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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 (zeige MRC1 ELISA Kits) genes, mlh1 (zeige MLH1 ELISA Kits), msh2 (zeige MSH2 ELISA Kits), and msh6, in zebrafish that develop tumors at low frequencies.
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 (zeige MKI67 ELISA Kits) 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 (zeige MSH2 ELISA Kits)-MSH6 complex
In colorectal neoplasms, negative expression of the MMR (zeige MRC1 ELISA Kits) proteins MLH1 (zeige MLH1 ELISA Kits), MSH2 (zeige MSH2 ELISA Kits) or MSH6 was seen in 15% (47 of 313) of the patients. Defect MLH1 (zeige MLH1 ELISA Kits) was most common and detected in 12% of the cases. Defect MLH1 (zeige MLH1 ELISA Kits) and MSH2 (zeige MSH2 ELISA Kits) were identified in each patient's normal adjacent mucosa.
unlike MutSbeta, MutSalpha may also act to protect against repeat contractions in the Fmr1 (zeige FMR1 ELISA Kits) gene
A total of 201 unique disease-predisposing mismatch repair gene mutations were identified in 369 Lynch syndrome families. These mutations affected MLH1 (zeige MLH1 ELISA Kits) in 40%, MSH2 (zeige MSH2 ELISA Kits) in 36%, MSH6 in 18% and PMS2 (zeige PMS2 ELISA Kits) in 6% of the families
There is a positive correlation between the expressions of hMSH2 (zeige MSH2 ELISA Kits) and hMSH6 between males (RHO=0.673 and p=0.001) and females with colorectal adenocarcinoma.
Individuals with Lynch syndrome and double-mutants in MSH6 and MSH2 (zeige MSH2 ELISA Kits) had normal MSH2 (zeige MSH2 ELISA Kits) expression, whereas MSH6 immunoexpression was lost in all evaluable cases.
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 (zeige MSH2 ELISA Kits)(-/-), Msh2 (zeige MSH2 ELISA Kits)(-/-)Msh6(-/-) and Msh2 (zeige MSH2 ELISA Kits)(-/-)Msh6(-/-)Msh3 (zeige MSH3 ELISA Kits)(-/-) mice confirm that MutSalpha but not MutSbeta plays an important role in class switch recombination
Msh6 deficiency resulted in somatic instability of a (GTG (zeige GGT1 ELISA Kits))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 (zeige MSH2 ELISA Kits), Msh3 (zeige MSH3 ELISA Kits), and Msh6 play overlapping and distinct roles during antibody diversification processes.
Data suggest that activation-induced cytidine deaminase (zeige AICDA ELISA Kits) has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2 (zeige MSH2 ELISA Kits)-Msh6, but not Msh3 (zeige MSH3 ELISA Kits), and DNA polymerase (zeige POLB ELISA Kits).
Mice nullizygous for both Msh2 (zeige MSH2 ELISA Kits) and Msh3 (zeige MSH3 ELISA Kits) and those nullizygous for both Msh3 (zeige MSH3 ELISA Kits) and Msh6 displayed the greatest overall increases in mutation frequencies compared with wild-type mice.
in Msh6(-/-)Ung (zeige UNG ELISA Kits)(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced.
p53 (zeige TP53 ELISA Kits) 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
, mutS homolog 6 (E. coli)
, DNA mismatch repair protein Msh6-like
, G/T mismatch-binding protein
, mutS-alpha 160 kDa subunit
, sperm-associated protein
, g/T mismatch-binding protein