The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Human Claspin Is Required for Replication Checkpoint Control
Open accessAbstract
Claspin is a newly identified protein that regulates Chk1 activation in Xenopus. In the present study we investigated the role of human Claspin in the DNA damage/replication checkpoint in mammalian cells. We observed that human Claspin is a cell cycle regulated protein that peaks at S/G2 phase. Claspin localizes in the nuclei, but it only associates with Chk1 following replication stress or other types of DNA damage. In addition, Claspin is phosphorylated in response to replication stress, and this phosphorylation appears to be required for its association with Chk1. Moreover, Claspin interacts with the checkpoint proteins ATR and Rad9. Given that both the ATR and Rad9-Rad1-Hus1 complexes are involved in Chk1 activation, it is possible that Claspin works as an adaptor molecule bringing these molecules together. Using small interfering RNA technology, we have shown that down-regulation of Claspin expression inhibits Chk1 activation in response to replication stress. More importantly, down-regulation of Claspin augments the premature chromatin condensation induced by hydroxyurea, inhibits the UV-induced reduction of DNA synthesis, and decreases cell survival. Taken together, these data imply a potentially critical role for Claspin in replication checkpoint control in mammalian cells.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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 [128]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells
Elbashir, S. M., Harborth, J., Lendeckel, W., Yalcin, A., Weber, K., & Tuschl, T. (2001) · Nature · doi:10.1038/35078107 · Cited by 9,456
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
Liu, Q., Guntuku, S., Cui, X.-S., Matsuoka, S., Cortez, D., Tamai, K., Luo, G., Carattini-Rivera, S., DeMayo, F., Bradley, A., et al. (2000) · Genes & Development · doi:10.1101/gad.14.12.1448 · Cited by 1,625
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
Sanchez, Y., Wong, C., Thoma, R. S., Richman, R., Wu, Z., Piwnica-Worms, H., & Elledge, S. J. (1997) · Science · doi:10.1126/science.277.5331.1497 · Cited by 1,320
ATR-Mediated Checkpoint Pathways Regulate Phosphorylation and Activation of Human Chk1
Zhao, H., & Piwnica-Worms, H. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.13.4129-4139.2001 · Cited by 1,091
(1999) · PubMed · Cited by 1,030
ATR disruption leads to chromosomal fragmentation and early embryonic lethality
Brown, E. J., & Baltimore, D. (2000) · Genes & Development · doi:10.1101/gad.14.4.397 · Cited by 951
Ataxia 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
Substrate Specificities and Identification of Putative Substrates of ATM Kinase Family Members
Kim, S.-T., Lim, D.-S., Canman, C. E., & Kastan, M. B. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.53.37538 · Cited by 810
Flagged first, then by citations
Research works printed but not linked: 3
- Sarkaria, 1999, Cancer Res., 59, 4375
- Busby, 2000, Cancer Res., 60, 2108
- Guo, 2002, Cell Growth Differ., 13, 77
Cited by
Sorted by citations
TopBP1 Activates the ATR-ATRIP Complex
Kumagai, A., Lee, J., Yoo, H. Y., & Dunphy, W. G. (2006) · Cell · doi:10.1016/j.cell.2005.12.041 · Cited by 787
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
Targeting the checkpoint kinases: chemosensitization versus chemoprotection
Zhou, B. S., & Bártek, J. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1296 · Cited by 401
Peschiaroli, A., Dorrello, N. V., Guardavaccaro, D., Venere, M., Halazonetis, T., Sherman, N. E., & Pagano, M. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.06.013 · Cited by 289
The Rad9-Hus1-Rad1 Checkpoint Clamp Regulates Interaction of TopBP1 with ATR
Lee, J., Kumagai, A., & Dunphy, W. G. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m704635200 · Cited by 294
Metadata
- Authors
- Chini, C. C. S., & Chen, J.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Chen, Junjie
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 278
- Issue
- 32
- Pages
- 30057-30062
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2137310763
- Cited by
- 244
- References
- 39
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 2 · 2023: 9 · 2022: 2 · 2021: 9 · 2020: 8 · 2019: 13 · 2018: 5 · 2017: 8 · 2016: 12 · 2015: 11 · 2014: 8 · 2013: 10 · 2012: 15
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Mayo Clinic
- National Institutes of Health
- National Cancer Institute (R01CA089239, R01 CA 89239, R01CA092312, CA92312)
- 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 › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- Claspin, S-phase checkpoint, DNA damage checkpoint, Chk1 activation, ATR, protein phosphorylation, replication stress, cell cycle regulation, chromatin condensation, hydroxyurea, adaptor proteins
- MeSH terms
- Carrier Proteins, Cell Cycle, Cell Line, Cell Survival, Chromatin, DNA, DNA Damage, DNA-Binding Proteins, Endonucleases, HeLa Cells, Humans, Hydroxyurea, Microscopy, Fluorescence, Mitosis, Phosphorylation, Precipitin Tests, Time Factors, Transfection, Tumor Cells, Cultured, Ultraviolet Rays, Down-Regulation, G2 Phase, S Phase, Protein Serine-Threonine Kinases, Cell Cycle Proteins, K562 Cells, Schizosaccharomyces pombe Proteins, Xenopus Proteins, RNA, Small Interfering, Adaptor Proteins, Signal Transducing, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
