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