4.8 Article

Chromatin Recruitment of DNA Repair Proteins: Lessons from the Fanconi Anemia and Double-Strand Break Repair Pathways

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MOLECULAR CELL
卷 32, 期 3, 页码 306-312

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CELL PRESS
DOI: 10.1016/j.molcel.2008.10.009

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  1. NIH [5PO1CA092584]

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In response to DNA damage, eukaryotic cells must rapidly load DNA repair proteins onto damaged chromatin. Chromatin recruitment often entails ubiquitination of a damage-specific DNA repair protein, interaction with a ubiquitin binding factor, assembly of a multisubunit DNA repair complex, and eventually a deubiquitination event once the DNA repair reaction has been completed. This review focuses on the recent discoveries in the Fanconi Anemia (FA) and DNA double-strand break (DSB) repair pathways, which underscore the importance of regulated chromatin loading in the DNA damage response. Interestingly, these two pathways share several features, suggesting a more general mechanism for DNA-repair regulation.

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