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MutS homolog 6

MSH6, p160
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MSH2, MLH1, PMS2, HAD, CAN
Papers using MSH6 antibodies
The reliability of immunohistochemistry as a prescreening method for the diagnosis of hereditary nonpolyposis colorectal cancer (HNPCC) – results of an international collaborative study
Kam Lee Suk et al., In The Indian Journal of Medical Research, 2000
... No.556349) at 1/200 dilution, MSH6 antibody (BD Biosciences Transduction Laboratories, USA, Cat ...
Papers on MSH6
Incidental germline variants in 1000 advanced cancers on a prospective somatic genomic profiling protocol.
Chen et al., Houston, United States. In Ann Oncol, Feb 2016
RESULTS: Of the 1000 patients who underwent sequencing, 43 had likely pathogenic germline variants: APC (1), BRCA1 (11), BRCA2 (10), TP53 (10), MSH2 (1), MSH6 (4), PALB2 (2), PTEN (2), TSC2 (1), and RB1 (1).
Nimotuzumab enhances temozolomide-induced growth suppression of glioma cells expressing mutant EGFR in vivo.
Nagane et al., Tokyo, Japan. In Cancer Med, Feb 2016
The post-treatment recurrent brain tumors exhibited a decrease in expression of the mismatch repair (MMR) proteins, MSH6 and MLH1, but their methylated MGMT status did not changed.
Moving Beyond the Androgen Receptor (AR): Targeting AR-Interacting Proteins to Treat Prostate Cancer.
Mitsiades et al., Houston, United States. In Horm Cancer, Feb 2016
In this review, we discuss the preclinical research that has been done, as well as clinical trials for prostate cancer, on inhibiting several important families of AR-interacting proteins, including chaperones (such as heat shock protein 90 (HSP90) and FKBP52), pioneer factors (including forkhead box protein A1 (FOXA1) and GATA-2), and AR transcriptional coregulators such as the p160 steroid receptor coactivators (SRCs) SRC-1, SRC-2, SRC-3, as well as lysine deacetylases (KDACs) and lysine acetyltransferases (KATs).
Whole-exome Sequencing analyses of Inflammatory Bowel Disease-associated Colorectal Cancers.
Papadopoulos et al., Bethesda, United States. In Gastroenterology, Feb 2016
RESULTS: Two specimens had somatic mutations in the DNA-proofreading or mismatch repair genes POLE, MLH1, and MSH6 and the tumor cells had a hypermutable phenotype.
Expression of the apoptosis repressor with caspase recruitment domain (ARC) in liver metastasis of colorectal cancer and its correlation with DNA mismatch repair proteins and p53.
Heikaus et al., Köln, Germany. In J Cancer Res Clin Oncol, Jan 2016
RESULTS: ARC expression level in colorectal cancer liver metastasis was independent from clinical data (i.e., age, gender, tumor size, tumor number or mucin production) but strongly correlated with MSH2 and MSH6 expression, which further supported the evidence for the regulatory role of MSH2 and MSH6 in apoptosis; i.e., in case of sufficient MSH2 and MSH6 expression, significantly higher ARC level is required to suppress the apoptosis.
Acute lymphoblastic leukemia and lymphoma in the context of constitutional mismatch repair deficiency syndrome.
Schlegelberger et al., Hannover, Germany. In Eur J Med Genet, Jan 2016
Causative mutations are found in DNA mismatch repair genes PMS2, MSH6, MSH2 or MLH1 that are well known in the context of Lynch syndrome.
Combined Microsatellite Instability, MLH1 Methylation Analysis, and Immunohistochemistry for Lynch Syndrome Screening in Endometrial Cancers From GOG210: An NRG Oncology and Gynecologic Oncology Group Study.
Mutch et al., Houston, United States. In J Clin Oncol, Jan 2016
One of the MSH6 Lynch mutations was identified in a patient whose tumor had intact MSH6 expression.
Disease-associated repeat instability and mismatch repair.
Pearson et al., Toronto, Canada. In Dna Repair (amst), Jan 2016
Recent advances have broadened our knowledge of both the MMR proteins involved in disease repeat expansions, including: MSH2, MSH3, MSH6, MLH1, PMS2, and MLH3, as well as the types of repeats affected by MMR, now including: (CAG)·(CTG), (CGG)·(CCG), and (GAA)·(TTC) repeats.
Review: Clinical aspects of hereditary DNA Mismatch repair gene mutations.
Hofstra et al., Groningen, Netherlands. In Dna Repair (amst), Jan 2016
UNASSIGNED: Inherited mutations of the DNA Mismatch repair genes MLH1, MSH2, MSH6 and PMS2 can result in two hereditary tumor syndromes: the adult-onset autosomal dominant Lynch syndrome, previously referred to as Hereditary Non-Polyposis Colorectal Cancer (HNPCC) and the childhood-onset autosomal recessive Constitutional Mismatch Repair Deficiency syndrome.
Obesity, Aspirin, and Risk of Colorectal Cancer in Carriers of Hereditary Colorectal Cancer: A Prospective Investigation in the CAPP2 Study.
Mathers et al., Tehrān, Iran. In J Clin Oncol, Dec 2015
In subgroup analysis, obesity was associated with 3.72× (95% CI, 1.41 to 9.81) greater CRC risk in patients with LS with MLH1 mutation, but no excess risk was observed in those with MSH2 or MSH6 mutation (P = .5).
[Gender-specific aspects of Lynch syndrome--an update].
Möslein et al., Wuppertal, Germany. In Z Gastroenterol, Aug 2015
The difference is especially notable in men with a MSH6-mutation.
Lynch syndrome in the 21st century: clinical perspectives.
Lynch et al., Omaha, United States. In Qjm, Aug 2015
At the genetic level, it is caused by a defective mismatch repair (MMR) system due to presence of germline defects in at least one of the MMR genes- MLH1, MSH2, MSH6, PMS2 or EPCAM.
Application of a 5-tiered scheme for standardized classification of 2,360 unique mismatch repair gene variants in the InSiGHT locus-specific database.
InSiGHT et al., In Nat Genet, 2014
The International Society for Gastrointestinal Hereditary Tumours (InSiGHT) undertook a collaborative effort to develop, test and apply a standardized classification scheme to constitutional variants in the Lynch syndrome-associated genes MLH1, MSH2, MSH6 and PMS2.
Tumor mismatch repair immunohistochemistry and DNA MLH1 methylation testing of patients with endometrial cancer diagnosed at age younger than 60 years optimizes triage for population-level germline mismatch repair gene mutation testing.
Spurdle et al., Adelaide, Australia. In J Clin Oncol, 2014
CONCLUSION: Population-level identification of patients with MMR mutation-positive endometrial cancer is optimized by stepwise testing for tumor MMR IHC loss in patients younger than 60 years, tumor MLH1 methylation in individuals with MLH1 IHC loss, and germline mutations in patients exhibiting loss of MSH6, MSH2, or PMS2 or loss of MLH1/PMS2 with absence of MLH1 methylation.
Risks of less common cancers in proven mutation carriers with lynch syndrome.
Vasen et al., Leipzig, Germany. In J Clin Oncol, 2013
The purpose of this retrospective cohort study was to provide risk estimates for these less common cancers in proven carriers of pathogenic mutations in the mismatch repair (MMR) genes MLH1, MSH2, and MSH6.
Myb-binding protein 1a (Mybbp1a) regulates levels and processing of pre-ribosomal RNA.
Németh et al., Regensburg, Germany. In J Biol Chem, 2012
Mybbp1a may play a dual role in the rRNA metabolism, potentially linking and coordinating ribosomal DNA transcription and pre-rRNA processing to allow for the efficient synthesis of ribosomes.
Decreased efficiency of MSH6 mRNA polyadenylation linked to a 20-base-pair duplication in Lynch syndrome families.
Vagner et al., In Cell Cycle, 2012
The duplication of S20 reduces MSH6 expression by lowering the efficiency of MSH6 mRNA polyadenylation.
Central role for PELP1 in nonandrogenic activation of the androgen receptor in prostate cancer.
Raj et al., Dallas, United States. In Mol Endocrinol, 2012
PELP1 may enable estradiol-induced androgen receptor (AR) signaling by forming a protein complex between AR, estrogen receptor beta, and PELP1 on the DNA, leading to the proliferation of prostate cancer cells in the absence of androgen.
Thirty-nine-year-old with familial colon cancer, and variant of undetermined significance in MSH6.
Morris et al., Scranton, United States. In Semin Oncol, 2012
The intriguing point in this case of familial colon cancer is the finding of two different variants at separate loci within the MSH6 gene.
Opposing function of MYBBP1A in proliferation and migration of head and neck squamous cell carcinoma cells.
Hess et al., Heidelberg, Germany. In Bmc Cancer, 2011
We provide experimental evidence that MYBBP1A is an important molecular switch in the regulation of tumor cell proliferation versus migration in head and neck squamous cell carcinoma cells.
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