Speed matters: How subtle changes in DNA end resection rate affect repair

The contribution of BRCA1 (breast cancer 1) to the repair of broken DNA is well established, but its real role at the molecular level is less well understood. By developing a new high-resolution, single-molecule technique, we have now shown that BRCA1 accelerates the processing of DNA breaks that subsequently engage in homologous recombination.

• Publication year

  2015

• Venue

  Molecular & Cellular Oncology

• Publication date

  2015-05-06

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4161/23723556.2014.982964PMID 27308460PMCID 4905430
• 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.

• BRCA1 accelerates CtIP-mediated DNA-end resection.

  2014cited by this paper
• The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression

  2013cited by this paper
• Prognostic value of CtIP/RBBP8 expression in breast cancer

  2013cited by this paper
• The DNA damage response and cancer therapy

  2012cited by this paper
• Mechanisms of BRCA1 tumor suppression.

  2012cited by this paper
• Regulation of homologous recombination in eukaryotes.

  2010influential reference
• Collaborative Action of Brca1 and CtIP in Elimination of Covalent Modifications from Double-Strand Breaks to Facilitate Subsequent Break Repair

  2010cited by this paper
• DNA resection in eukaryotes: deciding how to fix the break

  2010cited by this paper
• Mechanisms of double-strand break repair in somatic mammalian cells.

  2009influential reference
• CtIP-BRCA1 modulates the choice of DNA double-strand break repair pathway throughout the cell cycle

  2009cited by this paper

• No citing papers are available for this paper.