This work was supported by a grant from The National Natural Sciences Foundation of China (1999053905).
通过荧光分子标记和CONFOCAL技术检测方法,建立了TRAIL(TNF-related apoptosis inducing ligand, 一种类肿瘤坏死因子)诱导Novikoff细胞凋亡的模型,并探讨了TRAIL诱导凋亡的机制和Ap5A(P1, P5-Di(adenosine-5′)pentaphosphate)在其中的作用.结果显示:TRAIL可诱导Novikoff细胞凋亡,且具有剂量和时间依赖性,同时胞内钙离子浓度显著上调.Ap5A能延迟TRAIL诱导的Novikoff细胞凋亡,同时下调胞内钙离子浓度.TRAIL和Ap5A分别上调和下调胞内钙离子浓度的作用可能是其诱发和延迟Novikoff细胞凋亡的一个机制.
A novel model of TRAIL-induced apoptosis of Novikoff cells was constructed based on the observation using molecular fluorescence labelling and confocal microscopic techniques. The mechanism of TRAIL-induced apoptosis and the role of Ap5A [P1, P5-Di(adenosine-5′)pentaphosphate] during this process was investigatived. The results revealed that: 1) TRAIL-induced apoptosis is both dosage- and time- dependent, which correlates with the remarkable increase of [Ca2+] in Novikoff cells; 2) Ap5A retards the TRAIL-induced apoptosis as well as down-regulates [Ca2+] in Novikoff cells. These observations indicate that the mechanism of TRAIL-induced apoptosis and Ap5A retards it through down and up-regulating intracellular calcium concentration respectively.
赖秋安,刘彦信,郝雪梅,唐爱辉,卫威,王世强,孙久荣. Ap5A延迟TRAIL诱导Novikoff细胞的凋亡[J].生物化学与生物物理进展,2003,30(3):379-383
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