We have updated our privacy policy. If you have any question, contact us at privacy@scicrunch.org. Dismiss and don't show again

Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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

Nature | Apr 24, 1997

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

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants


Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.