms and optimize exercise protocols for maximum therapeutic benefit.
    Citation
    LU Dong-Lei, ZHANG Wen-Yu, TAN Si-Jie, YANG Feng-Ying.Exercise-induced Modulation of Ferroptosis: Potential Mechanisms for Improvement in Parkinsons Disease[J]..Export: BibTex EndNote
  • Objective Chronic stress can induce cognitive dysfunction, but the underlying mechanisms remain unknown. Studies have confirmed that the high mobility group box 1/Toll-like receptor 4 (HMGB1/TLR4) pathway is closely associated with cognitive impairment. Therefore, this research aimed to explore whether the HMGB1/TLR4 pathway involves in chronic stress-induced cognitive dysfunction.Methods The chronic unpredictable mild stress (CUMS) mouse model was established by randomly giving different types of stress every day for four consecutive weeks. Cognitive function was detected by novel object recognition test, Y-maze test, and Morris water maze test. The protein expressions of HMGB1, TLR4, B-cell lymphoma 2 (BCL2), and BCL2 associated X (BAX) were determined by Western blot. The damage of neurons in the hippocampal CA1 region was observed by hematoxylin-eosin (HE) staining.Results The protein expressions of HMGB1 and TLR4 were significantly increased in the hippocampus of chronic stress mice. Furthermore, inhibition of the HMGB1/TLR4 pathway induced by ethyl pyruvate (EP, a specific inhibitor of HMGB1) and TAK-242 (a selective inhibitor of TLR4) treatment attenuated cognitive impairment in chronic stress mice, according to the novel object recognition test, Y-maze test, and Morris water maze test. In addition, administration of EP and TAK-242 also mitigated the increase of apoptosis in the hippocampus of chronic stress mice.Conclusion These results indicate that the hippocampal HMGB1/TLR4 pathway contributes to chronic stress-induced apoptosis and cognitive dysfunction.
    Citation
    HU Wen, KUANG Xin, FENG Xin-Xiang, ZHONG Wen-Long, JIN Xin, JIANG Jia-Mei, ZOU Wei.Hippocampal HMGB1/TLR4 Pathway Mediates Cognitive Dysfunction in Chronic Stress Mice[J]..Export: BibTex EndNote
  • Integrated stress response (ISR) is an evolutionarily conserved intracellular signaling network. When the body encounters adverse stimuli, ISR is activated to assist cells, tissues, and the body in adapting to the changing environment and maintaining health by reprogramming genes. ISR is implicated in the onset and progression of various diseases, including cardiovascular disease, diabetes, obesity, cancer, and neurological disorders. A key factor in ISR is the eukaryotic initiation factor 2α (eIF2α) kinase. Four eIF2α kinases have been identified, namely general control non-derepressible-2 (GCN2), protein kinase double-stranded RNA-dependent (PKR), PKR-like ER kinase (PERK), and heme-regulated inhibitor (HRI). GCN2, PKR, PERK, and HRI kinases share a common kinase catalytic domain but have distinct regulatory domains that are activated by endoplasmic reticulum stress (ERS), viral infection, heme deficiency, and amino acid deficiency, respectively. Various stress conditions promote the phosphorylation of eIF2α at serine 51 by its 4 kinases. This inhibits the eIF2B-mediated GTP acquisition of eIF2α and reduces the translation rate. At the same time, ISR upregulates ATF4 expression. ATF4 and CCAAT-enhancer binding protein (CHOP) can promote downstream growth arrest and DNA damage-inducible protein 34 (GADD34) to mediate eIF2α dephosphorylation. At the same time, it can promote the downstream expression of Sestrin 2 (SESN2) protein, increase autophagy induced by mTORC1 and AMPK, and thereby reduce the risk of cardiovascular disease. Numerous animal and cellular studies have demonstrated that exercise, drugs, and molecular compounds can prevent and improve pathological myocardial hypertrophy, diabetic cardiomyopathy, ischemic cardiomyopathy, cardiotoxicity, and atherosclerosis by modulating ISR. The relevant mechanism involves gene knockout or inhibitors that directly inhibit the expression of eIF2α kinase. Aerobic exercise, editing of specific molecules, or drugs can indirectly inhibit the expression of eIF2α kinase, ultimately leading to the inhibition of the downstream expression of eIF2α/ATF4. In light of the significant pathological role of ISR in cardiovascular disease, current research on ISR primarily aims to develop medications that can regulate the upstream and downstream signaling activities of ISR. This involves targeting ISR to regulate intracellular protein homeostasis, ultimately aiming to delay or reverse the progression of cardiovascular disease. At present, drugs targeting ISR in cardiovascular disease research mainly include ISRIB, 4-PBA, and Salubrinal. ISRIB reverses eIF2α phosphorylation by suppressing the inhibitory effect of eIF2α on protein synthesis and blocking eIF2α/ATF4 signaling. 4-PBA can inhibit endoplasmic reticulum stress. Salubrinal inhibits eIF2α dephosphorylation by inhibiting the binding of GADD34-PP1 and CReP-PP1 complexes to eIF2α. In conclusion, the integrated stress response mediated by the four eIF2α kinases is essential for the body to adapt to various stress stimuli affecting the heart and blood vessels under normal or pathological conditions. Integrated stress response inhibitors should be promptly administered to clinical cardiovascular patients to assess their effectiveness in the onset and development of various cardiovascular diseases, as well as to evaluate potential side effects. Future studies are needed to explore the role and mechanism of eIF2α kinase-mediated integrative stress response in various diseases. It is also essential to investigate whether the integrative stress response yields different effects in various organs and can potentially exert cross-organ efficacy through inter-organ interaction.
    Citation
    SUN Zhong-Guang, LI Ting-Ting, ZHANG Ming-Chen, ZHANG Hui, CHEN Ming-Hua, FENG Li-Xu.The Role and Mechanism of eIF2α Kinase-mediated Integrated Stress Response in The Treatment of Cardiovascular Diseases[J]..Export: BibTex EndNote
  • Objective The inference of biogeographical ancestry (BGA) using DNA is a significant focus within anthropology and forensic science. Current methods often utilize dozens of ancestry-informative SNPs, employing principal component analysis (PCA) and likelihood ratios (LR) to ascertain individual ancestries. Nonetheless, the selection of these SNPs tends to be population-specific and shows limitations in population differentiation. With the development of high-throughput sequencing technologies, acquiring high-density SNP datasets has become easier, challenging traditional statistical models which are often reliant on prior assumptions and struggle with high-density genetic data. The integration of machine learning, which prioritizes data learning and algorithmic iteration over prior knowledge, has propelled forward new developments in BGA research. This study aims to construct a BGA inference model suitable for high-density SNP data, characterized by broad population applicability, higher accuracy, and strong generalization capabilities.Methods Initially, intersection sites of autosomes from the phase III data of the 1000 Genomes Project and commonly used commercial chips were selected to build a reference dataset after thorough site quality control and filtering. This dataset was analyzed using PCA and ADMIXTURE to study population clustering, ancestral component mixing, and genetic substructures. Utilizing spaces of different principal component (PC), combinations, this study visually assessed the PCs" capabilities to differentiate between continental and intercontinental populations. Following this, the study employed the supervised learning classification model XGBoost, establishing a multidimensional PC-based PCA-XGBoost model with hyperparameters set through ten-fold cross-validation and a greedy strategy. Subsequently, the model was optimized and evaluated based on the LR, considering accuracy and runtime to determine the optimal number of PCs and training rounds, culminating in the study"s optimal BGA inference model. Finally, the performance of the model was subsequently validated at national and regional levels using test sets from other public data to assess its post-optimization generalization capabilities.Results The reference dataset created contains 307 866 SNP sites. Top PCs reflect varying levels of population differentiation capabilities, with some PCs showing population specificity. Under smaller K values in ADMIXTURE results, genetic ancestral components between continents are elucidated, while larger K values reveal some specific ancestral components of certain populations within continents. The number of PCs and training rounds significantly affect the classification accuracy and efficiency of the XGBoost supervised model. With LR-based evaluation methods, the optimized PCA-XGBoost model achieved a continental prediction accuracy of over 98% in the reference set. For subcontinental population levels within the continents, the model achieved an accuracy of over 95% in the reference set and over 90% in the test set.Conclusion The reference dataset effectively represents the genetic substructures of populations at selected sites. Information derived from PC dimensions significantly aids in population differentiation and inference issues, and incorporating more PC dimensions as features in supervised learning models can increase the accuracy of BGA inference. The model of this study is suitable for high-density SNP data and is not confined to specific regional populations, offering enhanced population-wide applicability. Compared to previous ancestry inference models, the optimized PCA-XGBoost model demonstrates high intercontinental population predictive accuracy. LR-based evaluation methods further enhance the reliability of predictions. Additionally, the model"s strong generalization capabilities suggest that updating the reference population data could enable more detailed population analysis and inference.
    Citation
    YAO Hao-Tian, JIANG Li, WANG Chun-Nian, FAN Hong, LI Cai-Xia.Research on The Intercontinental Population Biogeographic Ancestral Inference Model Based on PCA-XGBoost Method[J]..Export: BibTex EndNote
  • Chimeric antigen receptor T (CAR-T) cell therapy is an innovative and cutting-edge treatment in the field of adoptive cell therapy. It represents an important milestone in personalized and precision medicine. T cell immunotherapy has gone through more than 30 years of development, making CAR-T cell therapy increasingly mature. Currently, CAR-T cell therapy has achieved significant success in the treatment of hematological system tumors, and the FDA has approved 6 CAR-T cell therapies for the treatment of hematopoietic cancers. However, on one hand, the preparation of CAR-T cells is a highly technical process involving multiple steps, each requiring precise operation and strict condition control to ensure the quality and activity of the cells. The high-quality materials, specialized equipment, and highly specialized personnel required in the production process have led to very high preparation costs for CAR-T cell therapy. The high cost has led to increased treatment fees, which may limit the popularization and accessibility of CAR-T therapy. On the other hand, CAR-T cell therapy faces a series of difficulties and challenges in the treatment of solid tumors. The first is the insufficient targeting and infiltration ability of CAR-T cells to tumors. The tumor microenvironment (TME) of solid tumors is usually composed of dense extracellular matrix, forming a physical barrier that severely limits the targeting and penetration ability of CAR-T cells to tumors. The second is the immunosuppressive factors in the TME. In the TME, there are a large number of immunosuppressive factors, such as interleukin-10, transforming growth factor β, and suppressive cells including regulatory T cells, tumor-associated macrophages, and myeloid-derived suppressor cells. These factors not only weaken the persistence of CAR-T cells but also severely hinder their effective anti-tumor effect. Finally, CAR-T cell therapy can cause serious cytotoxicity. The activation of CAR-T cells may cause cytokine release syndrome and attack normal cells expressing the CAR-T target antigen, causing "off-target" toxicity, and thus causing systemic inflammatory reactions and potential serious side effects. These factors lead to unsatisfactory therapeutic effects of CAR-T cell therapy. Fortunately, the advancement of nanotechnology has brought new hope to this field. In particular, nano drug delivery systems have become an extremely active research direction in the development of anti-tumor drugs. Nanoparticle delivery systems can address the challenges encountered by CAR-T cell therapy in treating solid tumors through various mechanisms. These mechanisms include enhancing tumor targeting and CAR-T cell penetration ability, regulating the tumor"s suppressive microenvironment, and overcoming the side effects of CAR-T cell therapy. The implementation of these strategies is expected to significantly improve the efficacy of CAR-T cell therapy in the treatment of solid tumors, thereby bringing more significant therapeutic effects to patients. This article focuses on the background of CAR-T therapy and solid tumor treatment, systematically reviews the application of nanotechnology in CAR-T cell preparation and solid tumor treatment in vitro and in vivo in recent years, and provides a forward-looking perspective on future development directions.
    Citation
    XU Lin, HU Bo, ZHENG Lu-Lu, JIANG Shao-Ping, RUAN Shao-Bo, HUANG Yuan-Yu.Application of Nanotechnology in CAR-T-based Cancer Therapy[J]..Export: BibTex EndNote
  • Proteins in biological systems rarely act alone, but instead bind with other biomolecules to trigger specific cellular reactions. These biomolecules are usually astonishing number of proteins self-assemble to form dimers, which are both in a relatively isolated state and in a protein interaction network and cascade. Dimerization can endow proteins with various structural and functional advantages, including improving stability, controlling the accessibility and specificity of active sites, and increasing complexity. The self-association of proteins to form dimers is a very common phenomenon, and the functional importance of homologous protein dimerization cannot be overestimated. It provides diversity and specificity in many pathways, and most cellular events, such as signal transduction, transcription cofactor recruitment, enzyme activation, and even pathogenic pathways, are significantly regulated through homologous protein-protein interactions. The regulation of protein dimerization is an important process for the growth and development of organisms under internal or external stimuli in the natural environment. Therefore, regulating the dimerization process of homologous proteins and understanding their molecular mechanisms are crucial for biomedical applications and analyzing complex biological regulatory networks. Proximity effects or physical proximity effects of molecules are essential regulatory factors in biological processes, which can be controlled through induced dimerization methods. The application range of induced proximity ranges from manipulating protein folding, activation, localization, and degradation to controlling gene transcription or cell therapy. The chemical induced dimerization (CID) system and light induced dimerization (LID) system based on proximity induction provide powerful tools for regulating the function of dimerized proteins, and have been gradually developed. The concept of CID was proposed as early as 1993, The basic principle of CID is that a small molecule controls the dimerization of a pair of proteins or domains, while binding two proteins and bringing them closer together. Small molecules in the CID system form ternary complexes with target proteins, which can bind to various sites, including "hotspot" and "allosteric sites". Small molecules play a role by regulating protein proximity. The light induced dimerization system uses photosensitive proteins to undergo conformational changes under light, thereby inducing protein interactions. Multiple photosensitive proteins derived from plants and microorganisms can undergo photo induced homologous interactions, and relying on LID systems, they can be used to study various biological processes, including cell signal transduction, microbial synthesis, and biomedical applications. In recent years, metal ions, nucleic acids, and molecular host guest systems have been proposed as new methods for orthogonal control of homologous protein dimerization, expanding the development and application of dimerization systems. In addition, the chemo-optogenetic approach combines the advantages of CID and LID systems and has also been applied in inducing protein dimerization. In this review, it is explained that through the CID system, The methods and applications of LID system and supramolecular chemistry to induce homologous protein dimerization are summarized, and the advantages and disadvantages of dimerization systems are discussed. The development direction of dimerization systems is also discussed, in order to provide some reference and ideas for the future application and development of homologous protein dimerization.
    Citation
    GUO Junxia, LIU Sen.Methods for Inducing Homologous Protein Dimerization[J]..Export: BibTex EndNote
  • Isocitrate dehydrogenase 1(IDH1)R132H is the most common mutated gene in grade II-III gliomas and oligodendrogliomas. Instead of activating telomerase(a reverse transcriptase which using RNA as a template to extend telomere length), the majority of IDH1R132H mutant glioma maintain telomere length through an alternative mechanism that relies on homologous recombination(HR), which is known as alterative lengthening of telomere(ALT).The phenotype of ALT mechanism include: ALT associated promyelocytic leukemia protein (PML)bodies(APBs); extrachromosomal telomeric DNA repeats such as C-and T-loops; telomeric sister chromatid exchange(T-SCE), and etc. The mechanism of ALT activation is not fully understood. Recent studies have shown that mutation IDH1 contributes to ALT phenotype in glioma cells in at least three key ways. Firstly, the IDH1R132H mutation mediates RAP1 down-regulation leading to telomere dysfunction, thus ensuring persistent endogenous telomeric DNA damage, which is important for ALT activation. Spontaneous DNA damage at telomeres may provide a substrate for mutation break-induced replication (BIR)-mediated ALT telomere lengthening, and it has been demonstrated that RAP1 inhibits TERRA(Telomeric Repeat-containing RNA, transcribed from telomeric DNA repeat sequences)transcription to down-regulate ALT telomere DNA replication stress and telomeric DNA damage, thereby inhibiting ALT telomere synthesis. Similarly, in ALT cells, knockdown of telomere-specific RNaseH1 nuclease triggers TERRA accumulation, which leads to increased replication pressure. Overexpression of RNaseH1, on the other hand, attenuates the recombination capacity of ALT telomeres, leading to telomere depletion, suggesting that RAP1 can regulate the level of replication pressure and thus ALT activity by controlling TERRA expression. Secondly, the IDH1R132H also alters the preference of the telomere damage repair pathway by down-regulating XRCC1, which inhibits the alternative non-homologous end joining(A-NHEJ)pathway at telomeres and alters cellular preference for the HR pathway to promote ALT. Finally, the IDH1R132H has a decreased affinity for isocitric acid and NADP+ and an increased affinity for α-ketoglutarate(α-KG)and NADPH, so that the mutant IDH1R132H catalysis the hydrogenation of α-KG to produce 2-hydroxyglutarate(2-HG)in a NADPH-dependent manner. Because 2-HG is structurally similar to α-KG, which maintains the trimethylation level of H3k9me3 by competitively inhibiting the activity of the α-KG-dependent histone demethylase KDM4B, and recruits heterochromatin protein HP1α to heterochromatinize telomeres, and promote ALT phenotypes in cooperation with the inactivating of ATRX. In addition, it has been shown that APBs contain telomeric chromatin, which is essentially heterochromatin, and HP1α is directly involved in the formation of APBs. Based on these studies, this article reviews the mechanism of IDH1R132H mediated telomere dysfunction and the preference of DNA repair pathway at telomeres in cooperate with ATRX loss to promote ALT, which may provide references for clinical targeted therapy of IDH1R132H mutant glioma.
    Citation
    YAN Si-Xiang, LI Yi-Fan, LI Yao, LI Yi-Xuan, LI Xiang-Xiu, TONG Jin-Kai, JIA Shu-Ting, DAN Ju-Hua.IDH1R132H Mutant Glioma and Its Compensatory Mechanisms for Maintaining Telomeres[J]..Export: BibTex EndNote
  • G-protein coupled receptors (GPCRs) are an essential family of proteins on the cell membrane, widely distributed in various types of tissues and cells. Typical GPCRs are composed of characteristic 7 transmembrane α-helix domains, extracellular domain and intracellular domain. They play a key role in transmitting information inside and outside cells. These receptors can sense and respond to a variety of external signals, including odor molecules, hormones, neurotransmitters, chemokines, and so on. thereby regulating the physiological functions and metabolic activities of cells. When external signal molecules bind, these receptors undergo conformational changes, thereby activating signal transduction pathways inside cells. The most common downstream signal pathway is the activation of G proteins, but it may also activate the β-arrestin signaling pathway. This series of signal transduction processes ultimately regulates physiological processes such as cell metabolism, proliferation, and differentiation, and also plays an important role in the occurrence and development of diseases. Due to its importance in regulating cell functions and participating in the development of diseases, GPCRs have become important targets in the field of drug research and development. The mechanism of action of many drugs is achieved by intervening in the GPCR signaling pathway. As important form of function regulating, dimerization has attracted widespread attention in the research of GPCR field. In the early days, the formation of GPCR dimerization and its effect on receptor function were mainly studied by immunoprecipitation, immunofluorescence and radioligand binding experiments in overexpression systems. Nowadays, with the continuous development of biochemical and biophysical methods, more and more GPCR dimers have been identified. GPCR dimer refers to the process in which two GPCR subunits bind to each other to form a complex. The same GPCR subunits form homodimers, and different GPCR subunits form heterodimers through direct interaction. Dimerization changes the activity, affinity, internalization, localization and transport, and signal transduction characteristics of GPCR, thereby producing more complex and delicate regulation of cellular physiological processes. In recent years, the research on GPCR dimers has been continuously deepened, revealing its important role in a variety of physiological and pathological processes. In general, the structure of GPCR dimers is complex and diverse, and its formation and stability are affected by many factors, including the specificity of receptor interaction interface, the conformational changes of receptor, and the regulation of intracellular and extracellular environment. By understanding the mechanism of GPCR dimerization, we can better understand the behavior of these receptors in signal transduction and provide new ideas and opportunities for the development of novel drug targets. More and more studies have reported the dimerization of GPCR and its structure and function regulation mechanism. This article reviews the research progress on the structure and function of GPCR dimers, and summarizes some research methods and technologies, which provide a basis for understanding the discovery of GPCR dimers, dimerization methods, structure and function regulation mechanisms, and further targeting GPCR dimers. Polymeric drug development provides a research basis.
    Citation
    LI Chuan-Bao, LI Chen-Hui, XUE Li.Structure and Function of GPCR Dimer[J]..Export: BibTex EndNote
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    FAN Zhi-Peng.Regulation of Mesenchymal Stem Cell Fate Commitment[J]..Export: BibTex EndNote
Journal Information
Sponsored by:Institute of Biophysics, The Chinese Academy of Sciences; Biophysical Society of China Edited by: Editorial Office of Progress in Biochemistry and Biophysics Published by:Editorial Office of PIBB Editor-in-Chief:HE Rong-Qiao Adress:15 Datun Road, Chaoyang District,Beijing 100101,China Telephone:86-10-64888459 Email:prog@ibp.ac.cn Journal inclusion:SCI, CA, Scopus, AJ ISSN    1000-3282 CN    11-2161/Q Current Issue
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Chinese Academy of SciencesInstitute of Biophysics, Chinese Academy of SciencesBiophysical Society of China