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Our meta-analysis results demonstrated that MSH3 rs26279 G > A polymorphism is associated with an increased risk of overall cancer, especially for the colorectal cancer and breast cancer.
The mismatch-binding protein MutS beta, a heterodimer of MSH2 and MSH3, activates ATR in response to DNA double-strand breaks.
Data show that single nucleotide polymorphisms in MutS homolog 3 (MSH3) had an impact on the chemotherapy response and prognosis of advanced non-small cell lung cancer (NCSLC) patients who were treated with platinum-based chemotherapy.
Our data present, for the first time, evidence that inherited MLH1 (show MLH1 ELISA Kits) c.-93G>A, MSH2 (show MSH2 ELISA Kits) c.211 + 9C>G, MSH3 c.3133G>A, and EXO1 (show EXO1 ELISA Kits) c.1765G>A abnormalities of DNA MMR (show MRC1 ELISA Kits) pathway are important determinants of head and neck squamous cell carcinoma
IL6 (show IL6 ELISA Kits) signaling disrupts the nuclear localization of hMSH3 and DNA repair, leading to elevated microsatellite alterations at selected tetranucleotide repeats in cancer cell lines.
Methylation of MSH3 together with exposure to tobacco smoke is involved in esophageal carcinogenesis.
MSH3 status can regulate the DNA damage response and extent of apoptosis induced by chemotherapy.
Single nucleotide polymorphisms in MSH3 are associated with myelodysplastic syndromes.
Oxidative stress, which causes a shift of hMSH3's subcellular location, may contribute to an hMSH3 loss-of-function phenotype by sequestering it to the cytosol
siRNA knockdown of the MutSbeta subunits MSH2 (show MSH2 ELISA Kits) or MSH3 impeded expansion of threshold-length CTG*CAG repeats.
MSH2 (show MSH2 ELISA Kits)-MSH3 suppresses chromosomal instability and modulates the tumor spectrum in p53 (show TP53 ELISA Kits)-deficient tumorigenesis.
naturally occurring MSH3 protein polymorphisms are modifiers of CAG repeat (show CELF3 ELISA Kits) instability, likely through variable MSH3 protein stability
Enhanced occupancy of Msh2 (show MSH2 ELISA Kits) and Msh3 proteins downstream of the FXN (show FXN ELISA Kits) expanded GAA (show GAA ELISA Kits) repeat, suggesting a model in which Msh2 (show MSH2 ELISA Kits)/3 dimers are recruited to this region to repair mismatches.
Stress treatment of mouse cells with ethanol or hydrogen peroxide caused the re-distribution of MSH3 into nuclear bodies containing the proliferating cell nuclear antigen (PCNA (show PCNA ELISA Kits)), a known binding partner of MutSbeta.
A (CTG)84 repeat was stable even in Msh3-deficient mice.
Data suggest that MutS homologues Msh2 (show MSH2 ELISA Kits), Msh3, and Msh6 (show MSH6 ELISA Kits) play overlapping and distinct roles during antibody diversification processes.
Data suggest that activation-induced cytidine deaminase (show AICDA ELISA Kits) has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2 (show MSH2 ELISA Kits)-Msh6 (show MSH6 ELISA Kits), but not Msh3, and DNA polymerase (show POLB ELISA Kits).
Frequencies and patterns in DNA mismatch repair in the context of mice deficient for Msh3.
The protein encoded by this gene forms a heterodimer with MSH2 to form MutS beta, part of the post-replicative DNA mismatch repair system. MutS beta initiates mismatch repair by binding to a mismatch and then forming a complex with MutL alpha heterodimer. This gene contains a polymorphic 9 bp tandem repeat sequence in the first exon. The repeat is present 6 times in the reference genome sequence and 3-7 repeats have been reported. Defects in this gene are a cause of susceptibility to endometrial cancer.
DNA mismatch repair protein Msh3
, DNA mismatch repair protein MSH3
, hypothetical protein
, divergent upstream protein
, mismatch repair protein 1
, protein repair-1
, protein repair-3