ArticleCell cycle (Georgetown, Tex.)2012
The conserved C terminus of Claspin interacts with Rad9 and promotes rapid activation of Chk1.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Therapeutic potential of PRMT1 as a critical survival dependency target in multiple myeloma.BMC cancer · 2025Article
- TRIM21 suppresses CHK1 activation by preferentially targeting CLASPIN for K63-linked ubiquitination.Nucleic acids research · 2022Article
- Cdc7 activates replication checkpoint by phosphorylating the Chk1-binding domain of Claspin in human cells.eLife · 2019Article
- Investigation of the Possible Role of RAD9 in Post-Diapaused Embryonic Development of the Brine ShrimpGenes · 2019Article
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- Article
- p53 and RAD9, the DNA Damage Response, and Regulation of Transcription Networks.Radiation research · 2017Review
- DNA mismatch repair and the DNA damage response.DNA repair · 2016Review
- Pathways to chromothripsis.Cell cycle (Georgetown, Tex.) · 2015Article
- Over expression of hRad9 protein correlates with reduced chemosensitivity in breast cancer with administration of neoadjuvant chemotherapy.Scientific reports · 2014Article
- HERC2/USP20 coordinates CHK1 activation by modulating CLASPIN stability.Nucleic acids research · 2014Article
- The ATR signaling pathway is disabled during infection with the parvovirus minute virus of mice.Journal of virology · 2014Article
- CHK1 and WEE1 inhibition combine synergistically to enhance therapeutic efficacy in acute myeloid leukemia ex vivo.Haematologica · 2014Article
- DNA damage sensing by the ATM and ATR kinases.Cold Spring Harbor perspectives in biology · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Claspin is a key mediator of the ATR-Chk1 checkpoint pathway. In response to DNA damage, Claspin interacts with Rad17 and Chk1 in a phosphorylation-dependent manner, enabling ATR to phosphorylate Chk1 efficiently. Claspin also interacts with Rad9, but how they interact and whether the interaction is functional remains unknown. Unexpectedly, our analysis of two splicing isoforms of Claspin provided an answer to these questions. The Claspin(1339) isoform contains an evolutionarily conserved C terminus, but the Claspin(1332) isoform does not. Although the transcripts encoding both Claspin isoforms coexist in HCT116 cells, Claspin(1339) is the predominant form responsible for Chk1 activation. When expressed in cells depleted of endogenous Claspin, both Claspin(1339) and Claspin(1332) are able to mediate Chk1 activation. However, the activation of Chk1 is delayed in Claspin(1332)-expressing cells compared with Claspin(1339)-expressing cells. Furthermore, only Claspin(1339) but not Claspin(1332) interacts with Rad9 efficiently. Together, these results suggest that the conserved C terminus of Claspin interacts with Rad9 and ensures timely activation of the ATR-Chk1 pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.