The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Human Claspin works with BRCA1 to both positively and negatively regulate cell proliferation
Open accessAbstract
Claspin is a homolog of Mrc1, a checkpoint protein required for the DNA replication checkpoint in yeast. In Xenopus , phosphorylated Claspin binds to xChk1 and regulates xChk1 activation in response to replication stress. In this study, we have shown that the human homolog of Claspin is required for resistance to multiple forms of genotoxic stress including UV, IR, and hydroxyurea. Phosphorylation of Claspin was found to depend on the ataxia telangiectasia mutated-Rad3 related (ATR) pathway. DNA damage induces the formation of a complex between Claspin and BRCA1, a second regulator of Chk1 activation. Claspin was found to control BRCA1 phosphorylation on serine 1524, a site whose phosphorylation is controlled by the ATR pathway. These results are consistent with a model in which ATR regulates Claspin phosphorylation in response to DNA damage and replication stress resulting in recruitment and phosphorylation of BRCA1. BRCA1 and Claspin then function to activate the tumor suppressor Chk1. Unexpectedly, we found that Claspin has a second, positive role in control of the cell cycle as Claspin overexpression increased cell proliferation. These results suggest that Claspin has properties of both a tumor suppressor and an oncogene.
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“Claspin, a Chk1-binding protein, is required for ATR-Chk1 checkpoint activation [127–129].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [129]
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Cites
Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes
Zou, L., & Elledge, S. J. (2003) · Science · doi:10.1126/science.1083430 · Cited by 2,693
Self-citationCell cycle checkpoint signaling through the ATM and ATR kinases
Abraham, R. T. (2001) · Genes & Development · doi:10.1101/gad.914401 · Cited by 1,966
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Self-citationLinkage 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
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Self-citationAtaxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro
Matsuoka, S., Rotman, G., Ogawa, A., Shiloh, Y., Tamai, K., & Elledge, S. J. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.190030497 · Cited by 849
Self-citationRadiosensitivity in ataxia-telangiectasia: a new explanation.
Painter, R. B., & Young, B. R. (1980) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.77.12.7315 · Cited by 795
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S-phase checkpoint proteins Tof1 and Mrc1 form a stable replication-pausing complex
Katou, Y., Kanoh, Y., Bando, M., Noguchi, H., Tanaka, H., Ashikari, T., Sugimoto, K., & Shirahige, K. (2003) · Nature · doi:10.1038/nature01900 · Cited by 649
ATM and ATR: networking cellular responses to DNA damage
Shiloh, Y. (2001) · Current Opinion in Genetics & Development · doi:10.1016/s0959-437x(00)00159-3 · Cited by 601
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TopBP1 Activates the ATR-ATRIP Complex
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Initiating Cellular Stress Responses
Bakkenist, C. J., & Kastan, M. B. (2004) · Cell · doi:10.1016/j.cell.2004.06.023 · Cited by 544
Eukaryotic Chromosome DNA Replication: Where, When, and How?
Masai, H., Matsumoto, S., You, Z., Yoshizawa-Sugata, N., & Oda, M. (2010) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.052308.103205 · Cited by 524
The Cdc14B-Cdh1-Plk1 Axis Controls the G2 DNA-Damage-Response Checkpoint
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Metadata
- Authors
- Lin, S.-Y., Li, K., Stewart, G. S., & Elledge, S. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2004-04-19
- Volume
- 101
- Issue
- 17
- Pages
- 6484-6489
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC404071
- OpenAlex
- W2129258256
- Cited by
- 156
- References
- 27
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 11 · 2023: 5 · 2022: 4 · 2021: 4 · 2020: 8 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 5 · 2015: 3 · 2014: 6 · 2013: 3 · 2012: 7
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- National Cancer Institute (F32CA093043)
- National Institute of General Medical Sciences (GM-44664, R37GM044664, R01GM044664)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Keywords
- Claspin, BRCA1, Chk1, ATR pathway, DNA damage response, genotoxic stress resistance, replication stress, cell proliferation, tumor suppressor, oncogenes, protein phosphorylation, hydroxyurea
- MeSH terms
- Base Sequence, Carrier Proteins, Cell Division, Cell Survival, DNA Damage, Humans, Oligoribonucleotides, Phosphorylation, Protein Binding, BRCA1 Protein, Xenopus Proteins, Adaptor Proteins, Signal Transducing
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