PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26021967-14 2015 The transcriptional analyses supported the participation of COMT in the folate pathway, which partakes in the complex network of genexgene and genexenvironment interactions of MDD etiopathogenesis. Folic Acid 72-78 catechol-O-methyltransferase Homo sapiens 60-64 17565222-0 2007 The influence of levodopa and the COMT inhibitor on serum vitamin B12 and folate levels in Parkinson"s disease patients. Folic Acid 74-80 catechol-O-methyltransferase Homo sapiens 34-38 18597513-3 2008 Folate differentially altered activity and expression of proteins involved in proliferation [e.g., PCNA], DNA repair [e.g., XRCC5, MSH2], apoptosis [e.g., BAG family chaperone protein, DIABLO and porin], cytoskeletal organization [e.g., actin, ezrin, elfin], and expression of proteins implicated in malignant transformation [COMT, Nit2]. Folic Acid 0-6 catechol-O-methyltransferase Homo sapiens 326-330 25728832-2 2015 The current study examined folate metabolism as a potential mechanism of CVD and neurocognitive deficits by: 1) using endothelial dysfunction as a biomarker of CVD, and 2) comparing enzymes associated with neurocognition, CVD, and critical to folate metabolism, methylenetetrahydrofolate reductase (MTHFR) and catechol-o-methyl transferase (COMT). Folic Acid 27-33 catechol-O-methyltransferase Homo sapiens 310-339 25728832-2 2015 The current study examined folate metabolism as a potential mechanism of CVD and neurocognitive deficits by: 1) using endothelial dysfunction as a biomarker of CVD, and 2) comparing enzymes associated with neurocognition, CVD, and critical to folate metabolism, methylenetetrahydrofolate reductase (MTHFR) and catechol-o-methyl transferase (COMT). Folic Acid 27-33 catechol-O-methyltransferase Homo sapiens 341-345 22370993-1 2012 Folate has been implicated in cardiovascular disease with atypical antipsychotic (AAPs) use, and individuals with methylenetetrahydrofolate reductase (MTHFR) and catechol-O-methyl transferase (COMT) variants are at greater risk. Folic Acid 0-6 catechol-O-methyltransferase Homo sapiens 193-197 22053698-0 2011 Modulatory effect of plasma folate and polymorphisms in one-carbon metabolism on catecholamine methyltransferase (COMT) H108L associated oxidative DNA damage and breast cancer risk. Folic Acid 28-34 catechol-O-methyltransferase Homo sapiens 114-118 22053698-1 2011 The present study was aimed to investigate the modulatory role of plasma folate and eight putatively functional polymorphisms of one-carbon metabolism on catecholamine methyltransferase (COMT)-mediated oxidative DNA damage and breast cancer risk. Folic Acid 73-79 catechol-O-methyltransferase Homo sapiens 187-191 19360465-3 2010 Of the analyzed genes, ERCC2, XRCC1, XRCC2, XRCC3 and Lig4 participate in DNA repair, TP53 in cell cycle check point control, AIB1, AR, COMT, CYP11A1, CYP17A1, CYP19A1, HSD17 and PGR in steroid hormone biosynthesis/metabolism/signaling, TYMS in folate metabolism and HER2, IL6, LRP1, TGFB and TGFBR1 affect cell growth. Folic Acid 245-251 catechol-O-methyltransferase Homo sapiens 136-140 18801628-2 2008 Polymorphic variants of genes encoding key enzymes of folate and methionine metabolism may have an impact on catecholamine catabolism conducted by catechol-O-methyltransferase. Folic Acid 54-60 catechol-O-methyltransferase Homo sapiens 147-175 17264883-3 2007 Many genetic factors play a role in folate-homocysteine metabolism, like functional polymorphism (Val108Met) in the Catechol-O-methyltransferase (COMT) gene. Folic Acid 36-42 catechol-O-methyltransferase Homo sapiens 116-144 17264883-3 2007 Many genetic factors play a role in folate-homocysteine metabolism, like functional polymorphism (Val108Met) in the Catechol-O-methyltransferase (COMT) gene. Folic Acid 36-42 catechol-O-methyltransferase Homo sapiens 146-150 14767563-7 2004 On the basis of the modulation of COMT-mediated methylation of catecholamines, it is mechanistically explained that hyperhomocysteinemia would be a pathogenic factor in PD whereas vitamins B6, B12, and folate would be a protective factor. Folic Acid 202-208 catechol-O-methyltransferase Homo sapiens 34-38 16917939-10 2006 Differences in allele frequency and/or significant gene-gene interactions were found for relevant genes encoding the reduced folate carrier (RFC 80G > A), transcobalamin II (TCN2 776G > C), catechol-O-methyltransferase (COMT 472G > A), methylenetetrahydrofolate reductase (MTHFR 677C > T and 1298A > C), and glutathione-S-transferase (GST M1). Folic Acid 125-131 catechol-O-methyltransferase Homo sapiens 196-224 11577006-0 2001 COMT genotype, micronutrients in the folate metabolic pathway and breast cancer risk. Folic Acid 37-43 catechol-O-methyltransferase Homo sapiens 0-4 11577006-3 2001 Folate, whose intake levels have also been associated with breast cancer risk, and other micronutrients in the folate metabolic pathway influence levels of SAM and S-adenosylhomocysteine (SAH), a COMT inhibitor generated by the demethylation of SAM. Folic Acid 0-6 catechol-O-methyltransferase Homo sapiens 196-200 11577006-3 2001 Folate, whose intake levels have also been associated with breast cancer risk, and other micronutrients in the folate metabolic pathway influence levels of SAM and S-adenosylhomocysteine (SAH), a COMT inhibitor generated by the demethylation of SAM. Folic Acid 111-117 catechol-O-methyltransferase Homo sapiens 196-200 11577006-9 2001 An increasing number of COMT(L) alleles was significantly associated with increased breast cancer risk in women with below median levels of folate (P(trend) = 0.05) or above median levels of homocysteine (P(trend) = 0.02). Folic Acid 140-146 catechol-O-methyltransferase Homo sapiens 24-28 11577006-10 2001 These findings are consistent with a role for certain folate pathway micronutrients in mediating the association between COMT genotype and breast cancer risk. Folic Acid 54-60 catechol-O-methyltransferase Homo sapiens 121-125