| MSH6 Aggravates the Hypoxic Microenvironment via Regulating HIF1A to Promote the Metastasis of Glioblastoma Multiforme. | MSH6 Aggravates the Hypoxic Microenvironment via Regulating HIF1A to Promote the Metastasis of Glioblastoma Multiforme.
Shi Y, Jiang J, Cui Y, Chen Y, Dong T, An H, Liu P. | 02/6/2021 |
| we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Smu and Sgamma3 regions | AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].
Ranjit S, Khair L, Linehan EK, Ucher AJ, Chakrabarti M, Schrader CE, Stavnezer J., Free PMC Article | 10/22/2011 |
| Data suggest that MSH6 protects B cells from neoplastic transformation by preserving genomic stability. | Msh6 protects mature B cells from lymphoma by preserving genomic stability.
Peled JU, Sellers RS, Iglesias-Ussel MD, Shin DM, Montagna C, Zhao C, Li Z, Edelmann W, Morse HC 3rd, Scharff MD., Free PMC Article | 03/26/2011 |
| 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 | MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sites.
Roa S, Li Z, Peled JU, Zhao C, Edelmann W, Scharff MD., Free PMC Article | 09/6/2010 |
| Synergism between Mgmt and Msh6 can be explained entirely by the suppression of alkylation-induced apoptosis when Msh6 is absent. | Alkylation-induced colon tumorigenesis in mice deficient in the Mgmt and Msh6 proteins.
Bugni JM, Meira LB, Samson LD., Free PMC Article | 01/21/2010 |
| 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 | O6-methylguanine-induced cell death involves exonuclease 1 as well as DNA mismatch recognition in vivo.
Klapacz J, Meira LB, Luchetti DG, Calvo JA, Bronson RT, Edelmann W, Samson LD., Free PMC Article | 01/21/2010 |
| These findings indicate that MutS alpha reduces spontaneous and IR-induced mutation in a cell type-dependant manner. | Role of the mismatch repair gene, Msh6, in suppressing genome instability and radiation-induced mutations.
Barrera-Oro J, Liu TY, Gorden E, Kucherlapati R, Shao C, Tischfield JA., Free PMC Article | 01/21/2010 |
| p53 and Msh6 are functionally interrelated and these tumor suppressors act together to accelerate tumorigenesis. | The associated contributions of p53 and the DNA mismatch repair protein Msh6 to spontaneous tumorigenesis.
Young LC, Keuling AM, Lai R, Nation PN, Tron VA, Andrew SE. | 01/21/2010 |
| 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. | Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6.
Hegan DC, Narayanan L, Jirik FR, Edelmann W, Liskay RM, Glazer PM., Free PMC Article | 01/21/2010 |
| Msh6 deficiency resulted in somatic instability of a (GTG)84 repeat. | Somatic expansion behaviour of the (CTG)n repeat in myotonic dystrophy knock-in mice is differentially affected by Msh3 and Msh6 mismatch-repair proteins.
van den Broek WJ, Nelen MR, Wansink DG, Coerwinkel MM, te Riele H, Groenen PJ, Wieringa B. | 01/21/2010 |
| in Msh6(-/-)Ung(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced. | Somatic hypermutation and class switch recombination in Msh6(-/-)Ung(-/-) double-knockout mice.
Shen HM, Tanaka A, Bozek G, Nicolae D, Storb U. | 01/21/2010 |
| role for Msh6 in protective cellular responses of primary cells to ultraviolet-B-induced mutagenesis and, hence, the prevention of skin cancer. | DNA mismatch repair protein Msh6 is required for optimal levels of ultraviolet-B-induced apoptosis in primary mouse fibroblasts.
Young LC, Peters AC, Maeda T, Edelmann W, Kucherlapati R, Andrew SE, Tron VA. | 01/21/2010 |
| 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. | A role for Msh6 but not Msh3 in somatic hypermutation and class switch recombination.
Martomo SA, Yang WW, Gearhart PJ., Free PMC Article | 01/21/2010 |
| Data suggest that MutS homologues Msh2, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes. | Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification.
Li Z, Scherer SJ, Ronai D, Iglesias-Ussel MD, Peled JU, Bardwell PD, Zhuang M, Lee K, Martin A, Edelmann W, Scharff MD., Free PMC Article | 01/21/2010 |