Document Detail

New roads to FA/BRCA pathway: H2AX.
MedLine Citation:
PMID:  17471025     Owner:  NLM     Status:  MEDLINE    
We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by gammaH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies.
Alex Lyakhovich; Jordi Surrallés
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-05-01
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  6     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-05-04     Completed Date:  2007-08-07     Revised Date:  2007-10-04    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1019-23     Citation Subset:  IM    
Group of Mutagenesis, Department of Genetics and Microbiology, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.
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MeSH Terms
BRCA2 Protein / metabolism*
Chromatin / metabolism
DNA Repair*
Fanconi Anemia / genetics,  metabolism*
Fanconi Anemia Complementation Group D2 Protein / metabolism*
Fanconi Anemia Complementation Group Proteins / metabolism
Histones / metabolism*
Models, Biological
Signal Transduction
Reg. No./Substance:
0/BRCA2 Protein; 0/Chromatin; 0/Fanconi Anemia Complementation Group D2 Protein; 0/Fanconi Anemia Complementation Group Proteins; 0/H2AFX protein, human; 0/H2AX protein, mouse; 0/Histones

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