ArticleCell cycle (Georgetown, Tex.)2012
The checkpoint transcriptional response: make sure to turn it off once you are satisfied.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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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
11 citing papers in PubMed.
- Article
- Checkpoint Regulation of Nuclear Tos4 Defines S Phase Arrest in Fission Yeast.G3 (Bethesda, Md.) · 2020Article
- Maintenance of genome stability: the unifying role of interconnections between the DNA damage response and RNA-processing pathways.Current genetics · 2018Review
- Diverse roles of Dpb2, the non-catalytic subunit of DNA polymerase ε.Current genetics · 2017Review
- The Intra-S Checkpoint Responses to DNA Damage.Genes · 2017Review
- Mutations in the Non-Catalytic Subunit Dpb2 of DNA Polymerase Epsilon Affect the Nrm1 Branch of the DNA Replication Checkpoint.PLoS genetics · 2017Article
- Review
- Checkpoint regulation of replication forks: global or local?Biochemical Society transactions · 2013Review
- Control of cell cycle transcription during G1 and S phases.Nature reviews. Molecular cell biology · 2013Review
- The DNA damage checkpoint response to replication stress: A Game of Forks.Frontiers in genetics · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The replication checkpoint signaling network monitors the presence of replication-induced lesions to DNA and coordinates an elaborate cellular response that includes ample transcriptional reprogramming. Recent work has established two major groups of replication stress-induced genes in Saccharomyces cerevisiae, the DNA damage response (DDR) genes and G 1/S cell cycle (CC) genes. In both cases, transcriptional activation is mediated via checkpoint-dependent inhibition of a transcriptional repressor (Crt1 for DDR and Nrm1 for CC) that participates in negative feedback regulation. This repressor-mediated regulation enables transcription to be rapidly repressed once cells have dealt with the replication stress. The recent finding of a new class of CC genes, named "switch genes," further uncovers a mode of transcription regulation that prevents overexpression of replication stress induced genes during G 1. Collectively, these findings highlight the need for mechanisms that tightly control replication stress-induced transcription, allowing rapid transcriptional activation during replication stress but also avoiding long-term hyperaccumulation of the induced protein product that may be detrimental to cell proliferation.
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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.