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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 (show MSH6 ELISA Kits) 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 (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 (+/+)) and deficient (Mpg (show MPG ELISA Kits) (-/-), Nth1 (-/-)) mouse embryonic fibroblasts following Msh2 knockdown, was examined.
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.
Loss of MSH2 expression is associated with colorectal carcinoma.
Findings indicate that carriers of the MSH5 (show MSH5 ELISA Kits) rs707939 T allele, the MSH2 rs6544991 C allele, the MSH3 (show MSH3 ELISA Kits) rs6151627 and rs6151670 G alleles, and the MSH3 (show MSH3 ELISA Kits) 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 (show EZH2 ELISA Kits)-H3K27me3 regulatory mechanism dynamically changes the expression levels of DNA mismatch repair gene MutS homolog 2, through epigenetic mark H3K27me3.
Genetic changes between MLH1 (show MLH1 ELISA Kits) and MSH2 were significantly positively correlated (p = 0.032). We also noted a positive correlation between genetic changes of MSH2 and DVL3 (show DVL3 ELISA Kits) 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 (show DUOXA1 ELISA Kits) is sufficient to cause rapid degradation via the ubiquitin-proteasome pathway.
human Pol alpha interacts with MSH2-MSH6 (show MSH6 ELISA Kits) complex
In colorectal neoplasms, negative expression of the MMR (show MRC1 ELISA Kits) proteins MLH1 (show MLH1 ELISA Kits), MSH2 or MSH6 (show MSH6 ELISA Kits) was seen in 15% (47 of 313) of the patients. Defect MLH1 (show MLH1 ELISA Kits) was most common and detected in 12% of the cases. Defect MLH1 (show MLH1 ELISA Kits) 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 (show FMR1 ELISA Kits) gene
Overexpression of Tinman and Pannier resulted in 20% of embryos with ectopic Hand and Sur (show ABCC8 ELISA Kits) expression. By adding MEF2 (show MYEF2 ELISA Kits) 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 (show MYEF2 ELISA Kits)-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