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细胞凋亡中的JNK信号传导

JNK signaling in apoptosis.

作者信息

Dhanasekaran D N, Reddy E P

机构信息

Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA.

出版信息

Oncogene. 2008 Oct 20;27(48):6245-51. doi: 10.1038/onc.2008.301.

DOI:10.1038/onc.2008.301
PMID:18931691
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3063296/
Abstract

Jun N-terminal kinases or JNKs play a critical role in death receptor-initiated extrinsic as well as mitochondrial intrinsic apoptotic pathways. JNKs activate apoptotic signaling by the upregulation of pro-apoptotic genes through the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and antiapoptotic proteins through distinct phosphorylation events. This review analyses our present understanding of the role of JNK in apoptotic signaling and the various mechanisms by which JNK promotes apoptosis.

摘要

Jun氨基末端激酶(JNK)在死亡受体启动的外源性以及线粒体介导的内源性凋亡途径中发挥关键作用。JNK通过特定转录因子的反式激活上调促凋亡基因,从而激活凋亡信号,或者通过不同的磷酸化事件直接调节线粒体促凋亡蛋白和抗凋亡蛋白的活性。这篇综述分析了我们目前对JNK在凋亡信号传导中的作用以及JNK促进凋亡的各种机制的理解。

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本文引用的文献

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Calphostin C-induced apoptosis is mediated by a tissue transglutaminase-dependent mechanism involving the DLK/JNK signaling pathway.钙泊三醇C诱导的细胞凋亡是由一种涉及DLK/JNK信号通路的组织转谷氨酰胺酶依赖性机制介导的。
Cell Death Differ. 2008 Sep;15(9):1522-31. doi: 10.1038/cdd.2008.77. Epub 2008 May 23.
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All JNKs can kill, but nuclear localization is critical for neuronal death.所有的应激活化蛋白激酶都具有杀伤作用,但核定位对于神经元死亡至关重要。
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Pin1 promotes cell death in NGF-dependent neurons through a mechanism requiring c-Jun activity.Pin1通过一种需要c-Jun活性的机制促进NGF依赖型神经元的细胞死亡。
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Distinct signaling pathways of microtubule inhibitors--vinblastine and Taxol induce JNK-dependent cell death but through AP-1-dependent and AP-1-independent mechanisms, respectively.微管抑制剂长春碱和紫杉醇的不同信号通路分别通过AP-1依赖和非AP-1依赖机制诱导JNK依赖的细胞死亡。
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Activating transcription factor 3 up-regulated by c-Jun NH(2)-terminal kinase/c-Jun contributes to apoptosis induced by potassium deprivation in cerebellar granule neurons.由c-Jun氨基末端激酶/c-Jun上调的激活转录因子3促进小脑颗粒神经元钾缺乏诱导的细胞凋亡。
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Thioredoxin and TRAF family proteins regulate reactive oxygen species-dependent activation of ASK1 through reciprocal modulation of the N-terminal homophilic interaction of ASK1.硫氧还蛋白和TRAF家族蛋白通过对ASK1 N端同源相互作用的相互调节,调控依赖活性氧的ASK1激活。
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Apoptosis: a review of programmed cell death.细胞凋亡:程序性细胞死亡综述
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