The DOI matches its Crossref record; 116 of the 116 references it cites were found in a registry or an index.
BRCA1: cell cycle checkpoint, genetic instability, DNA damage response and cancer evolution
Open accessAbstract
Germline mutations of the breast cancer associated gene 1 (BRCA1) predispose women to breast and ovarian cancers. BRCA1 is a large protein with multiple functional domains and interacts with numerous proteins that are involved in many important biological processes/pathways. Mounting evidence indicates that BRCA1 is involved in all phases of the cell cycle and regulates orderly events during cell cycle progression. BRCA1 deficiency, consequently causes abnormalities in the S-phase checkpoint, the G(2)/M checkpoint, the spindle checkpoint and centrosome duplication. The genetic instability caused by BRCA1 deficiency, however, also triggers cellular responses to DNA damage that blocks cell proliferation and induces apoptosis. Thus BRCA1 mutant cells cannot develop further into full-grown tumors unless this cellular defense is broken. Functional analysis of BRCA1 in cell cycle checkpoints, genome integrity, DNA damage response (DDR) and tumor evolution should benefit our understanding of the mechanisms underlying BRCA1 associated tumorigenesis, as well as the development of therapeutic approaches for this lethal disease.
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Cites
1 retracted
BRCA1 Phosphorylation by Aurora-A in the Regulation of G2 to M Transition
Ouchi, M., Fujiuchi, N., Sasai, K., Katayama, H., Minamishima, Y. A., Ongusaha, P. P., Deng, C., Sen, S., Lee, S. W., & Ouchi, T. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m311780200 · Cited by 199
Self-citationRetractedWAF1, a potential mediator of p53 tumor suppression
El-Deiry, W. S., Tokino, T., Velculescu, V. E., Levy, D. B., Parsons, R., Trent, J. M., Lin, D., Mercer, W. E., Kinzler, K. W., & Vogelstein, B. (1993) · Cell · doi:10.1016/0092-8674(93)90500-p · Cited by 8,321
Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
Farmer, H., McCabe, N., Lord, C. J., Tutt, A. N. J., Johnson, D. A., Richardson, T. B., Santarosa, M., Dillon, K. J., Hickson, I., Knights, C., et al. (2005) · Nature · doi:10.1038/nature03445 · Cited by 6,683
A Strong Candidate for the Breast and Ovarian Cancer Susceptibility Gene BRCA1
Miki, Y., Swensen, J., Shattuck-Eidens, D., Futreal, P. A., Harshman, K., Tavtigian, S., Liu, Q., Cochran, C., Bennett, L. M., Ding, W., et al. (1994) · Science · doi:10.1126/science.7545954 · Cited by 6,071
The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases.
Wade Harper, J. (1993) · Cell · doi:10.1016/0092-8674(93)90499-g · Cited by 5,651
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
Bryant, H. E., Schultz, N., Thomas, H. D., Parker, K. M., Flower, D., Lopez, E., Kyle, S., Meuth, M., Curtin, N. J., & Helleday, T. (2005) · Nature · doi:10.1038/nature03443 · Cited by 5,198
Molecular Mechanisms of Mammalian DNA Repair and the DNA Damage Checkpoints
Sancar, A., Lindsey-Boltz, L. A., Ünsal-Kaçmaz, K., & Linn, S. (2004) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.73.011303.073723 · Cited by 3,317
Genetic Heterogeneity and Penetrance Analysis of the BRCA1 and BRCA2 Genes in Breast Cancer Families
Ford, D., Easton, D. F., Stratton, M., Narod, S., Goldgar, D., Devilee, P., Bishop, D. T., Weber, B., Lenoir, G., Chang-Claude, J., et al. (1998) · The American Journal of Human Genetics · doi:10.1086/301749 · Cited by 3,037
Cell-cycle checkpoints and cancer
Kastan, M. B., & Bartek, J. (2004) · Nature · doi:10.1038/nature03097 · Cited by 2,836
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
Bartkova, J., Hořejší, Z., Koed, K., Krämer, A., Tort, F., Zieger, K., Guldberg, P., Sehested, M., Nesland, J. M., Lukas, C., et al. (2005) · Nature · doi:10.1038/nature03482 · Cited by 2,688
Cited by
53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks
Bunting, S. F., Callén, E., Wong, N., Chen, H.-T., Polato, F., Gunn, A., Bothmer, A., Feldhahn, N., Fernandez-Capetillo, O., Cao, L., et al. (2010) · Cell · doi:10.1016/j.cell.2010.03.012 · Cited by 1,671
Self-citationBouwman, P., Aly, A., Escandell, J. M., Pieterse, M., Bartkova, J., van der Gulden, H., Hiddingh, S., Thanasoula, M., Kulkarni, A., Yang, Q., et al. (2010) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.1831 · Cited by 1,001
Kim, H.-S., Patel, K., Muldoon-Jacobs, K., Bisht, K. S., Aykin-Burns, N., Pennington, J. D., van der Meer, R., Nguyen, P., Savage, J., Owens, K. M., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.11.023 · Cited by 785
Self-citationImpaired DNA Damage Response, Genome Instability, and Tumorigenesis in SIRT1 Mutant Mice
Wang, R.-H., Sengupta, K., Li, C., Kim, H.-S., Cao, L., Xiao, C., Kim, S., Xu, X., Zheng, Y., Chilton, B., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2008.09.001 · Cited by 769
Self-citationThe roles of BRCA1 and BRCA2 and associated proteins in the maintenance of genomic stability
Gudmundsdottir, K., & Ashworth, A. (2006) · Oncogene · doi:10.1038/sj.onc.1209874 · Cited by 622
Metadata
- Authors
- Deng, C.-X.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-03-06
- Volume
- 34
- Issue
- 5
- Pages
- 1416-1426
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- OpenAlex
- W1989059483
- Cited by
- 584
- References
- 116
- FWCI
- 19.62
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
