ATM and the Mre11 complex combine to recognize and signal DNA double-strand breaks

Lavin, MF (2007) ATM and the Mre11 complex combine to recognize and signal DNA double-strand breaks. Oncogene, 26 56: 7749-7758. doi:10.1038/sj.onc.1210880


Author Lavin, MF
Title ATM and the Mre11 complex combine to recognize and signal DNA double-strand breaks
Journal name Oncogene   Check publisher's open access policy
ISSN 0950-9232
Publication date 2007-01-01
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1038/sj.onc.1210880
Volume 26
Issue 56
Start page 7749
End page 7758
Total pages 10
Editor Reddy, E.P.
Jenkins, J.
Place of publication London
Publisher Nature Publishing Group
Collection year 2008
Language eng
Subject 320799 Neurosciences not elsewhere classified
C1
730104 Nervous system and disorders
Abstract The recognition and repair of DNA double-strand breaks (DSBs) is a complex process that draws upon a multitude of proteins. This is not surprising since this is a lethal lesion if left unrepaired and also contributes to genome instability and the consequential risk of cancer and other pathologies. Some of the key proteins that recognize these breaks in DNA are mutated in distinct genetic disorders that predispose to agent sensitivity, genome instability, cancer predisposition and/or neurodegeneration. These include members of the Mre11 complex (Mre11/Rad50/Nbs1) and ataxia-telangiectasia (A-T) mutated (ATM), mutated in the human genetic disorder A-T. The mre11 (MRN) complex appears to be the major sensor of the breaks and subsequently recruits ATM where it is activated to phosphorylate in turn members of that complex and a variety of other proteins involved in cell-cycle control and DNA repair. The MRN complex is also upstream of ATM and ATR (A-T-mutated and rad3-related) protein in responding to agents that block DNA replication. To date, more than 30 ATM-dependent substrates have been identified in multiple pathways that maintain genome stability and reduce the risk of disease. We focus here on the relationship between ATM and the MRN complex in recognizing and responding to DNA DSBs.
Keyword Biochemistry & Molecular Biology
Oncology
Cell Biology
Genetics & Heredity
ATM
Mre11 complex
DNA double strand breaks
signal transduction
functional consequences
Dependent Nuclear-dynamics
S-phase Checkpoint
In-vivo
Ionizing-radiation
Requires Atm
Mre11-rad50-nbs1 Complex
Saccharomyces-cerevisiae
Damage Response
Protein Complex
Repair Complex
Q-Index Code C1
Q-Index Status Confirmed Code
Additional Notes This document is a journal review.

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Excellence in Research Australia (ERA) - Collection
2008 Higher Education Research Data Collection
School of Medicine Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 154 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 155 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Tue, 19 Feb 2008, 01:52:56 EST