The BRCA1-interacting protein Abraxas is required for genomic stability and tumor suppression

Cell Rep. 2014 Aug 7;8(3):807-17. doi: 10.1016/j.celrep.2014.06.050. Epub 2014 Jul 24.


Germline mutations of BRCA1 confer hereditary susceptibility to breast and ovarian cancer. However, somatic mutation of BRCA1 is infrequent in sporadic breast cancers. The BRCA1 protein C terminus (BRCT) domains interact with multiple proteins and are required for BRCA1's tumor-suppressor function. In this study, we demonstrated that Abraxas, a BRCA1 BRCT domain-interacting protein, plays a role in tumor suppression. Abraxas exerts its function through binding to BRCA1 to regulate DNA repair and maintain genome stability. Both homozygous and heterozygous Abraxas knockout mice exhibited decreased survival and increased tumor incidence. The gene encoding Abraxas suffers from gene copy loss and somatic mutations in multiple human cancers including breast, ovarian, and endometrial cancers, suggesting that mutation and loss of function of Abraxas may contribute to tumor development in human patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • BRCA1 Protein / chemistry
  • BRCA1 Protein / metabolism*
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • DNA Repair
  • Female
  • Genomic Instability*
  • Germ-Line Mutation
  • HEK293 Cells
  • Homozygote
  • Humans
  • Mice
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / pathology
  • Protein Binding
  • Protein Structure, Tertiary


  • ABRAXAS1 protein, human
  • BRCA1 Protein
  • Carrier Proteins
  • FAM175A protein,mouse