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通过ASK1信号通路引发的氧化应激诱导疾病。

Oxidative Stress-Induced Diseases via the ASK1 Signaling Pathway.

作者信息

Soga Mayumi, Matsuzawa Atsushi, Ichijo Hidenori

机构信息

Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

出版信息

Int J Cell Biol. 2012;2012:439587. doi: 10.1155/2012/439587. Epub 2012 May 13.

DOI:10.1155/2012/439587
PMID:22654913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3359665/
Abstract

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that activates the downstream MAPKs, c-Jun N-terminal kinase (JNK) and p38. ASK1 is activated by various types of stress, such as oxidative stress, endoplasmic reticulum stress, and infection, and regulates various cellular functions. Recently, it has been reported that ASK1 is associated with various diseases induced by oxidative stress. In this review, we introduce recent findings of the regulatory mechanisms of ASK1 and the oxidative stress-induced diseases mediated by the ASK1 signaling pathway.

摘要

凋亡信号调节激酶1(ASK1)是一种丝裂原活化蛋白激酶(MAPK)激酶激酶,可激活下游的MAPK,即c-Jun氨基末端激酶(JNK)和p38。ASK1可被多种类型的应激激活,如氧化应激、内质网应激和感染,并调节多种细胞功能。最近,有报道称ASK1与氧化应激诱导的多种疾病有关。在本综述中,我们介绍了ASK1调控机制的最新研究结果以及由ASK1信号通路介导的氧化应激诱导疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6366/3359665/3f9dee6359b4/IJCB2012-439587.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6366/3359665/3f9dee6359b4/IJCB2012-439587.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6366/3359665/3f9dee6359b4/IJCB2012-439587.001.jpg

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Hypertens Res. 2012 Feb;35(2):194-200. doi: 10.1038/hr.2011.175. Epub 2011 Nov 17.
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