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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
Deletion of the MSH2 C-terminus severely affected the stability of the MSH2/MSH6 (Montrer MSH6 Kits ELISA) heterodimer and consequently strongly attenuated DNA mismatch repair. The C-terminal truncation MSH2 mutant predisposed mice to tumor formation.Mutations deleting the MSH2 C-terminus can therefore unambiguously be considered as pathogenic and a cause of Lynch syndrome.
Normal Msh2-deficient organoids showed increased inheritable transient cyst-like growth, which became independent of R-spondin. intestinal stem cell (ISC) proceeded faster in vitro than in vivo independent of the underlying genotype but more under Mutations in mismatch repair deficiency.
Study shows that MSH2-/- mice develop spontaneous thymic lymphomas.
Data show that in mutS homolog 2 protein Msh2(+/-) mice, azathioprine (Aza) induced a high incidence of microsatellite instability (MSI (Montrer EBP Kits ELISA)) 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 (Montrer ANGPTL2 Kits ELISA)-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
Gut (Montrer GUSB Kits ELISA) microbes did not induce colorectal cancer in APC (Montrer APC Kits ELISA)(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 (Montrer MSH3 Kits ELISA) suppresses chromosomal instability and modulates the tumor spectrum in p53 (Montrer TP53 Kits ELISA)-deficient tumorigenesis.
Results suggest that MSH2 is rate limiting for expansion in fragile X (Montrer FMR1 Kits ELISA) 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 (Montrer TERT Kits ELISA)-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (Montrer MPG Kits ELISA) (+/+), Nth1 (+/+)) and deficient (Mpg (Montrer MPG Kits ELISA) (-/-), Nth1 (-/-)) mouse embryonic fibroblasts following Msh2 knockdown, was examined.
Identification and characterization of novel knockout mutants of the three major MMR (Montrer MRC1 Kits ELISA) genes, mlh1 (Montrer MLH1 Kits ELISA), msh2, and msh6 (Montrer MSH6 Kits ELISA), in zebrafish that develop tumors at low frequencies.
Loss of MSH2 expression is associated with colorectal carcinoma.
Findings indicate that carriers of the MSH5 (Montrer MSH5 Kits ELISA) rs707939 T allele, the MSH2 rs6544991 C allele, the MSH3 (Montrer MSH3 Kits ELISA) rs6151627 and rs6151670 G alleles, and the MSH3 (Montrer MSH3 Kits ELISA) rs7709909 T allele have poor toxicity tolerance to platinum-based chemotherapy in non-small cell lung cancer patients.
Overexpression of MutL homolog 1 and MutS homolog 2 proteins have reversed prognostic implications for stage I-II colon cancer
MSH2 mutations contribute to colorectal cancer susceptibility in Algerian families with suspected Lynch syndrome.
The data suggest that EZH2 (Montrer EZH2 Kits ELISA)-H3K27me3 regulatory mechanism dynamically changes the expression levels of DNA mismatch repair gene MutS homolog 2, through epigenetic mark H3K27me3.
Genetic changes between MLH1 (Montrer MLH1 Kits ELISA) and MSH2 were significantly positively correlated (p = 0.032). We also noted a positive correlation between genetic changes of MSH2 and DVL3 (Montrer DVL3 Kits ELISA) genes (p = 0.034).
Here we demonstrate that in silico saturation mutagenesis and biophysical calculations of the structural stability of the human mismatch repair protein MSH2 correlate with cellular protein levels, turnover and function. Of 24 different MSH2 variants, some of which are linked to Lynch syndrome, a destabilization of as little as 3 kcal/mol (Montrer DUOXA1 Kits ELISA) is sufficient to cause rapid degradation via the ubiquitin-proteasome pathway.
human Pol alpha interacts with MSH2-MSH6 (Montrer MSH6 Kits ELISA) complex
In colorectal neoplasms, negative expression of the MMR (Montrer MRC1 Kits ELISA) proteins MLH1 (Montrer MLH1 Kits ELISA), MSH2 or MSH6 (Montrer MSH6 Kits ELISA) was seen in 15% (47 of 313) of the patients. Defect MLH1 (Montrer MLH1 Kits ELISA) was most common and detected in 12% of the cases. Defect MLH1 (Montrer MLH1 Kits ELISA) and MSH2 were identified in each patient's normal adjacent mucosa.
unlike MutSbeta, MutSalpha may also act to protect against repeat contractions in the Fmr1 (Montrer FMR1 Kits ELISA) gene
Overexpression of Tinman and Pannier resulted in 20% of embryos with ectopic Hand and Sur (Montrer ABCC8 Kits ELISA) expression. By adding MEF2 (Montrer MYEF2 Kits ELISA) alongside Tinman and Pannier, an expansion in expression of Hand and Sur (Montrer ABCC8 Kits ELISA) 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 (Montrer MYEF2 Kits ELISA)-dependent muscle differentiation can proceed.
Plasticity in Hox/PBC (Montrer DLAT Kits ELISA) 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 (Montrer TGFb Kits ELISA) contribute progressively to the elaboration of the expression pattern of the mesoderm-specific homeobox (Montrer PRRX1 Kits ELISA)-containing gene tinman (tin), and the overlap of wg and dpp (Montrer TGFb Kits ELISA) 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 (Montrer TGFb Kits ELISA) 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