Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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BRCA2 Protein / metabolism*
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Chromatin / metabolism
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DNA Repair*
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Fanconi Anemia / genetics
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Fanconi Anemia / metabolism*
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Fanconi Anemia Complementation Group D2 Protein / metabolism*
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Fanconi Anemia Complementation Group Proteins / metabolism
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Histones / metabolism*
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Humans
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Mice
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Models, Biological
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Phenotype
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Signal Transduction
Substances
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BRCA2 Protein
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Chromatin
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Fanconi Anemia Complementation Group D2 Protein
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Fanconi Anemia Complementation Group Proteins
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H2AX protein, human
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H2AX protein, mouse
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Histones