ReviewMutation research
Structural, molecular and cellular functions of MSH2 and MSH6 during DNA mismatch repair, damage signaling and other noncanonical activities.
Review in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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.
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Who cites it
81 citing papers in PubMed, 148 citations in OpenAlex.
- Linkage Analysis in Autoimmune Addison's Disease: NFATC1 as a Potential Novel Susceptibility Locus.PloS one · 2015Trial
- Immunohistochemical Expression of MSH2 and MSH6 Mismatch Repair Proteins and Their Pathological Correlations in Canine Primary Pulmonary Carcinoma.Animals : an open access journal from MDPI · 2026Article
- Divergent Roles of Canonical and Non-Canonical Mismatch Repair in Regulating Temozolomide Sensitivity in Glioblastoma.International journal of molecular sciences · 2026Review
- Family-Based Study RevealsInternational journal of molecular sciences · 2026Article
- Five dominant amino acid substitution signatures shape tumour immunity.Molecular systems biology · 2026Article
- Machine Learning-Based Pathomics Signature in Predicting MSH2 Expression and Prognosis in Gastric Cancer.Clinical and translational gastroenterology · 2026Article
- Case Report: CYLD cutaneous syndrome with malignant transformation to spiradenocarcinoma: cooperative effects of CYLD truncation and an MSH2 clamp-domain variant in an Ecuadorian patient.Frontiers in medicine · 2026Article
- TMT-based quantitative proteomic assessment of Vicia sativa induced neurotoxicity by β-cyano-L-alanine and γ-glutamyl-β-cyano-L-alanine in SH-SY5Y cells.Scientific reports · 2025Article
- Boosting Brain Clean-Up: Can Targeting UPS Genes Offer Neuroprotection?Molecular neurobiology · 2025Review
- FOXO3a upregulates DNA repair activities by transcriptional activation of target genes and provides the resistance to gamma radiation and the extension of lifespan in mouse.Biogerontology · 2025Article
- Therapeutic targeting of mismatch repair-deficient cancers.Nature reviews. Clinical oncology · 2025Review
- RNA/DNA-binding protein TDP43 regulates DNA mismatch repair genes with implications for genome stability.Nucleic acids research · 2025Article
- The hidden cost of somatic mutations on skeletal muscle regeneration.Nature aging · 2025Article
- Induced somatic mutation accumulation during skeletal muscle regeneration reduces muscle strength.Nature aging · 2025Article
- RNA/DNA Binding Protein TDP43 Regulates DNA Mismatch Repair Genes with Implications for Genome Stability.bioRxiv : the preprint server for biology · 2025Article
- Evolutionary Transcriptomics of Cancer Development.International journal of molecular sciences · 2025Article
- Elucidating the genetic mechanisms governing cytosine base editing outcomes through CRISPRi screens.Nature communications · 2025Article
- Dipeptidase-1-knockout mice develop invasive tumors with features of microsatellite-unstable colorectal cancer.JCI insight · 2025Article
- MicroRNA‑21‑5p expression in extracellular vesicles is increased in the blood of aging mice and in vascular endothelial cells induced by ionizing radiation.Experimental and therapeutic medicine · 2025Article
- Clinicopathological features of Lynch syndrome pedigrees with MSH2 c.351G>A gene variant.Molecular genetics & genomic medicine · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The field of DNA mismatch repair (MMR) has rapidly expanded after the discovery of the MutHLS repair system in bacteria. By the mid 1990s yeast and human homologues to bacterial MutL and MutS had been identified and their contribution to hereditary non-polyposis colorectal cancer (HNPCC; Lynch syndrome) was under intense investigation. The human MutS homologue 6 protein (hMSH6), was first reported in 1995 as a G:T binding partner (GTBP) of hMSH2, forming the hMutSα mismatch-binding complex. Signal transduction from each DNA-bound hMutSα complex is accomplished by the hMutLα heterodimer (hMLH1 and hPMS2). Molecular mechanisms and cellular regulation of individual MMR proteins are now areas of intensive research. This review will focus on molecular mechanisms associated with mismatch binding, as well as emerging evidence that MutSα, and in particular, MSH6, is a key protein in MMR-dependent DNA damage response and communication with other DNA repair pathways within the cell. MSH6 is unstable in the absence of MSH2, however it is the DNA lesion-binding partner of this heterodimer. MSH6, but not MSH2, has a conserved Phe-X-Glu motif that recognizes and binds several different DNA structural distortions, initiating different cellular responses. hMSH6 also contains the nuclear localization sequences required to shuttle hMutSα into the nucleus. For example, upon binding to O(6)meG:T, MSH6 triggers a DNA damage response that involves altered phosphorylation within the N-terminal disordered domain of this unique protein. While many investigations have focused on MMR as a post-replication DNA repair mechanism, MMR proteins are expressed and active in all phases of the cell cycle. There is much more to be discovered about regulatory cellular roles that require the presence of MutSα and, in particular, MSH6.
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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.