Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Deng, C.-X.
Right arrow Articles by Wang, R.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Deng, C.-X.
Right arrow Articles by Wang, R.-H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, 2003, Vol. 12, Review Issue 1 R113-R123
DOI: 10.1093/hmg/ddg082
© 2003 Oxford University Press

Roles of BRCA1 in DNA damage repair: a link between development and cancer

Chu-Xia Deng* and Rui-Hong Wang

Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, 10/9N105, National Institutes of Health, Bethesda, MD 20892, USA

Received October 23, 2002; Accepted January 29, 2003

DNA damage causes devastating problems for developing organisms. Recent studies reveal that BRCA1 plays essential roles in homologous recombinational repair, non-homologous end joining, and nucleotide excision repair. BRCA1 mediates these functions by interaction with components of the DNA repair machinery and by regulating expression of genes that are involved in these DNA damage repair pathways. Consequently, the absence of BRCA1 results in accumulation of chromosome damage, cell cycle abnormalities and apoptosis, leading to developmental abnormalities and adult tumorigenesis. In this review, we discuss recent advances regarding our understanding of the functions of BRCA1 in DNA damage repair and cellular responses that link development and cancer.

* To whom correspondence should be addressed. Tel: +1 3014027225; Fax: +1 3014801135; Email: chuxiad{at}bdg10.niddk.nih.gov


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 DevelopmentHome page
J. N. Pulvers and W. B. Huttner
Brca1 is required for embryonic development of the mouse cerebral cortex to normal size by preventing apoptosis of early neural progenitors
Development, June 1, 2009; 136(11): 1859 - 1868.
[Abstract] [Full Text] [PDF]

Home page
 Biol. Reprod.Home page
B. Xiong, S. Li, J.-S. Ai, S. Yin, Y.-C. OuYang, S.-C. Sun, D.-Y. Chen, and Q.-Y. Sun
BRCA1 Is Required for Meiotic Spindle Assembly and Spindle Assembly Checkpoint Activation in Mouse Oocytes
Biol Reprod, October 1, 2008; 79(4): 718 - 726.
[Abstract] [Full Text] [PDF]

Home page
 RadiologyHome page
S. Schrading and C. K. Kuhl
Mammographic, US, and MR Imaging Phenotypes of Familial Breast Cancer
Radiology, January 1, 2008; 246(1): 58 - 70.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
L. Cao, X. Xu, L. L. Cao, R.-H. Wang, X. Coumoul, S. S. Kim, and C.-X. Deng
Absence of full-length Brca1 sensitizes mice to oxidative stress and carcinogen-induced tumorigenesis in the esophagus and forestomach
Carcinogenesis, July 1, 2007; 28(7): 1401 - 1407.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. S. Kim, L. Cao, S.-C. Lim, C. Li, R.-H. Wang, X. Xu, R. Bachelier, and C.-X. Deng
Hyperplasia and Spontaneous Tumor Development in the Gynecologic System in Mice Lacking the BRCA1-{Delta}11 Isoform.
Mol. Cell. Biol., September 1, 2006; 26(18): 6983 - 6992.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
H.-S. Kim, H. Li, M. Cevher, A. Parmelee, D. Fonseca, F. E. Kleiman, and S. B. Lee
DNA Damage-Induced BARD1 Phosphorylation Is Critical for the Inhibition of Messenger RNA Processing by BRCA1/BARD1 Complex.
Cancer Res., May 1, 2006; 66(9): 4561 - 4565.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
C.-X. Deng
BRCA1: cell cycle checkpoint, genetic instability, DNA damage response and cancer evolution
Nucleic Acids Res., March 6, 2006; 34(5): 1416 - 1426.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
S. Beetstra, C. Salisbury, J. Turner, M. Altree, R. McKinnon, G. Suthers, and M. Fenech
Lymphocytes of BRCA1 and BRCA2 germ-line mutation carriers, with or without breast cancer, are not abnormally sensitive to the chromosome damaging effect of moderate folate deficiency
Carcinogenesis, March 1, 2006; 27(3): 517 - 524.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
S. Furuta, X. Jiang, B. Gu, E. Cheng, P.-L. Chen, and W.-H. Lee
Depletion of BRCA1 impairs differentiation but enhances proliferation of mammary epithelial cells
PNAS, June 28, 2005; 102(26): 9176 - 9181.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
E. H. van Beers, T. van Welsem, L. F.A. Wessels, Y. Li, R. A. Oldenburg, P. Devilee, C. J. Cornelisse, S. Verhoef, F. B.L. Hogervorst, L. J. van't Veer, et al.
Comparative Genomic Hybridization Profiles in Human BRCA1 and BRCA2 Breast Tumors Highlight Differential Sets of Genomic Aberrations
Cancer Res., February 1, 2005; 65(3): 822 - 827.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
K. Nakanishi, Y.-G. Yang, A. J. Pierce, T. Taniguchi, M. Digweed, A. D. D'Andrea, Z.-Q. Wang, and M. Jasin
Human Fanconi anemia monoubiquitination pathway promotes homologous DNA repair
PNAS, January 25, 2005; 102(4): 1110 - 1115.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
R.-H. Wang, H. Yu, and C.-X. Deng
A requirement for breast-cancer-associated gene 1 (BRCA1) in the spindle checkpoint
PNAS, December 7, 2004; 101(49): 17108 - 17113.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. S. Kim, L. Cao, C. Li, X. Xu, L. J. Huber, L. A. Chodosh, and C.-X. Deng
Uterus Hyperplasia and Increased Carcinogen-Induced Tumorigenesis in Mice Carrying a Targeted Mutation of the Chk2 Phosphorylation Site in Brca1
Mol. Cell. Biol., November 1, 2004; 24(21): 9498 - 9507.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
A. MacLaren, E. J. Black, W. Clark, and D. A. F. Gillespie
c-Jun-Deficient Cells Undergo Premature Senescence as a Result of Spontaneous DNA Damage Accumulation
Mol. Cell. Biol., October 15, 2004; 24(20): 9006 - 9018.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
D.-T. Bau, Y.-P. Fu, S.-T. Chen, T.-C. Cheng, J.-C. Yu, P.-E. Wu, and C.-Y. Shen
Breast Cancer Risk and the DNA Double-Strand Break End-Joining Capacity of Nonhomologous End-Joining Genes Are Affected by BRCA1
Cancer Res., July 15, 2004; 64(14): 5013 - 5019.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
X. Wang, R.-H. Wang, W. Li, X. Xu, M. C. Hollander, A. J. Fornace Jr., and C.-X. Deng
Genetic Interactions between Brca1 and Gadd45a in Centrosome Duplication, Genetic Stability, and Neural Tube Closure
J. Biol. Chem., July 9, 2004; 279(28): 29606 - 29614.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
C. Pipaon, J. A. Casado, J. A. Bueren, and J. L. Fernandez-Luna
Jun N-terminal kinase activity and early growth-response factor-1 gene expression are down-regulated in Fanconi anemia group A lymphoblasts
Blood, January 1, 2004; 103(1): 128 - 132.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
P. Hohenstein and R. Fodde
Of mice and (wo)men: genotype-phenotype correlations in BRCA1
Hum. Mol. Genet., October 15, 2003; 12(90002): R271 - 277.
[Abstract] [Full Text] [PDF]

Home page
 J BiochemHome page
J. H. Kim, K. C. Park, S. S. Chung, O. Bang, and C. H. Chung
Deubiquitinating Enzymes as Cellular Regulators
J. Biochem., July 1, 2003; 134(1): 9 - 18.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.