The DOI matches its Crossref record; 52 of the 54 references it cites were found in a registry or an index.
BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures.
Open accessAbstract
We report the identities of the members of a group of proteins that associate with BRCA1 to form a large complex that we have named BASC (B RCA1-a ssociated genome s urveillance c omplex). This complex includes tumor suppressors and DNA damage repair proteins MSH2, MSH6, MLH1, ATM, BLM, and the RAD50–MRE11–NBS1 protein complex. In addition, DNA replication factor C (RFC), a protein complex that facilitates the loading of PCNA onto DNA, is also part of BASC. We find that BRCA1, the BLM helicase, and the RAD50–MRE11–NBS1 complex colocalize to large nuclear foci that contain PCNA when cells are treated with agents that interfere with DNA synthesis. The association of BRCA1 with MSH2 and MSH6, which are required for transcription-coupled repair, provides a possible explanation for the role of BRCA1 in this pathway. Strikingly, all members of this complex have roles in recognition of abnormal DNA structures or damaged DNA, suggesting that BASC may serve as a sensor for DNA damage. Several of these proteins also have roles in DNA replication-associated repair. Collectively, these results suggest that BRCA1 may function as a coordinator of multiple activities required for maintenance of genomic integrity during the process of DNA replication and point to a central role for BRCA1 in DNA repair.
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“In addition to ATM, the members of the BASC include the mismatch repair proteins, MLH1, MSH2, and MSH6, the Bloom's syndrome helicase (BLM), and the Mre11-Rad50-NBS1 complex.”
From Cell cycle checkpoint signaling through the ATM and ATR kinases (2001) · cites this paper as Wang et al. 2000
In the citing paper
“Recent findings position ATM and ATR as critical upstream modulators of the breast cancer susceptibility protein, BRCA1”
From Cell cycle checkpoint signaling through the ATM and ATR kinases (2001) · cites this paper as Wang et al. 2000
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Citations
Cites
1 retracted
BRCA1 required for transcription-coupled repair of oxidative DNA damage
Gowen, L. C., Avrutskaya, A. V., Latour, A. M., Koller, B. H., & Leadon, S. A. (1998) · Science · doi:10.1126/science.281.5379.1009 · Cited by 496
RetractedA Strong Candidate for the Breast and Ovarian Cancer Susceptibility Gene BRCA1
Miki, Y., Swensen, J. J., Shattuck-Eidens, D. M., Futreal, P. A., Harshman, K., Tavtigian, S. V., Liu, Q., Cochran, C., Bennett, L. M., Ding, W., et al. (1994) · Science · doi:10.1126/science.7545954 · Cited by 6,069
Lessons from hereditary colorectal cancer
Kinzler, K. W., & Vogelstein, B. (1996) · Cell · doi:10.1016/s0092-8674(00)81333-1 · Cited by 4,919
A Single Ataxia Telangiectasia Gene with a Product Similar to PI-3 Kinase
Savitsky, K., Bar-Shira, A., Gilad, S., Rotman, G., Ziv, Y., Vanagaite, L., Tagle, D. A., Smith, S., Uziel, T., Sfez, S., et al. (1995) · Science · doi:10.1126/science.7792600 · Cited by 2,785
Activation of the ATM Kinase by Ionizing Radiation and Phosphorylation of p53
Canman, C. E., Lim, D.-S., Cimprich, K. A., Taya, Y., Tamai, K., Sakaguchi, K., Appella, E., Kastan, M. B., & Siliciano, J. D. (1998) · Science · doi:10.1126/science.281.5383.1677 · Cited by 2,042
Enhanced Phosphorylation of p53 by ATM in Response to DNA Damage
Banin, S., Moyal, L., Shieh, S.-Y., Taya, Y., Anderson, C. W., Chessa, L., Smorodinsky, N. I., Prives, C., Reiss, Y., Shiloh, Y., et al. (1998) · Science · doi:10.1126/science.281.5383.1674 · Cited by 1,797
Association of BRCA1 with Rad51 in Mitotic and Meiotic Cells
Scully, R., Chen, J., Plug, A., Xiao, Y., Weaver, D., Feunteun, J., Ashley, T., & Livingston, D. M. (1997) · Cell · doi:10.1016/s0092-8674(00)81847-4 · Cited by 1,459
The Bloom's syndrome gene product is homologous to RecQ helicases
Ellis, N. A., Groden, J. L., Ye, T.-Z., Straughen, J. E., Lennon, D. J., Ciocci, S., Proytcheva, M. A., & GERMAN, J. L. (1995) · Cell · doi:10.1016/0092-8674(95)90105-1 · Cited by 1,385
BRCA1 mutations in primary breast and ovarian carcinomas.
Futreal, P., Liu, Q., Shattuck-Eidens, D., Cochran, C., Harshman, K., Tavtigian, S., Bennett, L., Haugen-Strano, A., Swensen, J., & Miki, Y. (1994) · Science · doi:10.1126/science.7939630 · Cited by 1,378
Linkage of ATM to Cell Cycle Regulation by the Chk2 Protein Kinase
Matsuoka, S. (1998) · Science · doi:10.1126/science.282.5395.1893 · Cited by 1,322
Cited by
Sorted by citations
The DNA damage response: putting checkpoints in perspective
Zhou, B.-B. S., & Elledge, S. J. (2000) · Nature · doi:10.1038/35044005 · Cited by 3,213
Self-citationATM and related protein kinases: safeguarding genome integrity
Shiloh, Y. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1011 · Cited by 2,577
DNA double-strand breaks: signaling, repair and the cancer connection
Khanna, K. K., & Jackson, S. P. (2001) · Nature Genetics · doi:10.1038/85798 · Cited by 2,455
Cell cycle checkpoint signaling through the ATM and ATR kinases
Abraham, R. T. (2001) · Genes & Development · doi:10.1101/gad.914401 · Cited by 1,966
Cancer Susceptibility and the Functions of BRCA1 and BRCA2
Venkitaraman, A. R. (2002) · Cell · doi:10.1016/s0092-8674(02)00615-3 · Cited by 1,713
Metadata
- Authors
- Wang, Y., Cortez, D., Yazdi, P., Neff, N., Elledge, S. J., & Qin, J.
- Affiliations
- New York Blood Center (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2000-04-15
- Volume
- 14
- Issue
- 8
- Pages
- 927-939
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC316544
- OpenAlex
- W2127566231
- Cited by
- 1,221
- References
- 54
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 10 · 2023: 16 · 2022: 21 · 2021: 27 · 2020: 20 · 2019: 26 · 2018: 20 · 2017: 24 · 2016: 29 · 2015: 33 · 2014: 49 · 2013: 43 · 2012: 35
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Jane Coffin Childs Memorial Fund for Medical Research
- U.S. Bureau of Land Management
- U.S. Public Health Service (Q1187)
- National Institute of General Medical Sciences (GM-44664, R37GM044664, R01GM044664)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- BRCA1, BASC, DNA repair, MSH2, MSH6, MLH1, ATM, BLM helicase, PCNA, DNA damage recognition, genome stability, tumor suppressor proteins, nuclear foci
- MeSH terms
- Adenosine Triphosphatases, Cell Cycle, Cell Nucleus, DNA Repair, DNA Helicases, DNA-Binding Proteins, Endodeoxyribonucleases, Exodeoxyribonucleases, Fluorescent Antibody Technique, Fungal Proteins, HeLa Cells, Humans, Nuclear Proteins, Precipitin Tests, Protein Binding, Mass Spectrometry, Transcription, Genetic, Signal Transduction, Cell Cycle Proteins, BRCA1 Protein, Saccharomyces cerevisiae Proteins, Replication Protein C, RecQ Helicases
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