The role of LKB1 and AMPK in cellular responses to stress and damage

被引：169

作者：

Alexander, Angela

Walker, Cheryl L. ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Mol Carcinogenesis, Smithville, TX 78957 USA

来源：

FEBS LETTERS | 2011年 / 585卷 / 07期

关键词：

LKB1; AMPK; Apoptosis; Survival; Stress; DNA damage; ACTIVATED PROTEIN-KINASE; METABOLIC CHECKPOINT; GENOTOXIC STRESS; UPSTREAM KINASE; ENERGY STRESS; TUMOR-CELLS; PHOSPHORYLATION; AUTOPHAGY; P53; APOPTOSIS;

D O I：

10.1016/j.febslet.2011.03.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The LKB1 and AMPK proteins participate in an energy sensing cascade that responds to depletion of ATP, serving as a master regulator of metabolism that inhibits anabolic processes and stimulates catabolic processes. However in recent years, LKB1 and AMPK have been implicated in a variety of other cellular processes, both cytoplasmic and nuclear, such as control of cell polarity and regulation of gene transcription. In this review, we summarize the most recent discoveries regarding participation of LKB1 and AMPK in signaling pathways that respond to cellular stress and damage, and the relevance of this signaling for disease and therapy. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

收藏

页码：952 / 957

页数：6

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