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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

MutY homolog

MYH, MUTYH, hMYH, MutY homolog
This gene encodes a DNA glycosylase involved in oxidative DNA damage repair. The enzyme excises adenine bases from the DNA backbone at sites where adenine is inappropriately paired with guanine, cytosine, or 8-oxo-7,8-dihydroguanine, a major oxidatively damaged DNA lesion. The protein is localized to the nucleus and mitochondria. Mutations in this gene result in heritable predisposition to colon and stomach cancer. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: APC, HAD, CAN, AGE, OGG1
Papers on MYH
Exome sequencing identifies potential novel candidate genes in patients with unexplained colorectal adenomatous polyposis.
Aretz et al., Bonn, Germany. In Fam Cancer, Feb 2016
UNASSIGNED: In up to 30 % of patients with colorectal adenomatous polyposis, no germline mutation in the known genes APC, causing familial adenomatous polyposis, MUTYH, causing MUTYH-associated polyposis, and POLE or POLD1, causing Polymerase-Proofreading-associated polyposis can be identified, although a hereditary etiology is likely.
Resetting the epigenome for heart regeneration.
Hudson et al., Brisbane, Australia. In Semin Cell Dev Biol, Feb 2016
BMP, bone morphogenetic protein; Bvht, Braveheart; CBP, CREB-binding protein; Cdkn, cyclin dependent kinase inhibitor; DOT1L, disruptor of telomeric silencing-1; DNMTs, DNA methyltransferases; eRNAs, enhancer RNAs; ESCs, embryonic stem cells; FGF, fibroblast growth factor; FOX, Forkhead box; Gcn5, general control of amino acid synthesis protein 5; HATs, histone acetyl transferases; HDACs, histone deacteylases; H3K27, histone 3, lysine 27; HMTs, histone methyltransferases; Jmj, Jumonji; JMJD3, Jumonji domain-containing protein 3; KDMs, histone lysine demethylases; lncRNAs, long non-coding RNAs; Mhrt, Myheart; miRNAs, microRNAs; Myh, myosin heavy chain; PRC2, polycomb repressive complex 2; PSCs, pluripotent stem cells; PTM, post-translational modification; SIRTs, Sirtuins; SMYD1, SET and MYND domain containing 1; Srf, serum response factor; TET, Ten-eleven translocation; TGF-β, transforming growth factor beta; TFs, transcription factors; UTX, ubiquitously transcribed tetratricopeptide repeat, X chromosome.
Synergistic Actions of Ogg1 and Mutyh DNA Glycosylases Modulate Anxiety-like Behavior in Mice.
Bjørås et al., Oslo, Norway. In Cell Rep, Jan 2016
Ogg1 and Mutyh DNA glycosylases cooperate to prevent mutations caused by 8-oxoG, a major premutagenic DNA lesion associated with cognitive decline.
Functional Evaluation of 9 Missense-Type Variants of the Human DNA Glycosylase Enzyme MUTYH in the Japanese Population.
Sugimura et al., Hamamatsu, Japan. In Hum Mutat, Jan 2016
UNASSIGNED: Biallelic germline mutations of MUTYH, the gene encoding DNA glycosylase, cause MUTYH-associated polyposis (MAP), characterized by multiple colorectal adenomas and carcinoma(s).
Mutation analysis of MUTYH in Japanese colorectal adenomatous polyposis patients.
Arai et al., Tokyo, Japan. In Fam Cancer, Jan 2016
UNASSIGNED: Germline MUTYH mutations were investigated in 14 Japanese colorectal polyposis patients without germ line adenomatous polyposis coli (APC) gene mutations.
Potential role of Escherichia coli DNA mismatch repair proteins in colon cancer.
Khan, Riyadh, Saudi Arabia. In Crit Rev Oncol Hematol, Dec 2015
Interestingly, alteration in MutS, MutL complexes and MUTYH of mammalian cells may be involved in development of CRC.
Current status of familial gastrointestinal polyposis syndromes.
Turdean et al., Târgu-Mureş, Romania. In World J Gastrointest Oncol, Dec 2015
The following inherited polyposes syndromes were analyzed: familial adenomatous polyposis, the hamartomatous familial polyposes (Juvenile polyposis, Peutz-Jeghers syndrome, Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, hereditary mixed polyposis syndrome, Gorlin syndrome, Birt-Hogg-Dube syndrome, neurofibromatosis type I and multiple endocrine neoplasia syndrome 2B), Li-Fraumeni syndrome, and MUTYH-associated adenomatous polyposis.
High Prevalence of Hereditary Cancer Syndromes in Adolescents and Young Adults With Colorectal Cancer.
Vilar et al., Houston, United States. In J Clin Oncol, Dec 2015
RESULTS: Of the 193 patients with evaluable data, 35% had an identifiable hereditary cancer syndrome, including 23 with Lynch syndrome, 22 with mutation-negative Lynch syndrome, 16 with familial adenomatous polyposis, two with constitutional mismatch repair deficiency, two with biallelic MUTYH mutations, and one with Li-Fraumeni syndrome.
Hereditary Colorectal Cancer: Genetics and Screening.
Giardiello et al., Utrecht, Netherlands. In Surg Clin North Am, Oct 2015
This article focuses on genetic and clinical aspects of Lynch syndrome, familial adenomatous polyposis, and MUTYH-associated polyposis.
Genetic diagnosis of high-penetrance susceptibility for colorectal cancer (CRC) is achievable for a high proportion of familial CRC by exome sequencing.
Houlston et al., London, United Kingdom. In J Clin Oncol, Mar 2015
PATIENTS AND METHODS: To quantify the impact of germline mutation to familial CRC, we sequenced the mismatch repair genes (MMR) APC, MUTYH, and SMAD4/BMPR1A in 626 early-onset familial CRC cases ascertained through a population-based United Kingdom national registry.
[Retrospective NGS Study in High-risk Hereditary Cancer Patients at Masaryk Memorial Cancer Institute].
Foretová et al., In Klin Onkol, 2014
Various pathogenic or potentially pathogenic (missense, predicted splice site, in-frame insertion/deletion) mutations were detected in ATM, BRIP1, CDH1, CHEK2, ERCC2, ERCC3, ERCC4, FANCA, MC1R, MEN1, MRE11A, MUTYH, PALB2, RAD51C, RET, SDHB, STK11.
The genetic basis of familial adenomatous polyposis and its implications for clinical practice and risk management.
Balaguer et al., Barcelona, Spain. In Appl Clin Genet, 2014
Germline mutations in the APC gene were initially identified as responsible for FAP, and later, several studies have also implicated the MUTYH gene as responsible for this disease, usually referred to as MUTYH-associated polyposis (MAP).
Clinical evaluation of a multiple-gene sequencing panel for hereditary cancer risk assessment.
Ford et al., San Francisco, United States. In J Clin Oncol, 2014
Sixteen pathogenic variants were identified in ATM, BLM, CDH1, CDKN2A, MUTYH, MLH1, NBN, PRSS1, and SLX4 among 141 women without BRCA1/2 mutations.
Base excision repair gene polymorphisms are associated with inflammation in patients undergoing chronic hemodialysis.
Wang et al., Nanjing, China. In Biochem Biophys Res Commun, 2012
As predictors of mortality, plasma IL-1b and IL-6 levels were significantly higher in the hemodialysis patients than the healthy controls, and the increases were associated with the MUTYH c.972G > C and AluYb8MUTYH polymorphisms.
Prevalence and phenotypes of APC and MUTYH mutations in patients with multiple colorectal adenomas.
Syngal et al., Boston, United States. In Jama, 2012
Among patients with multiple colorectal adenomas, pathogenic APC and MUTYH mutation prevalence varied considerably by adenoma count, including within those with a classic polyposis phenotype.
MUTYH gene expression and alternative splicing in controls and polyposis patients.
Zeuzem et al., Frankfurt am Main, Germany. In Hum Mutat, 2012
MUTYH expression differed organ dependently, correlating with proliferative activity.Five transcripts were found to encode the biologically relevant products of the MUTYH gene.
MUTYH hotspot mutations in unselected colonoscopy patients.
Raedle et al., Homburg, Germany. In Colorectal Dis, 2012
Patients compound heterozygous for MUTYH pathogenic mutations and the p.Q338H variant may be at increased risk for mild polyposis or colorectal cancer.
Association between polymorphisms of the DNA base excision repair genes MUTYH and hOGG1 and age-related macular degeneration.
Szaflik et al., Łódź, Poland. In Exp Eye Res, 2012
Our findings suggest that the c.977C>G-hOGG1 polymorphism may be associated with dry AMD. Further studies are needed to determine possible association between AMD and the c.972G>C-MUTYH polymorphism.
DNA polymerases as potential therapeutic targets for cancers deficient in the DNA mismatch repair proteins MSH2 or MLH1.
Ashworth et al., London, United Kingdom. In Cancer Cell, 2010
Both SSLs were rescued by silencing the adenine glycosylase MUTYH, suggesting that lethality could be caused by the formation of lethal DNA breaks upon 8-oxoG accumulation.
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