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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 ELISA Kits)) 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 ELISA Kits)-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
Gut (show GUSB ELISA Kits) microbes did not induce colorectal cancer in APC (show APC ELISA Kits)(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 (show MSH3 ELISA Kits) suppresses chromosomal instability and modulates the tumor spectrum in p53 (show TP53 ELISA Kits)-deficient tumorigenesis.
Results suggest that MSH2 is rate limiting for expansion in fragile X (show FMR1 ELISA Kits) 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 ELISA Kits)-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (show MPG ELISA Kits) (+/+), Nth1 (show NTHL1 ELISA Kits) (+/+)) and deficient (Mpg (show MPG ELISA Kits) (-/-), Nth1 (show NTHL1 ELISA Kits) (-/-)) 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 ELISA Kits) CAG expansions in HTT (show HTT ELISA Kits) CAG knock-in mice.
Enhanced occupancy of Msh2 and Msh3 (show MSH3 ELISA Kits) proteins is detected downstream of the FXN (show FXN ELISA Kits) expanded GAA (show GAA ELISA Kits) 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 ELISA Kits) genes, mlh1 (show MLH1 ELISA Kits), msh2, and msh6 (show MSH6 ELISA Kits), in zebrafish that develop tumors at low frequencies.
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 ELISA Kits) and MSH2 would normally be reported as pathogenic based on widely accepted guidelines.
foot-drop is frequently associated with NEB (show NEB ELISA Kits) 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 ELISA Kits)) genes, MLH1 (show MLH1 ELISA Kits), MSH2, MSH6 (show MSH6 ELISA Kits), and PMS2 (show PMS2 ELISA Kits), 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 ELISA Kits), and EXO1 (show EXO1 ELISA Kits) genes were overexpressed in gastroesophageal cancers.
We identified several genes (FasL (show FASL ELISA Kits), MSH2, ABCC5 (show ABCC5 ELISA Kits), CASP3 (show CASP3 ELISA Kits), and CYP3A4 (show CYP3A4 ELISA Kits))that showed association with PFS in patients with osteosarcoma. These pharmacogenetic risk factors might be useful to predict treatment outcome
This retrospective cohort study investigated the risk factors associated with the development of colorectal cancer in patients with MLH1 (show MLH1 ELISA Kits) and MSH2 germline mutations.
The mismatch-binding protein MutS beta, a heterodimer of MSH2 and MSH3, activates ATR in response to DNA double-strand breaks.
Overexpression of Tinman and Pannier resulted in 20% of embryos with ectopic Hand and Sur (show ABCC8 ELISA Kits) expression. By adding MEF2 alongside Tinman and Pannier, an expansion in expression of Hand and Sur (show ABCC8 ELISA Kits) 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-dependent muscle differentiation can proceed.
Plasticity in Hox/PBC (show DLAT ELISA Kits) 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 ELISA Kits) contribute progressively to the elaboration of the expression pattern of the mesoderm-specific homeobox (show PRRX1 ELISA Kits)-containing gene tinman (tin), and the overlap of wg and dpp (show TGFb ELISA Kits) 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 ELISA Kits) 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