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Human Monoclonal Primary Antibody for WB - ABIN1882267
Leonardis: Gene symbol: msh2. Disease: hereditary nonpolyposis colorectal cancer. in Human genetics 2006
Show all 4 Pubmed References
Human Polyclonal Primary Antibody for IP, WB - ABIN151480
Wang, Qin: MSH2 and ATR form a signaling module and regulate two branches of the damage response to DNA methylation. in Proceedings of the National Academy of Sciences of the United States of America 2003
Cow (Bovine) Polyclonal Primary Antibody for IHC, WB - ABIN2776761
Wedrén, Lovmar, Humphreys, Magnusson, Melhus, Syvänen, Kindmark, Landegren, Fermér, Stiger, Persson, Baron, Weiderpass: Estrogen receptor alpha gene polymorphism and endometrial cancer risk--a case-control study. in BMC cancer 2009
Human Polyclonal Primary Antibody for ICC, IF - ABIN152052
Li, Wehrenberg, Waldman, Waldman: Mismatch tolerance during homologous recombination in mammalian cells. in DNA repair 2018
Single-Nucleotide Polymorphisms of the MSH2 is associated with Basal Cell Carcinoma.
MSH2-MSH3 (show MSH3 Antibodies) not only stimulates pol beta (show POLB Antibodies) to copy through the repeats but also enhances formation of the flap (show ALOX5AP Antibodies) precursor for expansion.
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.
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 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-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
Gut microbes did not induce colorectal cancer in APC(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 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.
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.
DNA mismatch repair protein Msh2
, mutS protein homolog 2
, mismatch repair protein
, MutS-like protein 2
, mismatch repair protein Msh2
, mutS-like protein 2
, mutS homolog 2, colon cancer, nonpolyposis type 1
, DNA mismatch repair protein MutS-homolog 2