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PMID: 10801460 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review

The Mre11 complex and ATM: collaborating to navigate S phase.

Current opinion in cell biology ·Vol. 12 ·No. 3 ·2000-06-00 ·Pages 293-6

Petrini JH

Abstract

Recently, findings regarding a group of cancer predisposition and chromosome instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telangiectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light on the unexpected role of recombinational DNA repair proteins in DNA-damage-dependent cell-cycle regulation. Mutations in the Mre11 complex cause A-TLD and NBS. In addition, functions of the Mre11 complex have been biochemically linked to ATM, the large protein kinase that is defective in ataxia-telangiectasia cells by the observation that Nbs1 is a bona fide substrate of the ATM kinase.

MeSH Terms
Animals Ataxia Telangiectasia/genetics,metabolism Ataxia Telangiectasia Mutated Proteins Cell Cycle Proteins DNA Damage DNA Repair DNA Replication DNA-Binding Proteins Endodeoxyribonucleases Exodeoxyribonucleases Fungal Proteins/genetics,metabolism Humans Protein Serine-Threonine Kinases/genetics,metabolism Recombination, Genetic S Phase/genetics,physiology Saccharomyces cerevisiae Proteins Tumor Suppressor Proteins
Chemicals
Cell Cycle Proteins DNA-Binding Proteins Fungal Proteins Saccharomyces cerevisiae Proteins Tumor Suppressor Proteins ATM protein, human Ataxia Telangiectasia Mutated Proteins Protein Serine-Threonine Kinases Endodeoxyribonucleases Exodeoxyribonucleases MRE11 protein, S cerevisiae
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Petrini J H
University of Wisconsin Medical School, Madison, WI 53706, USA. jpetrini@facstaff.wisc.edu
Article Info
Journal
Current opinion in cell biology
Abbr.
Curr Opin Cell Biol
ISSN
0955-0674
Published
2000-06-00
Pages
293-6
Language
English
Region
England
NLM ID
8913428
Subset
IM
Grants
NIGMS NIH HHS · GM59413 · United States
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