The roles of ASK family proteins in stress responses and diseases

被引：180

作者：

Hattori, Kazuki ^{[1
]}

Naguro, Isao ^{[1
]}

Runchel, Christopher ^{[1
]}

Ichijo, Hidenori ^{[1
]}

机构：

[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Lab Cell Signaling, Bunkyo Ku, Tokyo 1130033, Japan

来源：

CELL COMMUNICATION AND SIGNALING | 2009年 / 7卷

关键词：

SIGNAL-REGULATING KINASE; NEURONAL CELL-DEATH; AMYOTROPHIC-LATERAL-SCLEROSIS; SPECIES-DEPENDENT ACTIVATION; ENDOPLASMIC-RETICULUM; ER STRESS; ENDOTHELIAL DYSFUNCTION; SUPEROXIDE-DISMUTASE; CARDIAC-HYPERTROPHY; EXTRACELLULAR ATP;

D O I：

10.1186/1478-811X-7-9

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase family, which activates c-Jun N-terminal kinase and p38 in response to a diverse array of stresses such as oxidative stress, endoplasmic reticulum stress and calcium influx. In the past decade, various regulatory mechanisms of ASK1 have been elucidated, including its oxidative stress-dependent activation. Recently, it has emerged that ASK family proteins play key roles in cancer, cardiovascular diseases and neurodegenerative diseases. In this review, we summarize the recent findings on ASK family proteins and their implications in various diseases.

引用

页数：10

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