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Human Polyclonal MSH6 Primary Antibody for ICC, IF - ABIN151794
Cyr, Heinen: Hereditary cancer-associated missense mutations in hMSH6 uncouple ATP hydrolysis from DNA mismatch binding. in The Journal of biological chemistry 2008
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Human Polyclonal MSH6 Primary Antibody for IHC, IP - ABIN151795
Masih, Kunnev, Melendy: Mismatch Repair proteins are recruited to replicating DNA through interaction with Proliferating Cell Nuclear Antigen (PCNA). in Nucleic acids research 2008
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Human Monoclonal MSH6 Primary Antibody for ELISA, WB - ABIN1724694
Lynch, Lynch: What the physician needs to know about Lynch syndrome: an update. in Oncology (Williston Park, N.Y.) 2005
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Human Monoclonal MSH6 Primary Antibody for ICC, FACS - ABIN969293
Grindedal, Møller, Eeles, Stormorken, Bowitz-Lothe, Landrø, Clark, Kvåle, Shanley, Maehle: Germ-line mutations in mismatch repair genes associated with prostate cancer. in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2009
Human Monoclonal MSH6 Primary Antibody for ELISA, WB - ABIN969292
Becker, Creagh, ONeill: Rab39a binds caspase-1 and is required for caspase-1-dependent interleukin-1beta secretion. in The Journal of biological chemistry 2009
Cow (Bovine) Polyclonal MSH6 Primary Antibody for IHC, WB - ABIN2776759
Wedrén, Lovmar, Humphreys, Magnusson, Melhus, Syvänen, Kindmark, Landegren, Fermér, Stiger, Persson, Baron, Weiderpass: Estrogen receptor alpha gene polymorphism and endometrial cancer risk--a case-control study. in BMC cancer 2009
Human Monoclonal MSH6 Primary Antibody for ELISA, WB - ABIN966596
Hess, Mendillo, Mazur, Kolodner: Biochemical basis for dominant mutations in the Saccharomyces cerevisiae MSH6 gene. in Proceedings of the National Academy of Sciences of the United States of America 2006
Human Monoclonal MSH6 Primary Antibody for IHC (p) - ABIN4335859
Czink, Kloor, Goeppert, Fröhling, Uhrig, Weber, Meinel, Sutter, Weiss, Schirmacher, Doeberitz, Jäger, Springfeld: Successful immune checkpoint blockade in a patient with advanced stage microsatellite-unstable biliary tract cancer. in Cold Spring Harbor molecular case studies 2017
hMSH6 Glu39Gly polymorphism is associated with the risk of developing colorectal cancer in the Polish population.
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.
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.
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
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 (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
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 (show MKI67 Antibodies) 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 (show MRC1 Antibodies) genes, mlh1 (show MLH1 Antibodies), msh2 (show MSH2 Antibodies), 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 (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
Msh6 deficiency resulted in somatic instability of a (GTG (show GGT1 Antibodies))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 (show MSH2 Antibodies), Msh3 (show MSH3 Antibodies), and Msh6 play overlapping and distinct roles during antibody diversification processes.
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).
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.
in Msh6(-/-)Ung (show UNG Antibodies)(-/-) mice, mutations were mostly C,G transitions and class switch recombination was greatly reduced.
p53 (show TP53 Antibodies) 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