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Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2.

Inherited mutations in the human BRCA2 gene cause about half of the cases of early-onset breast cancer. The embryonic expression pattern of the mouse Brca2 gene is now defined and an interaction identified of the Brca2 protein with the DNA-repair protein Rad51. Developmental arrest in Brca2-deficient embryos, their radiation sensitivity, and the association of Brca2 with Rad51 indicate that Brca2 may be an essential cofactor in the Rad51-dependent DNA repair of double-strand breaks, thereby explaining the tumour-suppressor function of Brca2.

Pubmed ID: 9126738

Authors

  • Sharan SK
  • Morimatsu M
  • Albrecht U
  • Lim DS
  • Regel E
  • Dinh C
  • Sands A
  • Eichele G
  • Hasty P
  • Bradley A

Journal

Nature

Publication Data

April 24, 1997

Associated Grants

None

Mesh Terms

  • 3T3 Cells
  • Animals
  • BRCA2 Protein
  • Blastocyst
  • Brain
  • Cell Division
  • Cell Survival
  • DNA-Binding Proteins
  • Embryo, Mammalian
  • Embryonic and Fetal Development
  • Female
  • Gamma Rays
  • Gene Expression
  • Gene Targeting
  • Genes, Tumor Suppressor
  • In Situ Hybridization
  • Male
  • Mice
  • Molecular Sequence Data
  • Mutagenesis
  • Neoplasm Proteins
  • Polymerase Chain Reaction
  • Protein Binding
  • Rad51 Recombinase
  • Radiation Tolerance
  • Recombinant Fusion Proteins
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Stem Cells
  • Transcription Factors