ArticleCell cycle (Georgetown, Tex.)2013
Separation of intra-S checkpoint protein contributions to DNA replication fork protection and genomic stability in normal human fibroblasts.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Two fork protection complexes at the replication fork play distinct roles in fork progression and stress response.Research square · 2026Article
- A new model for coordinating the functions of TIMELESS at the replication fork.bioRxiv : the preprint server for biology · 2025Article
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- Implications ofCancers · 2020Article
- Article
- Roles of OB-Fold Proteins in Replication Stress.Frontiers in cell and developmental biology · 2020Review
- Article
- mTORC1 and DNA-PKcs as novel molecular determinants of sensitivity to Chk1 inhibition.Molecular oncology · 2016Article
- TIPIN depletion leads to apoptosis in breast cancer cells.Molecular oncology · 2015Article
- Inhibition of Survivin with YM155 Induces Durable Tumor Response in Anaplastic Thyroid Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- Identification of novel radiosensitizers in a high-throughput, cell-based screen for DSB repair inhibitors.Molecular cancer therapeutics · 2015Article
- Article
- Mechanisms of chromosomal instability in melanoma.Environmental and molecular mutagenesis · 2014Article
- Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?Cell cycle (Georgetown, Tex.) · 2013Article
- Exosomal-miR-129-2-3p derived fromGut microbesArticle
- The fork and the kinase: a DNA replication tale from a CHK1 perspective.Mutation research. Reviews in mutation researchReview
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The ATR-dependent intra-S checkpoint protects DNA replication forks undergoing replication stress. The checkpoint is enforced by ATR-dependent phosphorylation of CHK1, which are mediated by the TIMELESS-TIPIN complex and CLASPIN. Although loss of checkpoint proteins is associated with spontaneous chromosomal instability, few studies have examined the contribution of these proteins to unchallenged DNA metabolism in human cells that have not undergone carcinogenesis or crisis. Furthermore, the TIMELESS-TIPIN complex and CLASPIN may promote replication fork protection independently of CHK1 activation. Normal human fibroblasts (NHF) were depleted of ATR, CHK1, TIMELESS, TIPIN or CLASPIN and chromosomal aberrations, DNA synthesis, activation of the DNA damage response (DDR) and clonogenic survival were evaluated. This work demonstrates in NHF lines from two individuals that ATR and CHK1 promote chromosomal stability by different mechanisms that depletion of CHK1 produces phenotypes that resemble more closely the depletion of TIPIN or CLASPIN than the depletion of ATR, and that TIMELESS has a distinct contribution to suppression of chromosomal instability that is independent of its heterodimeric partner, TIPIN. Therefore, ATR, CHK1, TIMELESS-TIPIN and CLASPIN have functions for preservation of intrinsic chromosomal stability that is separate from their cooperation for activation of the intra-S checkpoint response to experimentally induced replication stress. These data reveal a complex and coordinated program of genome maintenance enforced by proteins known for their intra-S checkpoint function.
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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.