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

Methylthioadenosine phosphorylase

methylthioadenosine phosphorylase, MTAP, 5'-methylthioadenosine phosphorylase, MTA phosphorylase
This gene encodes an enzyme that plays a major role in polyamine metabolism and is important for the salvage of both adenine and methionine. The encoded enzyme is deficient in many cancers because this gene and the tumor suppressor p16 gene are co-deleted. Multiple alternatively spliced transcript variants have been described for this gene, but their full-length natures remain unknown. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p16, HAD, CAN, ACID, p15
Papers on methylthioadenosine phosphorylase
Unscrambling the genomic chaos of osteosarcoma reveals extensive transcript fusion, recurrent rearrangements and frequent novel TP53 aberrations.
Meza-Zepeda et al., Oslo, Norway. In Oncotarget, Jan 2016
By combining genomic and transcriptomic analysis, certain recurrent rearrangements were identified and further validated in patient biopsies, including a PMP22-ELOVL5 gene fusion, genomic structural variations affecting RB1, MTAP/CDKN2A and MDM2, and, most frequently, rearrangements involving TP53.
Pathway, in silico and tissue-specific expression quantitative analyses of oesophageal squamous cell carcinoma genome-wide association studies data.
Taylor et al., Bethesda, United States. In Int J Epidemiol, Jan 2016
After excluding genes with previous GWAS signals, candidate pathways (and genes) for ESCC risk included taste transduction (KEGG_hsa04742; TAS2R13, TAS2R42, TAS2R14, TAS2R46,TAS2R50), long-patch base excision repair (Reactome_pid; POLD2) and the metabolics pathway (KEGG_hsa01100; MTAP, GAPDH, DCTD, POLD2, AMDHD1).
Characterization of MTAP Gene Expression in Breast Cancer Patients and Cell Lines.
Ribeiro et al., Curitiba, Brazil. In Plos One, Dec 2015
MTAP is a ubiquitously expressed gene important for adenine and methionine salvage.
Characterization and Prognostic Significance of Methylthioadenosine Phosphorylase Deficiency in Nasopharyngeal Carcinoma.
Li et al., Kao-hsiung, Taiwan. In Medicine (baltimore), Dec 2015
The methylthioadenosine phosphorylase (MTAP) gene, located at chromosome 9p21, plays a critical role in tumorigenicity and disease progression in a wide variety of cancers.
Long Non-coding RNA ANRIL and Polycomb in Human Cancers and Cardiovascular Disease.
Walsh et al., New York City, United States. In Curr Top Microbiol Immunol, Aug 2015
UNASSIGNED: The long non-coding RNA CDKN2B-AS1, commonly referred to as the A ntisense N on-coding R NA in the I NK4 L ocus (ANRIL), is a 3.8-kb-long RNA transcribed from the short arm of human chromosome 9 on p21.3 that overlaps a critical region encompassing three major tumor suppressor loci juxtaposed to the INK4b-ARF-INK4a gene cluster and the methyl-thioadenosine phosphorylase (MTAP) gene.
Genomic Study of Cardiovascular Continuum Comorbidity.
Puzyrev et al., Tomsk, Russia. In Acta Naturae, Jul 2015
A total of 14 genetic variants were associated with a combination of several diseases of cardiovascular continuum (CVC), including those in the TAS2R38, SEZ6L, APOA2, KLF7, CETP, ITGA4, RAD54B, LDLR, and MTAP genes, along with intragenic variants rs1333048, rs1333049, and rs6501455.
6-thioguanine: a drug with unrealized potential for cancer therapy.
Bertino et al., New Brunswick, United States. In Oncologist, 2014
Although not yet tested in man, 6-TG has recently been proposed to treat a wide variety of cancers with a high frequency of homozygous deletion of the gene for methylthioadenosine phosphorylase (MTAP), often codeleted with the adjacent tumor suppressor CDKN2A (p16).
The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups.
Aparicio et al., Cambridge, United Kingdom. In Nature, 2012
By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4.
Entropy-driven binding of picomolar transition state analogue inhibitors to human 5'-methylthioadenosine phosphorylase.
Schramm et al., New York City, United States. In Biochemistry, 2011
A large negative heat capacity change of -600 cal/(mol K) upon inhibitor binding to MTAP is consistent with altered hydrophobic interactions and release of water.
Polymorphisms in nevus-associated genes MTAP, PLA2G6, and IRF4 and the risk of invasive cutaneous melanoma.
Duffy et al., Villejuif, France. In Twin Res Hum Genet, 2011
Polymorphisms in nevus-associated genes MTAP is associated with invasive cutaneous melanoma.
Comprehensive field synopsis and systematic meta-analyses of genetic association studies in cutaneous melanoma.
Stratigos et al., Athens, Greece. In J Natl Cancer Inst, 2011
In the supplementary meta-analyses, a locus at 9p21.3 (CDKN2A/MTAP) reached genome-wide statistical significance with CM and had strong epidemiological credibility.
Downregulation of methylthioadenosin phosphorylase by homozygous deletion in gastric carcinoma.
Kim et al., Seoul, South Korea. In Genes Chromosomes Cancer, 2011
The present study suggests that MTAP plays an important role in the regulation of gastric carcinogenesis.
Targeting tumors that lack methylthioadenosine phosphorylase (MTAP) activity: current strategies.
Lubin et al., New Brunswick, United States. In Cancer Biol Ther, 2011
Many solid tumors and hematologic malignancies lack expression of the enzyme methylthioadenosine phosphorylase (MTAP), due either to deletion of the MTAP gene or to methylation of the MTAP promoter.
Down-regulation of methylthioadenosine phosphorylase (MTAP) induces progression of hepatocellular carcinoma via accumulation of 5'-deoxy-5'-methylthioadenosine (MTA).
Hellerbrand et al., Regensburg, Germany. In Am J Pathol, 2011
MTAP deficiency results in accumulation of 5'-deoxy-5'-methylthioadenosine, which is associated with increased tumorigenicity.
9p21 DNA variants associated with coronary artery disease impair interferon-γ signalling response.
Frazer et al., San Diego, United States. In Nature, 2011
Using a new, open-ended approach to detect long-distance interactions, we find that in human vascular endothelial cells the enhancer interval containing the CAD locus physically interacts with the CDKN2A/B locus, the MTAP gene and an interval downstream of IFNA21.
[Detection of MTAP protein and gene expression in non-small cell lung cancer].
Ding et al., Weifang, China. In Zhongguo Fei Ai Za Zhi, 2011
The expression of MTAP protein in non-small cell lung cancer tissue was significantly lower than that in paracarcinomous tissue and borderline lung tissue.
Metabolic characteristics and importance of the universal methionine salvage pathway recycling methionine from 5'-methylthioadenosine.
Albers, Göteborg, Sweden. In Iubmb Life, 2009
MTA is first converted to 5'-methylthioribose-1-phosphate either by MTA phosphorylase or the combined action of MTA nucleosidase and 5'-methylthioribose kinase.
Genome-wide association study identifies variants at 9p21 and 22q13 associated with development of cutaneous nevi.
Spector et al., London, United Kingdom. In Nat Genet, 2009
We identified strongly associated variants in MTAP, a gene adjacent to the familial melanoma susceptibility locus CDKN2A on 9p21 (rs4636294, combined P = 3.4 x 10(-15)), as well as in PLA2G6 on 22q13.1 (rs2284063, combined P = 3.4 x 10(-8)).
Ewing sarcomas with p53 mutation or p16/p14ARF homozygous deletion: a highly lethal subset associated with poor chemoresponse.
Ladanyi et al., New York City, United States. In J Clin Oncol, 2005
Six cases with p16/p14ARF deletion were also studied for co-deletion of the contiguous methylthioadenosine phosphorylase gene, and this was detected in four cases.
Lymphoblastic leukemia with lymphomatous features associated with abnormalities of the short arm of chromosome 9.
Rowley et al., In N Engl J Med, 1985
These findings indicate that loss of chromosomal material in the region of 9p21-p22 is closely associated with lymphomatous ALL; by analogy with retinoblastoma, in which gene deletions are associated with an enzyme deficiency, this disease may be related to the loss of the enzyme methylthioadenosine phosphorylase, previously reported in some of these patients.
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