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TNF induced RIP3-dependent NADH depletion

Abstract

肿瘤坏死因子(tumornecrosisfactor,TNF)能诱导L929细胞产生相互作用蛋白3(receptor-interactingprotein3,RIP3)依赖的程序性细胞坏死,并且在该过程中,胞内的线粒体产生的活性氧(reactiveoxygenspecies,ROS)会积聚,同时当RIP3的表达水平敲低时,胞内ROS的积聚也受到了抑制。但是RIP3如何影响ROS的具体机制仍不清楚。 因为ROS的产生主要在线粒体电子传递链上,而还原型辅酶Ⅰ(NADH)和还原型辅酶Ⅱ(NADPH)又是电子传递链的底物,RIP3是否能通过改变电子传递链上NADH或者NADPH的消耗来影响ROS。我...TNF (Tumor necrosis factor) can induce necrosis in L929 cells which is RIP3 dependent. ROS (reactive oxygen species) production increase during this process which is also RIP3 dependent, RIP3 expression knockdown inhibits the accumulation of ROS. But the mechanism of how RIP3 affect the ROS production is unknown. ROS is generated mostly through the ETC (electron transport chain) of mitochondria, ...学位:理学硕士院系专业:生命科学学院_细胞生物学学号:2162012115244

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