Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2004 Nov;95(11):866-71.
doi: 10.1111/j.1349-7006.2004.tb02195.x.

Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage

Affiliations
Review

Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage

Kiyotsugu Yoshida et al. Cancer Sci. 2004 Nov.

Abstract

BRCA1 (BReast-CAncer susceptibility gene 1) and BRCA2 are tumor suppressor genes, the mutant phenotypes of which predispose to breast and ovarian cancers. Intensive research has shown that BRCA proteins are involved in a multitude of pivotal cellular processes. In particular, both genes contribute to DNA repair and transcriptional regulation in response to DNA damage. Recent studies suggest that BRCA proteins are required for maintenance of chromosomal stability, thereby protecting the genome from damage. New data also show that BRCAs transcriptionally regulate some genes involved in DNA repair, the cell cycle, and apoptosis. Many of these functions are mediated by a large number of cellular proteins that interact with BRCAs. The functions of BRCA proteins are also linked to distinct and specific phosphorylation events; however, the extent to which phosphorylation-activated molecular pathways contribute to tumor suppressor activity remains unclear. Finally, the reasons why mutations in BRCA genes lead to the development of breast and ovarian cancers are not clearly understood. Elucidation of the precise molecular functions of BRCAs is expected to improve our understanding of hereditary as well as sporadic mammary carcinogenesis.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Rosen EM, Fan S, Pestell RG, Goldberg ID. BRCA1 gene in breast cancer. J Cell Physiol 2003; 196: 19–41. - PubMed
    1. Hall JM, Lee MK, Newman B, Morrow JE, Anderson LA, Huey B, King MC. Linkage of early‐onset familial breast cancer to chromosome 17q21. Science 1990; 250: 1684–9. - PubMed
    1. Smith SA, Easton DF, Evans DG, Ponder BA. Allele losses in the region 17ql2–21 in familial breast and ovarian cancer involve the wild‐type chromosome. Nat Genet 1992; 2: 128–31. - PubMed
    1. Neuhausen SL, Marshall CJ. Loss of heterozygosity in familial tumors from three BRCAl‐linked kindreds. Cancer Res 1994; 54: 6069–72. - PubMed
    1. Miki Y, Swensen J, Shattuck‐Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science 1994; 266: 66–71. - PubMed

LinkOut - more resources

-