Molecular functions of ASK family in diseases caused by stress-induced inflammation and apoptosis

被引:2
|
作者
Kojima, Kazuki [1 ]
Ichijo, Hidenori [1 ]
Naguro, Isao [1 ]
机构
[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Cell Signaling, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan
来源
JOURNAL OF BIOCHEMISTRY | 2021年 / 169卷 / 04期
关键词
ASK family; ER stress; inflammation; MAPK cascade; oxidative stress; REGULATING KINASE 1; NEURONAL CELL-DEATH; NONALCOHOLIC STEATOHEPATITIS; DEPENDENT ACTIVATION; OXIDATIVE STRESS; THIOREDOXIN; INDUCTION; INVOLVEMENT; INHIBITION; EXPRESSION;
D O I
10.1093/jb/mvaa145
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
VCells are constantly exposed to various types of stress, and disruption of the proper response leads to a variety of diseases. Among them, inflammation and apoptosis are important examples of critical responses and should be tightly regulated, as inappropriate control of these responses is detrimental to the organism. In several disease states, these responses are abnormally regulated, with adverse effects. Apoptosis signal-regulating kinase (ASK) family members are stress-responsive kinases that regulate inflammation and apoptosis after a variety of stimuli, such as oxidative stress and endoplasmic reticulum stress. In this review, we summarize recent reports on the ASK family in terms of their involvement in inflammatory diseases, focussing on upstream stimuli that regulate ASK family members.
引用
收藏
页码:395 / 407
页数:13
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