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Human Monoclonal Primary Antibody für WB - ABIN1882267
Leonardis: Gene symbol: msh2. Disease: hereditary nonpolyposis colorectal cancer. in Human genetics 2006
Show all 4 Pubmed References
Human Polyclonal Primary Antibody für 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
Human Polyclonal Primary Antibody für ICC, IF - ABIN152052
Li, Wehrenberg, Waldman, Waldman: Mismatch tolerance during homologous recombination in mammalian cells. in DNA repair 2018
Cow (Bovine) Polyclonal Primary Antibody für 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 für ICC, IHC (p) - ABIN3043885
Zhang, Yue, Wang, Li, Xin, Pang, Zheng, Xie: Cisplatin upregulates MSH2 expression by reducing miR-21 to inhibit A549 cell growth. in Biomedicine & pharmacotherapy 2014
MSH2 Microsatellite Instability is associated with late stage Colorectal Cancer.
Study reports the case of a MSH2 missense variant, exon 3, c.482T>A, p.Val161Asp, found in a family fulfilling Amsterdam I criteria, Amsterdam II criteria and Bethesda guidelines, that on the basis of co-segregation with the disease, correlation with microsatellite instability, loss of MMR protein expression in tumour tissue and localization assay, is strongly suggested having a pathogenic role.
Hypomethylation of MSH2 gene is associated with chemotolerance of breast carcinoma.
Single-Nucleotide Polymorphisms of the MSH2 is associated with Basal Cell Carcinoma.
MSH2-MSH3 not only stimulates pol beta to copy through the repeats but also enhances formation of the flap precursor for expansion.
Cancer developed more often in mutation carriers, with no consistent difference between MLH1 and MSH2 carriers. More polyps (mostly adenomas) were detected in MLH1 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, 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, strongly suggesting a diagnosis of MTS.
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 and MSH2 was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR expression. Reduction of MSH6 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-Chk1 pathway.
Altered MSH2 expression detected in sporadic colon tumors pointing to its role in colorectal tumorigenesis
Among 13 gastric tumors showing no hMLH1 or hMSH2 expression, 8 MSI-H (high) and 5 MSI-L (low) were identified.
study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR) genes MLH1, MSH2, and MSH6 among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR genes
MSH2 rs2303425 Polymorphism is Associated with Early-Onset Breast Cancer.
Five out of twelve patients with defects in either of MSH2, RAD50 and NBN genes suffered from rare life-threatening AE, more frequently than in control group (p = 0.0005). When all detected variants were taken into account, the majority of patients (8 out of 15) suffered from life-threatening toxicity during chemotherapy.
MSH2 inversion of exons 1-7 was found in four probands previously suspected to have Lynch syndrome based on family history and tumor testing
Loss of MSH2 expression is associated with colorectal carcinoma.
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) 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 suppresses chromosomal instability and modulates the tumor spectrum in p53-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.
Toxicity, induced by tert-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (+/+), Nth1 (+/+)) and deficient (Mpg (-/-), Nth1 (-/-)) 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 CAG expansions in HTT CAG knock-in mice.
elevated mutation levels have little effect on the development of the fetus, even if a mutator phenotype appears at the organogenesis stage.
Enhanced occupancy of Msh2 and Msh3 proteins is detected downstream of the FXN expanded GAA 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
hMSH2 recruits ATR to DNA damage sites for activation during DNA damage-induced apoptosis.
MSH2 is all important for efficient alternative end-joining-mediated class-switch recombination region DNA breaks in B cells.
Azathioprine-induced carcinogenesis in mice depends on the number of functional copies of the Msh2 gene.
similar defects on switching in Msh2(-/-), Msh2(-/-)Msh6(-/-) and Msh2(-/-)Msh6(-/-)Msh3(-/-) mice confirm that MutSalpha but not MutSbeta plays an important role in class switch recombination
Msh2(LoxP/LoxP) mice in combination with appropriate Cre recombinase transgenes have excellent potential for preclinical modeling of Lynch syndrome.
Identification and characterization of novel knockout mutants of the three major MMR genes, mlh1, msh2, and msh6, 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