ArticleDNA repair2009
Regulation of repair choice: Cdk1 suppresses recruitment of end joining factors at DNA breaks.
Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 53 citations in OpenAlex.
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- Regulation of Error-Prone DNA Double-Strand Break Repair and Its Impact on Genome Evolution.Cells · 2020Review
- Microhomology-mediated end joining: Good, bad and ugly.Mutation research · 2018Review
- The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 nuclease-helicase at DNA double strand breaks.The Journal of biological chemistry · 2017Article
- Cell Cycle-Dependent Expression of Adeno-Associated Virus 2 (AAV2) Rep in Coinfections with Herpes Simplex Virus 1 (HSV-1) Gives Rise to a Mosaic of Cells Replicating either AAV2 or HSV-1.Journal of virology · 2017Article
- Article
- Stabilization of the metaphase spindle by Cdc14 is required for recombinational DNA repair.The EMBO journal · 2017Article
- The plant-specific CDKB1-CYCB1 complex mediates homologous recombination repair in Arabidopsis.The EMBO journal · 2016Article
- A plant solution to the CDK conundrum in the DNA damage response.The EMBO journal · 2016Article
- The Exonuclease Homolog OsRAD1 Promotes Accurate Meiotic Double-Strand Break Repair by Suppressing Nonhomologous End Joining.Plant physiology · 2016Article
- Risky business: Microhomology-mediated end joining.Mutation research · 2016Review
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Sumoylation influences DNA break repair partly by increasing the solubility of a conserved end resection protein.PLoS genetics · 2015Article
- Cdk1 restrains NHEJ through phosphorylation of XRCC4-like factor Xlf1.Cell reports · 2014Article
- Review
- High levels of BRC4 induced by a Tet-On 3G system suppress DNA repair and impair cell proliferation in vertebrate cells.DNA repair · 2014Article
- End resection at double-strand breaks: mechanism and regulation.Cold Spring Harbor perspectives in biology · 2014Review
- DNA double-strand break repair pathway choice and cancer.DNA repair · 2014Review
- Cdk1-dependent regulation of the Mre11 complex couples DNA repair pathways to cell cycle progression.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cell cycle plays a crucial role in regulating the pathway used to repair DNA double-strand breaks (DSBs). In Saccharomyces cerevisiae, homologous recombination is primarily limited to non-G(1) cells as the formation of recombinogenic single-stranded DNA requires CDK1-dependent 5' to 3' resection of DNA ends. However, the effect of cell cycle on non-homologous end joining (NHEJ) is not yet clearly defined. Using an assay to quantitatively measure the contributions of each repair pathway to repair product formation and cellular survival after DSB induction, we found that NHEJ is most efficient at G(1), and markedly repressed at G(2). Repression of NHEJ at G(2) is achieved by efficient end resection and by the reduced association of core NHEJ proteins with DNA breaks, both of which depend on the CDK1 activity. Importantly, repression of 5' end resection by CDK1 inhibition at G(2) alone did not fully restore either physical association of Ku/Dnl4-Lif1 with DSBs or NHEJ proficiency to the level at G(1). Expression of excess Ku can partially offset the inhibition of end joining at G(2). The results suggest that regulation of Ku/Dnl4-Lif1 affinity for DNA ends may contribute to the cell cycle-dependent modulation of NHEJ efficiency.
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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.