期刊
CELL CYCLE
卷 10, 期 1, 页码 23-27出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.10.1.14351
关键词
MAPKAP-kinase 2; p38MAPK; HuR; hnRNP A0; TIAR; PARN; DNA damage response; RNA-binding proteins; cell cycle checkpoint
类别
资金
- National Institutes of Health [GM68762, CA112967, ES015339]
- Deutsche Forschungsgemeinschaft [RE2246/1-1, RE2246/2-1, SFB-832]
- Deutsche Nierenstiftung
- Austrian Science Fund (FWF, Erwin-Schroedinger-Fellowship)
- Anna Fuller fund of New Haven
- David H. Koch Fund
- NATIONAL CANCER INSTITUTE [U54CA112967] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES015339] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P50GM068762] Funding Source: NIH RePORTER
In response to DNA damage, cells activate a complex, kinase-based signaling network that consists of two components-a rapid phosphorylation-driven signaling cascade that results in immediate inhibition of Cdk/cyclin complexes to arrest the cell cycle along with recruitment of repair machinery to damaged DNA, followed by a delayed transcriptional response that promotes cell cycle arrest through the induction of Cdk inhibitors, such as p21. In recent years a third layer of complexity has emerged that involves post-transcriptional control of mRNA stability, splicing and translation as a critical part of the DNA damage response. Here, we describe recent work implicating DNA damage-dependent modification of RNA-binding proteins that are responsible for some of these mRNA effects, highlighting recent work on post-transcriptional regulation of the cell cycle checkpoint protein/apoptosis inducer Gadd45 alpha by the checkpoint kinase MAPKAP Kinase-2.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据