ArticleSpringerPlus2014
Pcf1, a large subunit of CAF-1, required for maintenance of checkpoint kinase Cds1 activity.
Article in SpringerPlus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Crosstalk between H2A variant-specific modifications impacts vital cell functions.PLoS genetics · 2021Article
- Mutation in histone deacetylase clr6 promotes the survival of S. pombe cds1 null mutant in response to hydroxyurea.Molecular genetics and genomics : MGG · 2020Article
- An F-Box Protein, Mdm30, Interacts with TREX Subunit Sub2 To Regulate Cellular Abundance Cotranscriptionally in Orchestrating mRNA Export Independently of Splicing and Mitochondrial Function.Molecular and cellular biology · 2020Article
- Histone Chaperone Asf1 Is Required for the Establishment of Repressive Chromatin in Schizosaccharomyces pombe fbp1 Gene Repression.Molecular and cellular biology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Highly conserved chromatin assembly factor 1 (CAF-1) is required for histone deposition onto newly synthesized DNA to maintain genome stability. This study shows that the fission yeast Pcf1, the large subunit in CAF-1, is crucial for maintaining checkpoint kinase Cds1. Chromatin recruitment of Cds1 is enhanced by Pcf1 overproduction but is attenuated by the Δpcf1 mutation. Mutation of acetylation sites in the histone H4 tail abrogates the chromatin recruitment of Pcf1, which resembles that of Cds1 as reported previously. The present results provide evidence that chromatin recruitment of Pcf1, moderated by Clr6-HDAC activity, is essential for inactivating Cds1.
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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.