ArticleCell division2009
Regulation of chk1.
Article in Cell division, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- A C-degron regulates Chk1 kinase by allowing stability of inactive Chk1 and by making it short- lived upon activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CHK1 is an integral regulator of DNA replication in human cells.Cell death & disease · 2026Article
- CHK1 kinase inhibition: identification of allosteric hits using MD simulations, pharmacophore modeling, docking and MM-PBSA calculations.Molecular diversity · 2022Article
- Chk1 inhibitor-induced DNA damage increases BFL1 and decreases BIM but does not protect human cancer cell lines from Chk1 inhibitor-induced apoptosis.American journal of cancer research · 2022Article
- Candida albicans CHK1 gene from two-component system is essential for its pathogenicity in oral candidiasis.Applied microbiology and biotechnology · 2021Article
- Exploiting DNA repair pathways for tumor sensitization, mitigation of resistance, and normal tissue protection in radiotherapy.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- CHK2 is essential for spindle assembly and DNA repair during the first cleavage of mouse embryos.Aging · 2020Article
- Article
- Blocking c-Met and EGFR reverses acquired resistance of PARP inhibitors in triple-negative breast cancer.American journal of cancer research · 2020Article
- DNA Damage Response Pathways in Dinoflagellates.Microorganisms · 2019Article
- mTORC1/2 and Protein Translation Regulate Levels of CHK1 and the Sensitivity to CHK1 Inhibitors in Ewing Sarcoma Cells.Molecular cancer therapeutics · 2018Article
- Paths from DNA damage and signaling to genome rearrangements via homologous recombination.Mutation research · 2017Review
- Intramolecular autoinhibition of checkpoint kinase 1 is mediated by conserved basic motifs of the C-terminal kinase-associated 1 domain.The Journal of biological chemistry · 2017Article
- Inhibition of CHK1 sensitizes Ewing sarcoma cells to the ribonucleotide reductase inhibitor gemcitabine.Oncotarget · 2017Article
- Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.Neoplasia (New York, N.Y.) · 2017Article
- NSC30049 inhibits Chk1 pathway in 5-FU-resistant CRC bulk and stem cell populations.Oncotarget · 2017Article
- Translational research in radiation-induced DNA damage signaling and repair.Translational cancer research · 2017Article
- Control of Hsp90 chaperone and its clients by N-terminal acetylation and the N-end rule pathway.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Modification of tumour cell metabolism modulates sensitivity to Chk1 inhibitor-induced DNA damage.Scientific reports · 2017Article
- Inhibition of Chk1 with the small molecule inhibitor V158411 induces DNA damage and cell death in an unperturbed S-phase.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chk1 is a serine/threonine protein kinase that is the effector of the G2 DNA damage checkpoint. Chk1 homologs have a highly conserved N-terminal kinase domain, and a less conserved C-terminal regulatory domain of ~200 residues. In response to a variety of genomic lesions, a number of proteins collaborate to activate Chk1, which in turn ensures that the mitotic cyclin-dependent kinase Cdc2 remains in an inactive state until DNA repair is completed. Chk1 activation requires the phosphorylation of residues in the C-terminal domain, and this is catalyzed by the ATR protein kinase. How phosphorylation of the C-terminal regulatory domain activates the N-terminal kinase domain has not been elucidated, though some studies have suggested that this phosphorylation relieves an inhibitory intramolecular interaction between the N- and C-termini. However, recent studies in the fission yeast Schizosaccharomyces pombe have revealed that there is more to Chk1 regulation than this auto-inhibition model, and we review these findings and their implication to the biology of this genome integrity determinant.
Identifiers
What OpenQuestion holds
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.