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细胞凋亡中的信号转导通路。

Signal transduction pathways in apoptosis.

作者信息

McConkey D J, Orrenius S

机构信息

Department of Cell Biology, University of Texas MD Anderson Cancer Center, Houston 77030, USA.

出版信息

Stem Cells. 1996 Nov;14(6):619-31. doi: 10.1002/stem.140619.

DOI:10.1002/stem.140619
PMID:8948020
Abstract

Emerging evidence indicates that apoptosis is regulated by some of the same signal transduction pathways previously implicated in other physiological cellular responses, including alterations in intracellular Ca2+ compartmentalization, activation of protein kinases and phosphatases, alteratios in pH and oxidative stress. Interestingly, signals that promote apoptosis in one model can suppress cell death in another, indicating that cellular responses are determined by the intrinsic programming of the cell in question. This review will summarize current knowledge of the signal transduction pathways regulating apoptosis and discuss how they may be coupled to components of the molecular machinery for cell death.

摘要

新出现的证据表明,细胞凋亡是由一些先前涉及其他生理细胞反应的相同信号转导途径调控的,包括细胞内Ca2+ 分布的改变、蛋白激酶和磷酸酶的激活、pH值的变化以及氧化应激。有趣的是,在一种模型中促进细胞凋亡的信号在另一种模型中可能会抑制细胞死亡,这表明细胞反应是由所讨论细胞的内在程序决定的。本综述将总结目前关于调控细胞凋亡的信号转导途径的知识,并讨论它们如何与细胞死亡的分子机制成分相联系。

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Signal transduction pathways in apoptosis.细胞凋亡中的信号转导通路。
Stem Cells. 1996 Nov;14(6):619-31. doi: 10.1002/stem.140619.
2
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Making the connection: coupling of stress-activated ERK/MAPK (extracellular-signal-regulated kinase/mitogen-activated protein kinase) core signalling modules to extracellular stimuli and biological responses.建立联系:应激激活的ERK/MAPK(细胞外信号调节激酶/丝裂原活化蛋白激酶)核心信号模块与细胞外刺激及生物学反应的偶联。
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Modulation of nitric oxide-induced apoptotic death of HL-60 cells by protein kinase C and protein kinase A through mitogen-activated protein kinases and CPP32-like protease pathways.蛋白激酶C和蛋白激酶A通过丝裂原活化蛋白激酶和CPP32样蛋白酶途径对一氧化氮诱导的HL-60细胞凋亡死亡的调节作用。
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Protein kinase C-ERK1/2 signal pathway switches glucose depletion-induced necrosis to apoptosis by regulating superoxide dismutases and suppressing reactive oxygen species production in A549 lung cancer cells.蛋白激酶C-ERK1/2信号通路通过调节超氧化物歧化酶并抑制A549肺癌细胞中的活性氧生成,将葡萄糖剥夺诱导的坏死转变为凋亡。
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Cellular defense against H2O2-induced apoptosis via MAP kinase-MKP-1 pathway.细胞通过丝裂原活化蛋白激酶-MKP-1途径抵御过氧化氢诱导的细胞凋亡。
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