Browse our anti-MSH6 (MSH6) Antibodies

Human MutS Homolog 6 (E. Coli) (MSH6) interaction partners

1. our data suggests thatMSH6 Glu39Gly polymorphism is associated with the risk of developing sporadic colorectal cancer in polish population. Linkage to the female gender, onset above 60 years old and further increase of risk when combined with wild-type allele of PMS2 (show PMS2 Antibodies) IVS1-1121C >

2. hMSH6 Glu39Gly polymorphism is associated with the risk of developing colorectal cancer in the Polish population.

3. Expression of MSH6 and MSH2 (show MSH2 Antibodies) was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR (show ANTXR1 Antibodies) expression. Reduction of MSH6 and MSH2 (show MSH2 Antibodies) 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 (show ANTXR1 Antibodies)-Chk1 (show CHEK1 Antibodies) pathway.

4. Our results suggest that increased expression of MSH6, or other MMR (show MRC1 Antibodies), may be a new mechanism contributing to the acquired resistance during TMZ therapy; and may serve as an indicator to the resistance in GBM.

5. study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR (show MRC1 Antibodies)) genes MLH1 (show MLH1 Antibodies), MSH2 (show MSH2 Antibodies), 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 Antibodies) genes

6. MSH6 frameshift variants incompletely segregate with the Lynch syndrome phenotype in two families.

7. 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 Antibodies), TET2 (show TET2 Antibodies), TET3 (show TET3 Antibodies), KDM1A (show KDM1A Antibodies) and MSH6 were found in 25% of patients. TET2 (show TET2 Antibodies) or TET3 (show TET3 Antibodies), AKT1 (show AKT1 Antibodies) and RUNX1 (show RUNX1 Antibodies) were mutated in one patient each. ASXL1 (show ASXL1 Antibodies) was mutated within exon 12 in three cases

8. The MSH6 gene polymorphisms are likely to play an important role in the progression of AIDS in the northern Chinese population.

9. MSH6 mutations contribute to colorectal cancer susceptibility in Algerian families with suspected Lynch syndrome.

10. Neoadjuvant therapy in microsatellite-stable colorectal carcinoma induces concomitant loss of MSH6 and Ki-67 (show MKI67 Antibodies) expression.

Zebrafish MutS Homolog 6 (E. Coli) (MSH6) interaction partners

1. Studied MSH6 gene expression in developing zebrafish and the influence of MSH6 expression on the production of mismatch binding factors.

2. Identification and characterization of novel knockout mutants of the three major MMR (show MRC1 Antibodies) genes, mlh1 (show MLH1 Antibodies), msh2 (show MSH2 Antibodies), and msh6, in zebrafish that develop tumors at low frequencies.

Mouse (Murine) MutS Homolog 6 (E. Coli) (MSH6) interaction partners

1. we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Smu and Sgamma3 regions

2. Data suggest that MSH6 protects B cells from neoplastic transformation by preserving genomic stability.

3. similar defects on switching in Msh2 (show MSH2 Antibodies)(-/-), Msh2 (show MSH2 Antibodies)(-/-)Msh6(-/-) and Msh2 (show MSH2 Antibodies)(-/-)Msh6(-/-)Msh3 (show MSH3 Antibodies)(-/-) mice confirm that MutSalpha but not MutSbeta plays an important role in class switch recombination

4. Msh6 deficiency resulted in somatic instability of a (GTG (show GGT1 Antibodies))84 repeat.

5. role for Msh6 in protective cellular responses of primary cells to ultraviolet-B-induced mutagenesis and, hence, the prevention of skin cancer.

6. Data suggest that MutS homologues Msh2 (show MSH2 Antibodies), Msh3 (show MSH3 Antibodies), and Msh6 play overlapping and distinct roles during antibody diversification processes.

7. Data suggest that activation-induced cytidine deaminase (show AICDA Antibodies) has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2 (show MSH2 Antibodies)-Msh6, but not Msh3 (show MSH3 Antibodies), and DNA polymerase (show POLB Antibodies).

8. Mice nullizygous for both Msh2 (show MSH2 Antibodies) and Msh3 (show MSH3 Antibodies) and those nullizygous for both Msh3 (show MSH3 Antibodies) and Msh6 displayed the greatest overall increases in mutation frequencies compared with wild-type mice.

9. in Msh6(-/-)Ung (show UNG Antibodies)(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced.

10. p53 (show TP53 Antibodies) and Msh6 are functionally interrelated and these tumor suppressors act together to accelerate tumorigenesis.