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

Nature | Apr 24, 1997

http://www.ncbi.nlm.nih.gov/pubmed/9126738

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 RIS Download

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

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