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hMSH6 Glu39Gly polymorphism is associated with the risk of developing colorectal cancer in the Polish population.
Expression of MSH6 and MSH2 (Montrer MSH2 Protéines) was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR (Montrer ANTXR1 Protéines) expression. Reduction of MSH6 and MSH2 (Montrer MSH2 Protéines) 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 (Montrer ANTXR1 Protéines)-Chk1 (Montrer CHEK1 Protéines) pathway.
Our results suggest that increased expression of MSH6, or other MMR (Montrer MRC1 Protéines), 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 (Montrer MRC1 Protéines)) genes MLH1 (Montrer MLH1 Protéines), MSH2 (Montrer MSH2 Protéines), and MSH6 among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR (Montrer MRC1 Protéines) 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 (Montrer ASXL1 Protéines), TET2, TET3, KDM1A (Montrer KDM1A Protéines) and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 (Montrer AKT1 Protéines) and RUNX1 (Montrer RUNX1 Protéines) were mutated in one patient each. ASXL1 (Montrer ASXL1 Protéines) 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 (Montrer MKI67 Protéines) 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.
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 (Montrer MRC1 Protéines) genes, mlh1 (Montrer MLH1 Protéines), msh2 (Montrer MSH2 Protéines), 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 (Montrer GGT1 Protéines))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 (Montrer MSH2 Protéines), Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes.
Data suggest that activation-induced cytidine deaminase (Montrer AICDA Protéines) has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2 (Montrer MSH2 Protéines)-Msh6, but not Msh3, and DNA polymerase (Montrer POLB Protéines).
Mice nullizygous for both Msh2 (Montrer MSH2 Protéines) 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 (Montrer UNG Protéines)(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced.
p53 (Montrer TP53 Protéines) 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