期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 23, 期 21, 页码 7926-7936出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.23.21.7926-7936.2003
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资金
- NATIONAL CANCER INSTITUTE [P01CA094060, P01CA097403] Funding Source: NIH RePORTER
- NCI NIH HHS [P01 CA94060, P01 CA094060, P01 CA097403, P01 CA97403] Funding Source: Medline
The BRCA1 tumor suppressor has been implicated in the maintenance of chromosomal stability through homology-directed repair of DNA double-strand breaks. Much of the BRCA1 in cells forms a heterodimeric complex with a structurally related protein BARD1 We report that expression of truncated mouse or human BARD1 peptides capable of interacting with Brca1 results in a homologous-repair deficiency. Repair is mildly reduced in Brca1 wild-type cells and severely reduced in cells that harbor a Brca1 splice product deleted for exon 11. Nuclear localization of the Brca1 or BARD1 peptides is not compromised, implying that the repair deficiency is caused by a more direct effect on repair. The tumor suppressor activity of BRCA1 may require the participation of BARD1 to maintain chromosome integrity through the homologous-repair pathway.
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