ArticleGenetics2008
Functional interactions between Sae2 and the Mre11 complex.
Article in Genetics, 2008. 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
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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
39 citing papers in PubMed, 55 citations in OpenAlex.
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Meiotic prophase length modulates Tel1-dependent DNA double-strand break interference.PLoS genetics · 2024Article
- Nej1 interacts with Sae2 at DNA double-stranded breaks to inhibit DNA resection.The Journal of biological chemistry · 2022Article
- Functional and structural insights into the MRX/MRN complex, a key player in recognition and repair of DNA double-strand breaks.Computational and structural biotechnology journal · 2020Review
- CDK and Mec1/Tel1-catalyzed phosphorylation of Sae2 regulate different responses to DNA damage.Nucleic acids research · 2019Article
- Article
- Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context.Frontiers in molecular biosciences · 2019Review
- Sae2 antagonizes Rad9 accumulation at DNA double-strand breaks to attenuate checkpoint signaling and facilitate end resection.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Regulatory control of DNA end resection by Sae2 phosphorylation.Nature communications · 2018Article
- Fumarase is involved in DNA double-strand break resection through a functional interaction with Sae2.Current genetics · 2018Article
- Genetic Separation of Sae2 Nuclease Activity from Mre11 Nuclease Functions in Budding Yeast.Molecular and cellular biology · 2017Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
- Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
- DNA End Resection: Nucleases Team Up with the Right Partners to Initiate Homologous Recombination.The Journal of biological chemistry · 2015Review
- Tetrameric Ctp1 coordinates DNA binding and DNA bridging in DNA double-strand-break repair.Nature structural & molecular biology · 2015Article
- Sumoylation influences DNA break repair partly by increasing the solubility of a conserved end resection protein.PLoS genetics · 2015Article
- Functional interplay between the 53BP1-ortholog Rad9 and the Mre11 complex regulates resection, end-tethering and repair of a double-strand break.PLoS genetics · 2015Article
- When two is not enough: a CtIP tetramer is required for DNA repair by Homologous Recombination.Nucleus (Austin, Tex.) · 2015Article
- Sae2 promotes dsDNA endonuclease activity within Mre11-Rad50-Xrs2 to resect DNA breaks.Nature · 2014Article
- End resection at double-strand breaks: mechanism and regulation.Cold Spring Harbor perspectives in biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The Mre11 complex functions in double-strand break (DSB) repair, meiotic recombination, and DNA damage checkpoint pathways. Sae2 deficiency has opposing effects on the Mre11 complex. On one hand, it appears to impair Mre11 nuclease function in DNA repair and meiotic DSB processing, and on the other, Sae2 deficiency activates Mre11-complex-dependent DNA-damage-signaling via the Tel1-Mre11 complex (TM) pathway. We demonstrate that SAE2 overexpression blocks the TM pathway, suggesting that Sae2 antagonizes Mre11-complex checkpoint functions. To understand how Sae2 regulates the Mre11 complex, we screened for sae2 alleles that behaved as the null with respect to Mre11-complex checkpoint functions, but left nuclease function intact. Phenotypic characterization of these sae2 alleles suggests that Sae2 functions as a multimer and influences the substrate specificity of the Mre11 nuclease. We show that Sae2 oligomerizes independently of DNA damage and that oligomerization is required for its regulatory influence on the Mre11 nuclease and checkpoint functions.
Indexed as
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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.