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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
Msh2 deficiency causes dysmyelination of the axonal projections in the corpus callosum. Evoked action potentials in the myelinated corpus callosum projections of Msh2-null mice were smaller than wild-type mice, whereas unmyelinated axons showed no difference.
Deletion of the MSH2 C-terminus severely affected the stability of the MSH2/MSH6 (show MSH6 Antibodies) 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 Antibodies)) 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 Antibodies)-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
Gut (show GUSB Antibodies) microbes did not induce colorectal cancer in APC (show APC Antibodies)(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 Antibodies) suppresses chromosomal instability and modulates the tumor spectrum in p53 (show TP53 Antibodies)-deficient tumorigenesis.
Results suggest that MSH2 is rate limiting for expansion in fragile X (show FMR1 Antibodies) premutation mouse model and that MSH2 levels may be a key factor that accounts for tissue-specific differences in expansion risk.
Identification and characterization of novel knockout mutants of the three major MMR (show MRC1 Antibodies) genes, mlh1 (show MLH1 Antibodies), msh2, and msh6 (show MSH6 Antibodies), in zebrafish that develop tumors at low frequencies.
Cancer developed more often in mutation carriers, with no consistent difference between MLH1 (show MLH1 Antibodies) and MSH2 carriers. More polyps (mostly adenomas) were detected in MLH1 (show MLH1 Antibodies) carriers. The majority (13 of 21) of malignant tumours occurred in organs for which there is no recommended surveillance, and were lethal in three patients.
SNP Rs2303428 of MSH2 is associated with hepatocellular carcinoma prognosis in a Chinese population.
Expression of MSH2 in patients with colon cancer may promote the expression of the obesity gene MC4R (show MC4R Antibodies), potentially contributing to body weight gains
An increased risk of breast cancer in MSH2 mutation carriers was demonstrated in a Canadian familial cancer registry.
Loss of MSH2 protein is correlated with MSH2 inactivation, hypermutation, and higher tumor-infiltrating lymphocyte density, and appears most common among very high-grade primary tumors, for which routine screening may be warranted if validated in additional cohorts.
Immunohistochemistry revealed loss of expression of proteins MSH2 and MSH6 (show MSH6 Antibodies), strongly suggesting a diagnosis of MTS (show TIMM8A Antibodies).
Authors revealed a novel pathologic mutation on the MSH2 gene (G504 splicing) that associates with Lynch syndrome. Systematical comparison of the mutation landscape revealed that multiple cancers in the proband were evolutionarily independent.
Expression of MSH6 (show MSH6 Antibodies) and MSH2 was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR (show ANTXR1 Antibodies) expression. Reduction of MSH6 (show MSH6 Antibodies) and MSH2 expression at the messenger RNA and protein levels could be involved in direct Pituitary Adenoma proliferation by promoting cell-cycle progression or decreasing the rate of apoptosis through interference with the function of the ATR (show ANTXR1 Antibodies)-Chk1 (show CHEK1 Antibodies) pathway.
Altered MSH2 expression detected in sporadic colon tumors pointing to its role in colorectal tumorigenesis
Among 13 gastric tumors showing no hMLH1 (show MLH1 Antibodies) or hMSH2 expression, 8 MSI (show MSI1 Antibodies)-H (high) and 5 MSI (show MSI1 Antibodies)-L (low) were identified.
Overexpression of Tinman and Pannier resulted in 20% of embryos with ectopic Hand and Sur (show ABCC8 Antibodies) expression. By adding MEF2 (show MYEF2 Antibodies) alongside Tinman and Pannier, an expansion in expression of Hand and Sur (show ABCC8 Antibodies) 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 Antibodies)-dependent muscle differentiation can proceed.
Plasticity in Hox/PBC (show DLAT Antibodies) 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 Antibodies) contribute progressively to the elaboration of the expression pattern of the mesoderm-specific homeobox (show PRRX1 Antibodies)-containing gene tinman (tin), and the overlap of wg and dpp (show TGFb Antibodies) 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 Antibodies) 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