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Our results suggest that increased expression of MSH6, or other MMR (show MRC1 Proteins), may be a new mechanism contributing to the acquired resistance during TMZ therapy; and may serve as an indicator to the resistance in GBM.
study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR (show MRC1 Proteins)) genes MLH1 (show MLH1 Proteins), MSH2 (show MSH2 Proteins), and MSH6 among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR (show MRC1 Proteins) genes
MSH6 frameshift variants incompletely segregate with the Lynch syndrome phenotype in two families.
Patients with mutations 6 showed higher rate of achieving major molecular response than those<6 (P=0.0381). Mutations in epigenetic regulator, ASXL1 (show ASXL1 Proteins), TET2, TET3, KDM1A (show KDM1A Proteins) and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 (show AKT1 Proteins) and RUNX1 (show RUNX1 Proteins) were mutated in one patient each. ASXL1 (show ASXL1 Proteins) was mutated within exon 12 in three cases
The MSH6 gene polymorphisms are likely to play an important role in the progression of AIDS in the northern Chinese population.
MSH6 mutations contribute to colorectal cancer susceptibility in Algerian families with suspected Lynch syndrome.
Neoadjuvant therapy in microsatellite-stable colorectal carcinoma induces concomitant loss of MSH6 and Ki-67 (show MKI67 Proteins) expression.
High MSH6 expression is associated with the development of genetic instability and is linked to tumor aggressiveness and early PSA recurrence in prostate cancer.
human Pol alpha interacts with MSH2 (show MSH2 Proteins)-MSH6 complex
In colorectal neoplasms, negative expression of the MMR (show MRC1 Proteins) proteins MLH1 (show MLH1 Proteins), MSH2 (show MSH2 Proteins) or MSH6 was seen in 15% (47 of 313) of the patients. Defect MLH1 (show MLH1 Proteins) was most common and detected in 12% of the cases. Defect MLH1 (show MLH1 Proteins) and MSH2 (show MSH2 Proteins) were identified in each patient's normal adjacent mucosa.
Studied MSH6 gene expression in developing zebrafish and the influence of MSH6 expression on the production of mismatch binding factors.
Identification and characterization of novel knockout mutants of the three major MMR (show MRC1 Proteins) genes, mlh1 (show MLH1 Proteins), msh2 (show MSH2 Proteins), and msh6, in zebrafish that develop tumors at low frequencies.
we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Smu and Sgamma3 regions
Data suggest that MSH6 protects B cells from neoplastic transformation by preserving genomic stability.
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
Msh6 deficiency resulted in somatic instability of a (GTG (show GGT1 Proteins))84 repeat.
role for Msh6 in protective cellular responses of primary cells to ultraviolet-B-induced mutagenesis and, hence, the prevention of skin cancer.
Data suggest that MutS homologues Msh2 (show MSH2 Proteins), Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes.
Data suggest that activation-induced cytidine deaminase (show AICDA Proteins) has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2 (show MSH2 Proteins)-Msh6, but not Msh3, and DNA polymerase (show POLB Proteins).
Mice nullizygous for both Msh2 (show MSH2 Proteins) and Msh3 and those nullizygous for both Msh3 and Msh6 displayed the greatest overall increases in mutation frequencies compared with wild-type mice.
in Msh6(-/-)Ung (show UNG Proteins)(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced.
p53 (show TP53 Proteins) and Msh6 are functionally interrelated and these tumor suppressors act together to accelerate tumorigenesis.
This gene encodes a protein similar to the MutS protein. In E. coli, the MutS protein helps in the recognition of mismatched nucleotides, prior to their repair. A highly conserved region of approximately 150 aa, called the Walker-A adenine nucleotide binding motif, exists in MutS homologs. The encoded protein of this gene combines with MSH2 to form a mismatch recognition complex that functions as a bidirectional molecular switch that exchanges ADP and ATP as DNA mismatches are bound and dissociated. Mutations in this gene have been identified in individuals with hereditary nonpolyposis colon cancer (HNPCC) and endometrial cancer.
DNA mismatch repair protein Msh6
, G/T mismatch-binding protein
, mutS-alpha 160 kDa subunit
, sperm-associated protein
, mutS homolog 6 (E. coli)
, DNA mismatch repair protein Msh6-like
, g/T mismatch-binding protein
, LOW QUALITY PROTEIN: DNA mismatch repair protein Msh6