ArticleGenetics2006
Antagonism of Chk1 signaling in the G2 DNA damage checkpoint by dominant alleles of Cdr1.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- XPG-related nucleases are hierarchically recruited for double-stranded rDNA break resection.The Journal of biological chemistry · 2019Article
- H2A.Z-dependent regulation of cohesin dynamics on chromosome arms.Molecular and cellular biology · 2014Article
- Regulatory motifs in Chk1.Cell cycle (Georgetown, Tex.) · 2013Article
- Initiation of DNA damage responses through XPG-related nucleases.The EMBO journal · 2013Article
- Brc1-dependent recovery from replication stress.Journal of cell science · 2012Article
- Nse1-dependent recruitment of Smc5/6 to lesion-containing loci contributes to the repair defects of mutant complexes.Molecular biology of the cell · 2011Article
- Transformation/transcription domain-associated protein (TRRAP)-mediated regulation of Wee1.Genetics · 2010Article
- Smc5-Smc6-dependent removal of cohesin from mitotic chromosomes.Molecular and cellular biology · 2009Article
- Regulation of chk1.Cell division · 2009Article
- Turning off the G2 DNA damage checkpoint.DNA repair · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Activation of the Chk1 protein kinase by DNA damage enforces a checkpoint that maintains Cdc2 in its inactive, tyrosine-15 (Y15) phosphorylated state. Chk1 downregulates the Cdc25 phosphatases and concomitantly upregulates the Wee1 kinases that control the phosphorylation of Cdc2. Overproduction of Chk1 causes G(2) arrest/delay independently of DNA damage and upstream checkpoint genes. We utilized this to screen fission yeast for mutations that alter sensitivity to Chk1 signaling. We describe three dominant-negative alleles of cdr1, which render cells supersensitive to Chk1 levels, and suppress the checkpoint defects of chk1Delta cells. Cdr1 encodes a protein kinase previously identified as a negative regulator of Wee1 activity in response to limited nutrition, but Cdr1 has not previously been linked to checkpoint signaling. Overproduction of Cdr1 promotes checkpoint defects and exacerbates the defective response to DNA damage of cells lacking Chk1. We conclude that regulation of Wee1 by Cdr1 and possibly by related kinases is an important antagonist of Chk1 signaling and represents a novel negative regulation of cell cycle arrest promoted by this checkpoint.
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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.