ArticleCell cycle (Georgetown, Tex.)2011
Timeless functions independently of the Tim-Tipin complex to promote sister chromatid cohesion in normal human fibroblasts.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- ATR-CHK1 Axis Inhibitors in Gastric Cancer Treatment.International journal of molecular sciences · 2025Review
- Article
- The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023Review
- The Interplay of Cohesin and the Replisome at Processive and Stressed DNA Replication Forks.Cells · 2021Review
- Functional Coupling between DNA Replication and Sister Chromatid Cohesion Establishment.International journal of molecular sciences · 2021Review
- TIMELESS inhibits breast cancer cell invasion and metastasis by down-regulating the expression of MMP9.Cancer cell international · 2021Article
- TIMELESS Promotes Tumor Progression by Enhancing Macrophages Recruitment in Ovarian Cancer.Frontiers in oncology · 2021Article
- SDE2 integrates into the TIMELESS-TIPIN complex to protect stalled replication forks.Nature communications · 2020Article
- Implications ofCancers · 2020Article
- Interaction of the Warsaw breakage syndrome DNA helicase DDX11 with the replication fork-protection factor Timeless promotes sister chromatid cohesion.PLoS genetics · 2018Article
- TIMELESS Suppresses the Accumulation of Aberrant CDC45·MCM2-7·GINS Replicative Helicase Complexes on Human Chromatin.The Journal of biological chemistry · 2016Article
- Tim/Timeless, a member of the replication fork protection complex, operates with the Warsaw breakage syndrome DNA helicase DDX11 in the same fork recovery pathway.Nucleic acids research · 2016Article
- Article
- TIPIN depletion leads to apoptosis in breast cancer cells.Molecular oncology · 2015Article
- Tipin functions in the protection against topoisomerase I inhibitor.The Journal of biological chemistry · 2014Article
- Mechanisms of cohesin-mediated gene regulation and lessons learned from cohesinopathies.Biochimica et biophysica acta · 2014Review
- Linking chromosome duplication and segregation via sister chromatid cohesion.Methods in molecular biology (Clifton, N.J.) · 2014Review
- A high resolution genomic portrait of bladder cancer: correlation between genomic aberrations and the DNA damage response.Oncogene · 2013Article
- The human Tim-Tipin complex interacts directly with DNA polymerase epsilon and stimulates its synthetic activity.The Journal of biological chemistry · 2013Article
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9 authors at 1 institution in 1 country.
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Abstract
The Timeless-Tipin complex and Claspin are mediators of the ATR-dependent activation of Chk1 in the intra-S checkpoint response to stalled DNA replication forks. Tim-Tipin and Claspin also contribute to sister chromatid cohesion (SCC) in various organisms, likely through a replication-coupled process. Some models of the establishment of SCC posit that interactions between cohesin rings and replisomes could result in physiological replication stress requiring fork stabilization. The contributions of Timeless, Tipin, Claspin, Chk1 and ATR to SCC were investigated in genetically stable, human diploid fibroblast cell lines. Whereas Timeless, Tipin and Claspin showed similar contributions to UVC-induced activation of Chk1, siRNA-mediated knockdown of Timeless induced a 100-fold increase in sister chromatid discohesion, whereas the inductive effects of knocking down Tipin, Claspin and ATR were 4-20-fold. Knockdown of Chk1 did not significantly affect SCC. Consistent findings were obtained in two independently derived human diploid fibroblast lines and support a conclusion that SCC in human cells is strongly dependent on Timeless but independent of Chk1. Furthermore, the 10-fold difference in discohesion observed when depleting Timeless versus Tipin indicates that Timeless has a function in SCC that is independent of the Tim-Tipin complex, even though the abundance of Timeless is reduced when Tipin is targeted for depletion. A better understanding of how Timeless, Tipin and Claspin promote SCC will elucidate non-checkpoint functions of these proteins at DNA replication forks and inform models of the establishment of SCC.
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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.