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The expression of AtMutSgamma (MSH7 and MSH2) in Saccharomyces cerevisiae suggest that AtMutSgamma affects yeast genomic stability by recognizing specific mismatches.
The contribution of MutSalpha (MSH2-MSH6) to ultraviolet-induced DNA lesion repair and cell cycle regulation was investigated.
reported that AtMSH2 has a broad range of anti-recombination effects: it suppresses recombination between divergent direct repeats in somatic cells or between homologues from different ecotypes during meiosis
Data show that in mutS homolog 2 protein Msh2(+/-) mice, azathioprine (Aza) induced a high incidence of microsatellite instability (MSI (show EBP Proteins)) lymphomas in a dose-dependent manner.
In Msh2-/- mice, red meat enhanced survival compared to control (p<0.01) and lowered total tumour burden compared to resistant starch (p<0.167).
Angptl2 (show ANGPTL2 Proteins)-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
Gut (show GUSB Proteins) microbes did not induce colorectal cancer in APC (show APC Proteins)(Min/+)MSH2(-/-) mice through an inflammatory response or the production of DNA mutagens but rather by providing carbohydrate-derived metabolites such as butyrate that fuel hyperproliferation of MSH2(-/-) colon epithelial cells.
MSH2-MSH3 suppresses chromosomal instability and modulates the tumor spectrum in p53 (show TP53 Proteins)-deficient tumorigenesis.
Results suggest that MSH2 is rate limiting for expansion in fragile X (show FMR1 Proteins) premutation mouse model and that MSH2 levels may be a key factor that accounts for tissue-specific differences in expansion risk.
Toxicity, induced by tert (show TERT Proteins)-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (show MPG Proteins) (+/+), Nth1 (+/+)) and deficient (Mpg (show MPG Proteins) (-/-), Nth1 (-/-)) mouse embryonic fibroblasts following Msh2 knockdown, was examined.
Medium-spiny striatal neurons-specific deletion of Msh2 was sufficient to eliminate the vast majority of striatal HTT (show HTT Proteins) CAG expansions in HTT (show HTT Proteins) CAG knock-in mice.
Enhanced occupancy of Msh2 and Msh3 proteins is detected downstream of the FXN (show FXN Proteins) expanded GAA (show GAA Proteins) repeat, suggesting a model in which Msh2/3 dimers are recruited to this region to repair mismatches.
we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Smu and Sgamma3 regions
Identification and characterization of novel knockout mutants of the three major MMR (show MRC1 Proteins) genes, mlh1 (show MLH1 Proteins), msh2, and msh6 (show MSH6 Proteins), in zebrafish that develop tumors at low frequencies.
In Lynch syndrome families, prostate cancer was associated with mutations in MSH2 with loss of the mismatch repair protein.
Loss of MSH-2/MSH-6 (show MSH6 Proteins) expression was correlated with the right-colon location, poor and mucinous differentiation in colorectal adenocarcinoma.
The proportion of deaths from extra-colonic cancer was significantly higher in Japanese families with Lynch syndrome with MSH2 mutation
Studies indicate that each of the three neoplasm protein variants in BRCA1, BRCA2 (show BRCA2 Proteins) and MSH2 would normally be reported as pathogenic based on widely accepted guidelines.
foot-drop is frequently associated with NEB gene mutations . This result supports the indication deriving from the yeast model that BRCA1 driven tumorigenesis may be modulated by MSH2.
Pathogenic mutations were only confined to MSH2 and identified in 28.8% of Singapore families with Hereditary Colorectal Cancer.
Heterozygous germline mutations in any of the mismatch repair (MMR (show MRC1 Proteins)) genes, MLH1 (show MLH1 Proteins), MSH2, MSH6 (show MSH6 Proteins), and PMS2 (show PMS2 Proteins), cause Lynch syndrome (LS), an autosomal dominant cancer predisposition syndrome.
Authors propose an Alu-mediated recombination model to explain the origin of the cryptic paracentric inversion of MSH2 exons 2-6 causes Lynch syndrome.
MSH2, MSH6 (show MSH6 Proteins), and EXO1 (show EXO1 Proteins) genes were overexpressed in gastroesophageal cancers.
We identified several genes (FasL (show FASL Proteins), MSH2, ABCC5 (show ABCC5 Proteins), CASP3 (show CASP3 Proteins), and CYP3A4 (show CYP3A4 Proteins))that showed association with PFS in patients with osteosarcoma. These pharmacogenetic risk factors might be useful to predict treatment outcome
Overexpression of Tinman and Pannier resulted in 20% of embryos with ectopic Hand and Sur (show ABCC8 Proteins) expression. By adding MEF2 (show MYEF2 Proteins) alongside Tinman and Pannier, an expansion in expression of Hand and Sur (show ABCC8 Proteins) was observed.
Findings provide mechanistic insight into the brake on myogenesis that occurs during mesoderm specification: twist and tin expression at early stages in turn activate the myogenic inhibitor Him; yet, once Twist or Tin levels decline at mid-embryogenesis, Him is no longer expressed in the mesoderm, and MEF2 (show MYEF2 Proteins)-dependent muscle differentiation can proceed.
Plasticity in Hox/PBC (show DLAT Proteins) interaction modes is a common molecular strategy for shaping Hox transcriptional activities.
The enhancers active in the heart progenitor cells and the heart generally are dependent on tinman gene activity, whereas those active in non-cardiac mesoderm are often bound neutrally by Tinman
Genetic interaction analysis shows that spir functionally interacts with Dorsocross, tin, and pannier to properly specify the cardiac fate.
Tin is a direct regulator of midline in fly heart development.
wg and dpp (show TGFb Proteins) contribute progressively to the elaboration of the expression pattern of the mesoderm-specific homeobox (show PRRX1 Proteins)-containing gene tinman (tin), and the overlap of wg and dpp (show TGFb Proteins) in the presence of tin-expressing cells directs cardiac-specific differentiation
We show that salivary gland posterior migration requires the activities of genes that position the visceral mesoderm precursors, such as heartless, thickveins, and tinman, but does not require a differentiated visceral mesoderm.
one of the major functions of mid and H15 during cardioblast development is the re-activation of tin expression at a stage when the induction of tin by Dpp (show TGFb Proteins) in the dorsal mesoderm has ceased
dSUR is regulated by tinman and plays a protective role against hypoxic stress and pacing-induced heart failure
This locus is frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). When cloned, it was discovered to be a human homolog of the E. coli mismatch repair gene mutS, consistent with the characteristic alterations in microsatellite sequences (RER+ phenotype) found in HNPCC. Two transcript variants encoding different isoforms have been found for this gene.
mismatch repair protein
, DNA mismatch repair protein Msh2
, mutS protein homolog 2
, mismatch repair protein Msh2
, mutS-like protein 2
, MutS-like protein 2