BRCA1 accelerates CtIP-mediated DNA-end resection.

DNA-end resection is a highly regulated and critical step in the response and repair of DNA double-strand breaks. In higher eukaryotes, CtIP regulates resection by integrating cellular signals via its posttranslational modifications and protein-protein interactions, including cell-cycle-controlled interaction with BRCA1. The role of BRCA1 in DNA-end resection is not clear. Here, we develop an assay to study DNA resection in higher eukaryotes at high resolution. We demonstrate that the BRCA1-CtIP interaction, albeit not essential for resection, modulates the speed at which this process takes place.

• Publication year

  2014

• Venue

  Cell Reports

• Publication date

  2014-10-23

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.celrep.2014.08.076PMID 25310973
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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