anti-MSH6 (MSH6) Antikörper

Human MutS Homolog 6 (E. Coli) (MSH6) Interaktionspartner

1. This deletion in Lynch Syndrome results in the loss of a 3246bp-sized fragment in MSH6 gene exons 5-9 which represents the coding regions of the MSH6 ATPase domain. This novel mutation has yet to be documented in the International Society for Gastrointestinal Hereditary Tumours (InSiGHT) database. This mutation resulted in MSH6 protein losing gene mismatch repair function, and further caused the microsatellite instable.

2. Report loss of MSH2 and MSH6 expression in sporadic deficient mismatch repair colorectal cancer due to MLH1 promoter hypermethylation.

3. Results show that mutations in MSH6 were less prevalent in a cohort of patients diagnosed with Lynch syndrome, and MSH6 mutation carriers presented with colorectal and endometrial cancer at later age.

4. MSH6 Microsatellite Instability is associated with late stage Colorectal Cancer.

5. Our data demonstrate that two Lynch syndrome (LS) genes, MSH6 and PMS2, are associated with an increased risk for breast cancer and should be considered when ordering genetic testing for individuals who have a personal and/or family history of breast cancer

6. discover a translocation disrupting MLH1 and three mutations in MSH6 and PMS2 that increase endometrial, colorectal, brain and ovarian cancer risk

7. Whole exome sequencing in triple negative breast cancer cases revealed MSH6 rs2020912 (MAF: 56.25% vs. 1.04%, OR 122.13, 95% CI 12.29-2985.48) are risk factors for triple negative breast cancer.

8. CSE1L expression was correlated with MSH6 expression in tumor samples and was associated with poor prognosis in patients with osteosarcoma. Taken together, our results demonstrate that the CSE1L-MSH6 axis has an important role in osteosarcoma progression.

9. 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 IVS1-1121C >

10. Results from a study on gene expression variability markers in early-stage human embryos shows that is a putative expression variability marker for the 3-day, 8-cell embryo stage.

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

12. Expression of MSH6 and MSH2 was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR expression. Reduction of MSH6 and MSH2 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-Chk1 pathway.

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

14. study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR) genes MLH1, MSH2, and MSH6 among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR genes

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

16. Patients with mutations 6 showed higher rate of achieving major molecular response than those<6 (P=0.0381). Mutations in epigenetic regulator, ASXL1, TET2, TET3, KDM1A and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 and RUNX1 were mutated in one patient each. ASXL1 was mutated within exon 12 in three cases

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

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

19. Neoadjuvant therapy in microsatellite-stable colorectal carcinoma induces concomitant loss of MSH6 and Ki-67 expression.

20. High MSH6 expression is associated with the development of genetic instability and is linked to tumor aggressiveness and early PSA recurrence in prostate cancer.

Zebrafish MutS Homolog 6 (E. Coli) (MSH6) Interaktionspartner

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 genes, mlh1, msh2, and msh6, in zebrafish that develop tumors at low frequencies.

Mouse (Murine) MutS Homolog 6 (E. Coli) (MSH6) Interaktionspartner

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(-/-), Msh2(-/-)Msh6(-/-) and Msh2(-/-)Msh6(-/-)Msh3(-/-) 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)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, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes.

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

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

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

10. p53 and Msh6 are functionally interrelated and these tumor suppressors act together to accelerate tumorigenesis.

11. These findings indicate that MutS alpha reduces spontaneous and IR-induced mutation in a cell type-dependant manner.

12. Synergism between Mgmt and Msh6 can be explained entirely by the suppression of alkylation-induced apoptosis when Msh6 is absent.

13. ablation of either Msh6 or Exo1 function in the Mgmt-null mouse renders these rapidly proliferating tissues alkylation-resistant. The Msh6 defect confers total alkylation resistance