Authors:
HC Reinhardt, IG Cannell, S Morandell, MB Yaffe
Journal name: 
Cell Cycle
Citation info: 
10(1):23-27
Abstract: 
In response to DNA damage, cells activate a complex, kinase-based signaling network that consist 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 Gadd45a by the checkpoint kinase MAPKAP Kinase-2.
DOI: 
http://doi.org/10.4161/cc.10.1.14351
E-pub date: 
31 Dec 2010
Users with this publication listed: 
Ian Cannell