Journal
DNA REPAIR
Volume 8, Issue 9, Pages 1047-1054Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2009.04.012
Keywords
Chk1; Chk2; Rad53; Rad9; Mre11; Nbs1; Rad50; ATR; ATM; Tel1; Cell cycle; Checkpoint; Transcription; Apoptosis; DNA repair; Recombination
Categories
Funding
- NIH NRSA
- Lymphoma Society Special Fellows
- Joel and Jean Smilow initiativ
Ask authors/readers for more resources
The cellular DNA damage response (DDR) is activated by many types of DNA lesions. Upon recognition of DNA damage by sensor proteins, an intricate signal transduction network is activated to coordinate diverse cellular outcomes that promote genome integrity. Key components of the DDR in mammalian cells are the checkpoint effector kinases Chk1 and Chk2 (referred to henceforth as the effector kinases; orthologous to spChk1 and spCds1 in the fission yeast S. pombe and scChk1 and scRad53 in the budding yeast S. cerevisiae). These evolutionarily conserved and structurally divergent kinases phosphorylate numerous substrates to regulate the DDR. This review will focus on recent advances in our understanding of the structure, regulation, and functions of the effector kinases in the DDR, as well as their potential roles in human disease. (C) 2009 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available