ArticleDNA repair2007
Mutations affecting a putative MutLalpha endonuclease motif impact multiple mismatch repair functions.
Article in DNA repair, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 55 citations in OpenAlex.
- Suppression of transcription-replication conflicts by sequence-coordinated actions of TRDMT1 and MutLα.Nature communications · 2026Article
- Mismatch repair MLH complexes make distinct contributions to post-replicative mismatch repair versus trinucleotide repeat expansions.bioRxiv : the preprint server for biology · 2026Article
- The structure of the MutL-CTD:processivity-clamp complex provides insight regarding strand discrimination in non-methyl-directed DNA mismatch repair.Nucleic acids research · 2025Article
- PMS2 mutation spectra in Norway and risk of cancer for carriers of pathogenic variants.Hereditary cancer in clinical practice · 2024Article
- Resolution of sequence divergence for repeat-mediated deletions shows a polarity that is mediated by MLH1.Nucleic acids research · 2023Article
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- Mismatch recognition and subsequent processing have distinct effects on mitotic recombination intermediates and outcomes in yeast.Nucleic acids research · 2019Article
- The Major Replicative Histone Chaperone CAF-1 Suppresses the Activity of the DNA Mismatch Repair System in the Cytotoxic Response to a DNA-methylating Agent.The Journal of biological chemistry · 2016Article
- An intact Pms2 ATPase domain is not essential for male fertility.DNA repair · 2016Article
- DNA mismatch repair and the DNA damage response.DNA repair · 2016Review
- Review
- Eukaryotic Mismatch Repair in Relation to DNA Replication.Annual review of genetics · 2015Review
- PCNA and Msh2-Msh6 activate an Mlh1-Pms1 endonuclease pathway required for Exo1-independent mismatch repair.Molecular cell · 2014Article
- Mlh2 is an accessory factor for DNA mismatch repair in Saccharomyces cerevisiae.PLoS genetics · 2014Article
- Postreplicative mismatch repair.Cold Spring Harbor perspectives in biology · 2013Review
- Review
- Structure of the MutLα C-terminal domain reveals how Mlh1 contributes to Pms1 endonuclease site.Nature structural & molecular biology · 2013Article
- MSH6- or PMS2-deficiency causes re-replication in DT40 B cells, but it has little effect on immunoglobulin gene conversion or on repair of AID-generated uracils.Nucleic acids research · 2013Article
- Mismatch-mediated error prone repair at the immunoglobulin genes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2011Review
- An update on targeted gene repair in mammalian cells: methods and mechanisms.Journal of biomedical science · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in DNA mismatch repair (MMR) lead to increased mutation rates and higher recombination between similar, but not identical sequences, as well as resistance to certain DNA methylating agents. Recently, a component of human MMR machinery, MutLalpha, has been shown to display a latent endonuclease activity. The endonuclease active site appears to include a conserved motif, DQHA(X)(2)E(X)(4)E, within the COOH-terminus of human PMS2. Substitution of the glutamic acid residue (E705) abolished the endonuclease activity and mismatch-dependent excision in vitro. Previously, we showed that the PMS2-E705K mutation and the corresponding mutation in Saccharomyces cerevisiae were both recessive loss of function alleles for mutation avoidance in vivo. Here, we show that mutations impacting this endonuclease motif also significantly affect MMR-dependent suppression of homeologous recombination in yeast and responses to S(n)1-type methylating agents in both yeast and mammalian cells. Thus, our in vivo results suggest that the endonuclease activity of MutLalpha is important not only in MMR-dependent mutation avoidance but also for recombination and damage response functions.
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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.