ArticleMolecular and cellular biology2007
Mechanisms of checkpoint kinase Rad53 inactivation after a double-strand break in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 70 citations in OpenAlex.
- Fmp45 promotes Rad53 dephosphorylation via Ptc2 interaction to attenuate checkpoint signaling and maintain genome stability.Journal, genetic engineering & biotechnology · 2025Article
- The regulatory subunits of CK2 complex mediate DNA damage response and virulence in Candida Glabrata.BMC microbiology · 2023Article
- Homologous recombination suppresses transgenerational DNA end resection and chromosomal instability in fission yeast.Nucleic acids research · 2023Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- Mec1Cell reports · 2019Article
- DNA Damage Stress: Cui Prodest?International journal of molecular sciences · 2019Review
- On the Interplay of the DNA Replication Program and the Intra-S Phase Checkpoint Pathway.Genes · 2019Review
- PP2C phosphatases promote autophagy by dephosphorylation of the Atg1 complex.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Recovery from the DNA Replication Checkpoint.Genes · 2016Review
- A Genome-Wide Screen with Nicotinamide to Identify Sirtuin-Dependent Pathways in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2015Article
- Tryptophan-Dependent Control of Colony Formation After DNA Damage via Sea3-Regulated TORC1 Signaling in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2015Article
- Yeast PP4 interacts with ATR homolog Ddc2-Mec1 and regulates checkpoint signaling.Molecular cell · 2015Article
- When genome integrity and cell cycle decisions collide: roles of polo kinases in cellular adaptation to DNA damage.Systems and synthetic biology · 2014Review
- Use of quantitative mass spectrometric analysis to elucidate the mechanisms of phospho-priming and auto-activation of the checkpoint kinase Rad53 in vivo.Molecular & cellular proteomics : MCP · 2014Article
- Deacetylase Rpd3 facilitates checkpoint adaptation by preventing Rad53 overactivation.Molecular and cellular biology · 2013Article
- Article
- DNA damage checkpoint triggers autophagy to regulate the initiation of anaphase.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Saccharomyces cerevisiae, double-strand breaks (DSBs) activate DNA checkpoint pathways that trigger several responses including a strong G(2)/M arrest. We have previously provided evidence that the phosphatases Ptc2 and Ptc3 of the protein phosphatase 2C type are required for DNA checkpoint inactivation after a DSB and probably dephosphorylate the checkpoint kinase Rad53. In this article we have investigated further the interactions between Ptc2 and Rad53. We showed that forkhead-associated domain 1 (FHA1) of Rad53 interacts with a specific threonine of Ptc2, T376, located outside its catalytic domain in a TXXD motif which constitutes an optimal FHA1 binding sequence in vitro. Mutating T376 abolishes Ptc2 interaction with the Rad53 FHA1 domain and results in adaptation and recovery defects following a DSB. We found that Ckb1 and Ckb2, the regulatory subunits of the protein kinase CK2, are necessary for the in vivo interaction between Ptc2 and the Rad53 FHA1 domain, that Ckb1 binds Ptc2 in vitro and that ckb1Delta and ckb2Delta mutants are defective in adaptation and recovery after a DSB. Our data thus strongly suggest that CK2 is the kinase responsible for the in vivo phosphorylation of Ptc2 T376.
Indexed as
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.