ArticlePloS one2009
The role of specific checkpoint-induced S-phase transcripts in resistance to replicative stress.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- An essential role for dNTP homeostasis following CDK-induced replication stress.Journal of cell science · 2019Article
- The Intra-S Checkpoint Responses to DNA Damage.Genes · 2017Review
- ATM/CHK/p53 Pathway Dependent Chemopreventive and Therapeutic Activity on Lung Cancer by Pterostilbene.PloS one · 2016Article
- DNA replication stress differentially regulates G1/S genes via Rad53-dependent inactivation of Nrm1.The EMBO journal · 2012Article
- Phosphorylation of the MBF repressor Yox1p by the DNA replication checkpoint keeps the G1/S cell-cycle transcriptional program active.PloS one · 2011Article
- Yox1 links MBF-dependent transcription to completion of DNA synthesis.EMBO reports · 2011Article
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 at 1 institution in 1 country.
Funding
Abstract
Checkpoint activation during S phase modulates transcription. In response to replication arrest, the fission yeast Cds1 checkpoint kinase maintains the normal S-phase transcriptional program by regulating MBF, the S-phase transcription factor. We show that similar regulation occurs in response to DNA damage during S-phase. We test the relative contributions to replication-stress resistance of transcriptional regulation and the two other major checkpoint functions: cell-cycle arrest and fork stabilization. We show that, although transcriptional regulation provides only modest resistance relative to fork stabilization, it contributes significantly to cell survival. Finally, we investigate the roles of two specific transcripts: mik1 and mrc1. These results demonstrate the general importance of checkpoint regulation of G1/S transcription in response to replicative stress and elucidate the specific roles of Mik1 and Mrc1 in the 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.