PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18023073-2 2008 The purpose of the present study was to determine whether the tyrosine hydroxylase (TH) val81met and catechol-O-methyltransferase (COMT) val158met polymorphisms are associated with the antidepressant effect of milnacipran, a serotonin/noradrenaline reuptake inhibitor. Serotonin 225-234 catechol-O-methyltransferase Homo sapiens 131-135 22483292-7 2012 As serotonin interacts with dopamine and dopamine availability is influenced by COMT SNPs, an association between the COMT gene and response to treatment, based on the various pharmacogenetics/pharmacogenomics studies about COMT gene published to date, is explored in this overview. Serotonin 3-12 catechol-O-methyltransferase Homo sapiens 80-84 18520162-6 2008 In this article, we review existing data on the effects of genetic variation in the dopamine and serotonin systems (catechol-O-methyltransferase, the serotonin-transporter-linked polymorphic region) on the morphometric, metabolic and functional characteristics of the cerebral cortex and limbic structures. Serotonin 97-106 catechol-O-methyltransferase Homo sapiens 116-144 17335389-6 2007 COMT is involved in the catabolism of dopamine, and TPH is the rate-limiting enzyme for serotonin synthesis. Serotonin 88-97 catechol-O-methyltransferase Homo sapiens 0-4 9326274-2 1997 Uptake and cellular retention of 3H-catecholamines was increased by up to fourfold by two COMT inhibitors, tropolone and Ro 41-0960, with potencies similar to those for inhibition of COMT activity, whereas the uptake of two transporter substrates that are not substrates for COMT, [3H]serotonin and [3H]MPP+, was unaffected. Serotonin 285-294 catechol-O-methyltransferase Homo sapiens 90-94 28443016-5 2017 Interestingly, (i) the expression of three of these six genes (COMT, DBH, NOS1) are highly variable; (ii) three of these six genes (COMT, DBH, TPH1) are involved in DA or serotonin metabolism, biosynthesis and/or neurotransmission; and (iii) five of these six genes (AR, BDNF, COMT, DBH, NOS1) have been implicated in the development, onset and/or propagation of schizophrenia. Serotonin 171-180 catechol-O-methyltransferase Homo sapiens 63-67 28443016-5 2017 Interestingly, (i) the expression of three of these six genes (COMT, DBH, NOS1) are highly variable; (ii) three of these six genes (COMT, DBH, TPH1) are involved in DA or serotonin metabolism, biosynthesis and/or neurotransmission; and (iii) five of these six genes (AR, BDNF, COMT, DBH, NOS1) have been implicated in the development, onset and/or propagation of schizophrenia. Serotonin 171-180 catechol-O-methyltransferase Homo sapiens 132-136 28443016-5 2017 Interestingly, (i) the expression of three of these six genes (COMT, DBH, NOS1) are highly variable; (ii) three of these six genes (COMT, DBH, TPH1) are involved in DA or serotonin metabolism, biosynthesis and/or neurotransmission; and (iii) five of these six genes (AR, BDNF, COMT, DBH, NOS1) have been implicated in the development, onset and/or propagation of schizophrenia. Serotonin 171-180 catechol-O-methyltransferase Homo sapiens 132-136 27821364-1 2016 The monoamine oxidases (MAOA/B) and catechol-O-methyltransferase (COMT) enzymes break down regulatory components within serotonin and dopamine pathways, and polymorphisms within these genes are candidates for OCD susceptibility. Serotonin 120-129 catechol-O-methyltransferase Homo sapiens 36-64 27821364-1 2016 The monoamine oxidases (MAOA/B) and catechol-O-methyltransferase (COMT) enzymes break down regulatory components within serotonin and dopamine pathways, and polymorphisms within these genes are candidates for OCD susceptibility. Serotonin 120-129 catechol-O-methyltransferase Homo sapiens 66-70 27959337-9 2016 WGCNA revealed significant correlations between serotonin metabolism and hub genes with known functions in serotonin metabolism, for example, HTR2A and COMT. Serotonin 48-57 catechol-O-methyltransferase Homo sapiens 152-156 27959337-9 2016 WGCNA revealed significant correlations between serotonin metabolism and hub genes with known functions in serotonin metabolism, for example, HTR2A and COMT. Serotonin 107-116 catechol-O-methyltransferase Homo sapiens 152-156 17944104-4 2007 5-HTT and COMT genes, regulating activity of serotonin and dopamine respectively, are related with accuracy of orientation in time. Serotonin 45-54 catechol-O-methyltransferase Homo sapiens 10-14 16257094-4 2006 The present study sought to evaluate the relationship between such behavioral endophenotypes in AD and genetic variations in dopamine- or serotonin-related genes, such as catechol-O-methyltransferase (COMT) or 5-HTT gene-linked promoter region (5-HTTLPR), and apolipoprotein E (APOE). Serotonin 138-147 catechol-O-methyltransferase Homo sapiens 171-199 16257094-4 2006 The present study sought to evaluate the relationship between such behavioral endophenotypes in AD and genetic variations in dopamine- or serotonin-related genes, such as catechol-O-methyltransferase (COMT) or 5-HTT gene-linked promoter region (5-HTTLPR), and apolipoprotein E (APOE). Serotonin 138-147 catechol-O-methyltransferase Homo sapiens 201-205 15900225-1 2005 OBJECTIVES: Catechol-O-methyltransferase plays a central role in the metabolism of biogenic amines such as norepinephrine, dopamine and serotonin. Serotonin 136-145 catechol-O-methyltransferase Homo sapiens 12-40 14520117-2 2003 Catechol-O-methyltransferase and monoamine oxidase enzymes are important agents in the metabolic inactivation of these neurotransmitters (ie, dopamine, serotonin, and norepinephrine). Serotonin 152-161 catechol-O-methyltransferase Homo sapiens 0-28 23965265-2 2013 This study investigates whether social cognition varies with genetic variations of COMT and tryptophan hydroxylase-2 (TPH2), which modulate dopamine and serotonin neurotransmissions respectively, and thereby emotion regulation. Serotonin 153-162 catechol-O-methyltransferase Homo sapiens 83-87 22483292-7 2012 As serotonin interacts with dopamine and dopamine availability is influenced by COMT SNPs, an association between the COMT gene and response to treatment, based on the various pharmacogenetics/pharmacogenomics studies about COMT gene published to date, is explored in this overview. Serotonin 3-12 catechol-O-methyltransferase Homo sapiens 118-122 22483292-7 2012 As serotonin interacts with dopamine and dopamine availability is influenced by COMT SNPs, an association between the COMT gene and response to treatment, based on the various pharmacogenetics/pharmacogenomics studies about COMT gene published to date, is explored in this overview. Serotonin 3-12 catechol-O-methyltransferase Homo sapiens 118-122 21302344-2 2011 Well-characterized common functional polymorphisms in the genes MAOA, COMT, and 5HTTLPR each have predictable effects on the availability of the monoamine neurotransmitters dopamine, noradrenaline, and serotonin. Serotonin 202-211 catechol-O-methyltransferase Homo sapiens 70-74 21519306-10 2011 CONCLUSION: This study suggests that gene interactions between genetic variants in COMT, 5-HTR2A and tryptophan hydroxylase gene would be associated with ASPD and influence the dopamine rewards pathways and modulate serotonin levels in ASPD. Serotonin 216-225 catechol-O-methyltransferase Homo sapiens 83-87 21575337-1 2011 OBJECTIVE: To investigate the association between aggressive behaviors and catechol-O-methyltransferase (COMT) single nucleotide polymorphism at position 158 from a valine to a methionine (Val158Met) as well as serotonin (5-HT) transporter gene linked polymorphic region (5-HTTLPR) in children. Serotonin 211-220 catechol-O-methyltransferase Homo sapiens 105-109 22500608-0 2012 Serotonin-induced hypersensitivity via inhibition of catechol O-methyltransferase activity. Serotonin 0-9 catechol-O-methyltransferase Homo sapiens 53-81 22500608-3 2012 Here we show that serotonin also inhibits catechol O-methyltransferase (COMT), an enzyme that contributes to modultion the perception of pain, via non-competitive binding to the site bound by catechol substrates with a binding affinity comparable to the binding affinity of catechol itself (K(i) = 44 muM). Serotonin 18-27 catechol-O-methyltransferase Homo sapiens 42-70 22500608-3 2012 Here we show that serotonin also inhibits catechol O-methyltransferase (COMT), an enzyme that contributes to modultion the perception of pain, via non-competitive binding to the site bound by catechol substrates with a binding affinity comparable to the binding affinity of catechol itself (K(i) = 44 muM). Serotonin 18-27 catechol-O-methyltransferase Homo sapiens 72-76 22500608-5 2012 Binding of serotonin to the catalytic site inhibits the access of SAM, thus preventing methylation of COMT substrates. Serotonin 11-20 catechol-O-methyltransferase Homo sapiens 102-106 22500608-7 2012 Our results suggest that inhibition of COMT via serotonin binding contributes to pain hypersensitivity, providing additional strategies for the treatment of clinical pain conditions. Serotonin 48-57 catechol-O-methyltransferase Homo sapiens 39-43 19690620-1 2009 BACKGROUND: Candidate genes of psychological importance include 5HT2A, 5HT2C, and COMT, implicated in the serotonin, noradrenaline and dopamine pathways, which also may be involved in regulation of energy balance. Serotonin 106-115 catechol-O-methyltransferase Homo sapiens 82-86