Document Detail


Direct activation of the ATM protein kinase by the Mre11/Rad50/Nbs1 complex.
MedLine Citation:
PMID:  15064416     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The complex containing the Mre11, Rad50, and Nbs1 proteins (MRN) is essential for the cellular response to DNA double-strand breaks, integrating DNA repair with the activation of checkpoint signaling through the protein kinase ATM (ataxia telangiectasia mutated). We demonstrate that MRN stimulates the kinase activity of ATM in vitro toward its substrates p53, Chk2, and histone H2AX. MRN makes multiple contacts with ATM and appears to stimulate ATM activity by facilitating the stable binding of substrates. Phosphorylation of Nbs1 is critical for MRN stimulation of ATM activity toward Chk2, but not p53. Kinase-deficient ATM inhibits wild-type ATM phosphorylation of Chk2, consistent with the dominant-negative effect of kinase-deficient ATM in vivo.
Authors:
Ji-Hoon Lee; Tanya T Paull
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  304     ISSN:  1095-9203     ISO Abbreviation:  Science     Publication Date:  2004 Apr 
Date Detail:
Created Date:  2004-04-05     Completed Date:  2004-04-14     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  93-6     Citation Subset:  IM    
Affiliation:
Department of Molecular Genetics and Microbiology, Institute of Cellular and Molecular Biology, University of Texas at Austin, 1 University Station, A4800, Austin, TX 78712, USA.
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MeSH Terms
Descriptor/Qualifier:
Ataxia Telangiectasia / genetics
Cell Cycle Proteins / genetics,  metabolism*
DNA / metabolism
DNA Repair Enzymes*
DNA-Binding Proteins / metabolism*
Enzyme Activation
Histones / metabolism
Humans
Mutation
Mutation, Missense
Nuclear Proteins / genetics,  metabolism*
Phosphorylation
Protein Binding
Protein-Serine-Threonine Kinases / genetics,  metabolism*
Recombinant Proteins / metabolism
Tumor Suppressor Protein p53 / metabolism
Tumor Suppressor Proteins
Grant Support
ID/Acronym/Agency:
CA94008/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/H2AFX protein, human; 0/Histones; 0/MRE11A protein, human; 0/NBN protein, human; 0/Nuclear Proteins; 0/Rad50 protein, human; 0/Recombinant Proteins; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; 9007-49-2/DNA; EC 2.7.1.11/checkpoint kinase 2; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein; EC 6.5.1.-/DNA Repair Enzymes

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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