ライフサイエンスコーパス: COMT

1 COMT activity can also be regulated pharmacologically by

2 COMT activity specifically alters long-latency component

3 COMT genetic overactivity produced a selective overdrive

4 COMT genotype did not predict hits or d'.

5 COMT genotype was not related to working memory in this

6 COMT is a druggable biological target for the treatment

7 COMT modulates catecholamine metabolism, and polymorphis

8 COMT selectively and reversibly modulated the recall of

9 COMT Val158Met genotype data were also obtained from chi

10 COMT-Val-tg mice displayed increased N40 latency and dec

11 irty-four COMT Met(158)Met (Met-COMT) and 33 COMT Val(158)Val (Val-COMT) men were given a single 200-

12 cused on the development of centrally active COMT inhibitors, which can be valuable assets for neurol

13 o determine the effects of the high-activity COMT allele on electrophysiological markers, including t

14 ect not found in subjects with high-activity COMT diplotypes (hazard ratio = 1.42; 95% confidence lim

15 hermore, smokers who carry the high-activity COMT-Val allele are more prone to cognitive deficits and

16 TMD incidence in subjects with low-activity COMT diplotypes (hazard ratio = 2.35; 95% confidence lim

17 with COMT diplotypes coding for low-activity COMT, signifying impaired catabolism of catecholamines.

18 ore developed a novel mouse model of altered COMT activity.

19 restored normal event-related activity among COMT-Val-tg mice, suggesting one mechanism through which

20 ciated with disease duration (P = 0.02), and COMT rs6267 T allele (P < 0.01).

21 Span Q = 0.006; Block Design Q = 0.076), and COMT (Behavioral Assessment System for Children-2 Attent

22 .65, 95% CI: 0.53-0.79, P=1.81 x 10(-5)) and COMT rs4680 (Val (G) allele: OR=1.27, 95% CI: 1.14-1.42,

23 ) and in 18 metabolites between C57BL/6J and COMT(-/-) mice (p < 0.05).

24 best predicted by fractional anisotropy and COMT genotype.

25 nd epistasis between the same AKT1, BDNF and COMT functional variants on schizophrenia risk, and phar

26 is with functional polymorphisms in BDNF and COMT--genes also implicated in MTL biology related to AK

27 eic acid 3-O-methyltransferases (CCoAOMT and COMT) and a form of cinnamyl alcohol dehydrogenase (ChCA

28 ergic signaling: DRD2, DRD3, DRD4, DAT1, and COMT.

29 We concluded that depression and COMT rs4680 "GG" and "GA" genotypes and COMT rs6267 "GT"

30 lly significant interaction of diagnosis and COMT genotype was observed, such that schizophrenia hete

31 and COMT rs4680 "GG" and "GA" genotypes and COMT rs6267 "GT" genotype contribute to pain in PD patie

32 um, BDNF Val66Met for CA4/dentate gyrus, and COMT Val158Met for CA2/3 volume changes.

33 g that overall, females outperform males and COMT knockout males outperform their wild-type littermat

34 with respect to other olfactory measures and COMT haplotypes is warranted.

35 infants with NAS, variants in the OPRM1 and COMT genes were associated with a shorter length of hosp

36 046, ERbeta rs1256049, ERbeta rs4986938, and COMT rs4680) among 702 Singapore Chinese female lung can

37 food-restriction condition enhanced sex and COMT differences, revealing that overall, females outper

38 ple regression to examine effects of sex and COMT genotype on N-Back hits, false positives, discrimin

39 manipulations revealed a variety of sex- and COMT-dependent effects.

40 These findings illuminate complex sex- and COMT-related effects and their interactions with environ

41 action between prenatal maternal smoking and COMT Val(158)Met in conduct problems and crime in the 19

42 SLC6A4(serotonin reuptake transporter), and COMT(catecholamine O-methyltransferase).

43 identified through our integrative approach, COMT and FMO3, increase apoptosis and decrease cell viab

44 To functionally assess COMT inactivation of vesicular release of DA we used fas

45 ings are of translational relevance, because COMT inhibitors are used in the adjunctive treatment of

46 vidence was found for an association between COMT genotypes and conduct scores or for an interaction

47 There was no association between COMT genotypes and events or interaction between COMT ge

48 us of depression and the association between COMT rs6267 "GT" genotype and pain severity remained sig

49 on region, and possible associations between COMT variants and neuropsychiatric manifestations in 22q

50 a nominally significant interaction between COMT and sex on false positives, but this was not in the

51 genotypes and events or interaction between COMT genotypes and HVAL concentrations.We report, for th

52 nificantly mediated the relationship between COMT genotype and inhibitory proficiency as indexed by s

53 Our analysis identifies a trend between COMT genotype with scarring, with rs4680 genetic variati

54 t time demonstrate an interaction of BDNF by COMT on human cortical plasticity.

55 ivity of children with ADHD was modulated by COMT polymorphism, with Met-carriers exhibiting signific

56 y can also be regulated pharmacologically by COMT inhibitors.

57 ever, despite the established role played by COMT genetic variation in executive functions, its impac

58 ferences in WM performance were predicted by COMT val(158)met status.

59 o of three brown midrib12 mutants that carry COMT gene missense mutations, we determined the apo-form

60 potent inhibition of peripheral and cerebral COMT within the nanomolar range.

61 UFV2, RAB18, as well as ADCYAP1, BDNF, CNR1, COMT, DRD2, DTNBP1, GAD1, GRIA1, GRIN2B, HTR2A, NRG1, RE

62 There are three common COMT haplotypes in the human population reported to have

63 small low nanomolar potent, SAM competitive COMT inhibitors are reported.

64 ey demonstrate the importance of considering COMT genotype when examining the therapeutic potential o

65 When considering COMT genotype and chronic pain suffering, TMD patients w

66 pes in Native Americans include OPRM1, CRN1, COMT, GABRA2, MAOA, and HTR3-B.

67 Current COMT inhibitors carry a high risk for toxic effects to h

68 nts were selected from the DRD2, DRD3, DAT1, COMT, DDC, GRIN2B, ADRA2C, SERT, TPH2, HTR2A, OPRK1 and

69 viduals who carried a larger number of DAT1, COMT, DRD2, and DRD4 alleles associated with higher DA t

70 chronically-curtailed sleep and demonstrate COMT-related treatment responses and risk factors for sy

71 ing approach to discover noncatechol derived COMT inhibitors which bind at the SAM binding pocket.

72 Genotyped DNA from blood samples determined COMT diplotypes.

73 Together, the TMD diagnosis, COMT (158)Met substitution, and pain chronicity explaine

74 rticipants were also genotyped for different COMT alleles.

75 immersion varied in subjects with different COMT genotypes.

76 For CpG sites at genes of the dopaminergic (COMT, ANKK1) and the neurotrophic (BDNF, NGFR) system, a

77 netic mutation reducing expression of either COMT or DTNBP1 alone produced working memory advantages,

78 indicate that the OB preferentially employs COMT enzymatic inactivation of vesicular release of DA.

79 ine receptor DRD4 48 bp VNTR, and the enzyme COMT SNP rs4680.

80 sured the amount of the DA breakdown enzyme, COMT, present in the OB.

81 isms in genes encoding dopaminergic enzymes (COMT, DBH, DDC, MAOA, MAOB, and TH), dopamine receptors

82 Here we examine COMT in relation to N-Back working memory task performan

83 didate genes for schizophrenia (for example, COMT, DISC1, DTNBP1 and NRG1).

84 3, BDNF, SLC6A4, CSNK1E, SLC6A2, DRD2, FAAH, COMT, OPRM1).

85 isease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 ver

86 We calculated the Kd values for COMT, SAHH, and PRDM2 (24.1 +/- 2.2 muM, 6.0 +/- 2.9 muM

87 Thirty-four COMT Met(158)Met (Met-COMT) and 33 COMT Val(158)Val (Val

88 iabetic mice with a transplanted kidney from COMT(-/-) mice.

89 genes related to dopamine metabolism (e.g., COMT, DAT1, and AKT1) may moderate the effects of cannab

90 silencing of the non-memory permissive gene COMT in the hippocampus.

91 mice overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote memories (>50 da

92 Depending on genotype, COMT inhibition can enhance or impair working memory and

93 significantly higher in participants having COMT rs4680 "GG" and "GA" genpotypes than those having "

94 yltransferase (COMT) genotype activity (high COMT compared with low or intermediate COMT genotype act

95 DRD3, DRD2, CYP2D6, HTR2A, COMT, HSPG2 and SOD2 genes have variants that may increa

96 158Met mouse lines, which carry either human COMT Val or Met alleles via gene targeting.

97 uable for understanding the effects of human COMT Val158Met polymorphism on cortical development and

98 ese mice (1) support the argument that human COMT Val158Met polymorphism modulates behavioral functio

99 hat transgenic mice overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote m

100 mployed transgenic mice expressing the human COMT-Val variant to determine the effects of the high-ac

101 ium of AdoMet was previously shown to impair COMT activity by interfering with methyl donor-acceptor

102 her, we hypothesised that any differences in COMT(-/-) mice would be resolved following treatment wit

103 f variations, such as ethnic differences, in COMT genetic effects on the cortico-cerebellar executive

104 ocol for the BDNF Val/Val vs Met genotype in COMT Met homozygotes only (ANOVA, p = 0.027).

105 Loss of function mutations in COMT reduces syringyl (S) lignin subunits and improves b

106 iated effects of functional polymorphisms in COMT, DRD2 and AKT1 genes on prefrontal-parietal and pre

107 (eg, increased spatial novelty preference in COMT-Met mice vs wild-type mice).

108 ormalize the aberrant metabolomic profile in COMT(-/-) mice; as this treatment moves into clinical tr

109 o rescue the altered remote memory recall in COMT-Val-tg mice and increased PFC dopamine levels.

110 There was an approximately 50% reduction in COMT mRNA, protein, and enzyme activity levels in 22q11.

111 ly specific: COMT-Met mice had reductions in COMT abundance and activity, compared with wild-type mic

112 rences in metabolites (p < 0.05) remained in COMT(-/-) mice.

113 odified through complex genetic variation in COMT.

114 izes, these data indicate that variations in COMT val(158)met may predict the nature of WM improvemen

115 tiple neuropsychiatric risk genes, including COMT, IFNG, MIR200B, SYNGAP1, and VIPR2 showed associati

116 Individual COMT SNPs (val158met, rs737865, and rs165599) modulated

117 variants within the COMT gene that influence COMT biology and confound conclusions based on associati

118 a significant interaction of tDCS intensity, COMT genotype, and WM task.

119 (high COMT compared with low or intermediate COMT genotype activity).

120 synapses, the DA catalytic pathway involving COMT predominates over re-uptake in OB.

121 absent soluble COMT expression and very low COMT activity in two 22q11.2DS individuals.

122 The cellular distribution of MB-COMT in cortical neurons remains unclear and the orienta

123 l that the C-terminal catalytic domain of MB-COMT is in the extracellular space, which suggests that

124 ns remains unclear and the orientation of MB-COMT on the cellular membrane is controversial.

125 Analyses of MB-COMT orientation with computer simulation, flow cytometr

126 extracellular space, which suggests that MB-COMT can inactivate synaptic and extrasynaptic dopamine

127 We measured COMT messenger (m)RNA and protein expression and enzyme

128 lele, DAT1 10-repeat allele, and the Met/Met COMT genotype, and with a greater number of these genoty

129 In the placebo group, Met-COMT subjects outperformed Val-COMT subjects on the 2- b

130 roups: it worsened N-back performance in Met-COMT subjects but enhanced it in Val-COMT subjects.

131 Tolcapone made Met-COMT subjects less risk averse but Val-COMT subjects mor

132 Thirty-four COMT Met(158)Met (Met-COMT) and 33 COMT Val(158)Val (Val-COMT) men were given

133 OO and wine consumption and a high metabolic COMT capacity for methylation are key factors for high H

134 tial of disrupting mitochondrial metabolism (COMT, UFD1L, DGCR8, MRPL40, PRODH, SLC25A1, TXNRD2, T10,

135 ology to the catecholamine methyltransferase COMT that is linked to schizophrenia, cause deafness.

136 he sorghum caffeic acid O-methyltransferase (COMT) and is one of the key enzymes in monolignol biosyn

137 (F5H) and caffeic acid O-methyltransferase (COMT) from Liquidambar styraciflua confirmed the product

138 rphisms in the catechol-O-methyltransferase (COMT) gene affect the relationship.

139 orphism of the catechol-O-methyltransferase (COMT) gene is an important regulator of dopamine in the

140 58)Met) in the catechol-O-methyltransferase (COMT) gene is associated with changes in executive perfo

141 The catechol-O-methyltransferase (COMT) gene is located in the obligatory deletion region,

142 ariants in the catechol-O-methyltransferase (COMT) gene result in a different catabolism of dopamine

143 articular, the catechol-O-methyltransferase (COMT) gene, located on chromosome 22q11.2, regulates cat

144 158Met) in the catechol-O-methyltransferase (COMT) gene, whose protein product degrades synaptically

145 ariants of the catechol-O-methyltransferase (COMT) gene.

146 e (ABCB1), and catechol-o-methyltransferase (COMT) genes are associated with risk for opioid addictio

147 stratified by catechol-O-methyltransferase (COMT) genotype activity (high COMT compared with low or

148 Human catechol O-methyltransferase (COMT) has emerged as a model for understanding enzyme-ca

149 Catechol O-methyltransferase (COMT) inhibitors are an established treatment for end-of

150 Catechol-O-methyltransferase (COMT) is a key enzyme for inactivation and metabolism of

151 phism of human catechol-o-methyltransferase (COMT) is one of the most well-studied single-nucleotide

152 Catechol O-methyltransferase (COMT) is the enzyme responsible for the O-methylation of

153 Catechol-O-methyltransferase (COMT) metabolizes dopamine.

154 Catechol-O-methyltransferase (COMT) modulates dopamine levels in the prefrontal cortex

155 Additionally, catechol-O-methyltransferase (COMT) polymorphism has been reported to be associated wi

156 l and HVAL and catechol-O-methyltransferase (COMT) rs4680 genotypes were measured.After multivariable

157 DA [indexed by catechol-O-methyltransferase (COMT) Val(158)Met genotype and, at a finer scale, COMT e

158 ionally taking catechol-O-methyltransferase (COMT) Val158Met and kidney and brain (KIBRA) rs17070145

159 The catechol-O-methyltransferase (COMT) val158met polymorphism has received attention in s

160 he sorghum caffeic acid O-methyltransferase (COMT) was combined with 35S::SbF5H through cross-pollina

161 c variation in catechol-O-methyltransferase (COMT), a regulatory enzyme that controls dopamine availa

162 expression of catechol-O-methyltransferase (COMT), along with a lower level of DNA methylation, in i

163 Catechol-O-methyltransferase (COMT), an important therapeutic target in the treatment

164 lymorphisms in catechol-O-methyltransferase (COMT), DRD2, and DRD4 were evaluated.

165 , catalyzed by catechol-O-methyltransferase (COMT), is investigated using binding isotope effects (BI

166 nts in a gene, catechol-O-methyltransferase (COMT), regulating catechol neurotransmitter catabolism.

167 For catechol-O-methyltransferase (COMT), the Val(158)Met polymorphism (rs4680) markedly af

168 1 (CNR1), and catechol-o-methyltransferase (COMT), was strongly associated with overall poor perform

169 the mammalian catechol-O-methyltransferase (COMT), which can effect the sequential hydroxylation of

170 it human liver catechol-O-methyltransferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+

171 olymorphism in catechol-O-methyltransferase (COMT).

172 ydroxylase and catechol-O-methyltransferase (COMT).

173 lymorphism for catechol-O-methyltransferase (COMT).

174 (specifically catechol-O-methyltransferase [COMT] polymorphisms) impacts its activation are currentl

175 se [F5H1], caffeic acid O-methyltransferase [COMT], and cinnamyl alcohol dehydrogenase6 [CAD6], two m

176 Compared with wild-type diabetic mice, COMT(-/-) mice had decreased hyperfiltration, decreased

177 transferase from Selaginella moellendorffii, COMT, the coding sequence of which is clustered together

178 ent the first SAM-competitive small-molecule COMT co-complex crystal structure.

179 st in DA terminals, the OB contains 50% more COMT per unit of tissue.

180 Moreover, COMT knockout mice were more impulsive compared with wil

181 allele was introduced into the native mouse COMT gene to produce COMT-Met mice, which were compared

182 spectrometric study of wild type and mutant COMT, comparing temperature dependences of HDX against c

183 8; 95% CI: 1.09-1.48; p = 0.002) but neither COMT genotypes nor the possible interaction between gene

184 New nitrocatechol COMT inhibitors based on naturally occurring caffeic aci

185 um metabolic profiles of pregnant Nos3(-/-), COMT(-/-) and C57BL/6J mice were made using a kit from B

186 pone: performance of wild-type mice, but not COMT-Met mice, was improved on the 5-choice serial react

187 several high-impact genes, including NOTCH4, COMT, CACNA1C and DRD3 which are related to calcium home

188 voltammetry and pharmacological blockade of COMT.

189 the phenotypic and molecular consequences of COMT deficiency under optimal and water stress environme

190 stry behind the discovery and development of COMT inhibitors; (iii) to discuss how the physicochemica

191 current study was to evaluate the effect of COMT hemizygosity and molecular haplotypes on gene expre

192 Our findings confirm a robust effect of COMT hemizygosity on COMT activity and show complex inte

193 working memory predicts that the effects of COMT inhibition will differ according to COMT genotype.

194 These sexually dimorphic effects of COMT on inhibitory brain activation have important impli

195 Moreover, copy number elevations of COMT or Tbx1 reduced the proliferation of adult neural s

196 a significant increase in the expression of COMT was found in dopaminergic neurons of isogenic PARK2

197 The frequencies of COMT rs4680 "A" allele were higher in PD patients with p

198 clic voltammetry, we show that inhibition of COMT increases DA signals approximately 2-fold.

199 ore, a significant (P = 0.04) interaction of COMT diplotype and time-varying stress showed that a pos

200 ymorphism, was associated with low levels of COMT expression and with the presence of psychosis and l

201 th, but it cannot compensate for the loss of COMT activity in monolignol synthesis.

202 of SbF5H did not compensate for the loss of COMT activity.

203 al and molecular consequences due to loss of COMT on root growth and adaptation to water deficit rema

204 ransporter (DAT)-Cre mice, overexpression of COMT, specifically in dopaminergic neurons of the substa

205 rs4680, a single nucleotide polymorphism of COMT, and randomly allocated to either propranolol 60 mg

206 when examining the therapeutic potential of COMT inhibitors.

207 : (i) to summarize the physiological role of COMT inhibitors in central and peripheral nervous system

208 Association studies of COMT and working memory in healthy volunteers have yield

209 These findings suggest that upregulation of COMT, likely resulting from DNA hypomethylation, in dopa

210 between various Val-containing haplotypes on COMT-3' untranslated region extended mRNA, soluble COMT

211 firm a robust effect of COMT hemizygosity on COMT activity and show complex interactions of variants

212 estigate the potential effects of smoking on COMT-mediated electrophysiological activity.

213 om inattention by overexpression of OPRD1 or COMT, respectively, as well as a distinct cluster of epi

214 No sex- or COMT-dependent differences were present in the basic acq

215 itive performance in males, and particularly COMT knockout males, but not in females.

216 a single 200-mg dose of the brain-penetrant COMT inhibitor tolcapone or placebo in a randomized, dou

217 It is possible COMT is not meaningfully associated with working memory

218 compounds represent a novel series of potent COMT inhibitors that might be further optimized to new d

219 d into the native mouse COMT gene to produce COMT-Met mice, which were compared with their wild-type

220 We demonstrate interactions of the proteins COMT and SAHH with SAH-CC with biotin used in conjunctio

221 the physicochemical properties of recognized COMT inhibitors are understood to exert influence over t

222 for the COMT rs4680 Met allele that reduces COMT enzyme activity showed a relatively more efficient

223 llele to assess the hypothesis that reducing COMT enzymatic activity interacts with genotype to incre

224 mechanistic information, regiocomplementary COMT variants were engineered that deliver either meta-

225 doMet are accepted by the regiocomplementary COMT mutants and can be used to prepare alkylated catech

226 e the clinical benefits of the most relevant COMT inhibitors.

227 .69; confidence interval: 1.12-2.55), rs4680 COMT (odds ratio (OR): 1.40; confidence interval: 1.04-1

228 perenne) and dicot alfalfa (Medicago sativa) COMTs.

229 Val(158)Met genotype and, at a finer scale, COMT enzyme activity].

230 (5CSRTT) to investigate the effects of sex, COMT genotype, and their interactions with environmental

231 d the recall of remote memories as silencing COMT Val overexpression starting from 30 days after the

232 t model based on five of the candidate SNPs (COMT, NTRK1, ErbB4, CLU, and HFE) explained approximatel

233 " mutation is associated with absent soluble COMT expression and very low COMT activity in two 22q11.

234 ' untranslated region extended mRNA, soluble COMT and membrane-bound proteins, and enzyme activity.

235 he development of improved and more specific COMT inhibitors.

236 The model proved highly specific: COMT-Met mice had reductions in COMT abundance and activ

237 ally, we examined how the frequently studied COMT Val(158)Met polymorphism interacted with an environ

238 These results demonstrate that COMT genetic variations modulate the retrieval of remote

239 ared with striatum, supporting the idea that COMT enzymatic breakdown, rather than DAT recycling, is

240 e robust; however, despite observations that COMT is estrogenically catabolized, sex differences in i

241 king memory in healthy young adults, or that COMT effects are detectable only in assessments reflecti

242 e Val(158)Met polymorphism, and suggest that COMT's effects are most prominent when the dopamine syst

243 The COMT 158A>G AG/GG genotype was associated with shortened

244 The COMT c.472 A alleles associated with decreased syncope i

245 The COMT inhibitor, tolcapone, increased the DA signal appro

246 The COMT rs4680 A allele was positively associated with lung

247 The COMT Val(158)Met polymorphism influences its activity, a

248 The COMT Val158Met polymorphism modulates cortical dopaminer

249 Cortical synaptic dopamine monitored by the COMT Val158Met polymorphism influenced prefrontal contro

250 erved in schizophrenia are influenced by the COMT val158met polymorphism.

251 ad lower E2 levels, while those carrying the COMT Val/Val alleles had higher E2 levels compared to Me

252 ory paradigm, individuals homozygous for the COMT rs4680 Met allele that reduces COMT enzyme activity

253 Average valence force constants for the COMT TS show significant differences from early BEBOVIB

254 A polymorphism in the COMT gene (rs4680), associated with prefrontal dopaminer

255 unction was indexed by a polymorphism in the COMT gene, differences of which reflect dopamine levels

256 otype at the Val(158)Met polymorphism in the COMT gene.

257 ingle-nucleotide polymorphisms (SNPs) in the COMT, NTRK1, BDNF, ErbB4, CLU, and HFE genes, and invest

258 ingle-nucleotide polymorphisms (SNPs) of the COMT gene and their haplotypes moderate the association

259 ne whether variants in the rs4680 SNP of the COMT gene are associated with post-burn pruritus and sca

260 ferences emerged after administration of the COMT inhibitor tolcapone: performance of wild-type mice,

261 nts, indicating that the introduction of the COMT overcame the inefficiency of the native pine methyl

262 was associated with hypermethylation of the COMT promoter at a conserved CpG site in exon II.

263 Research on the COMT gene continues to yield interesting findings, inclu

264 CONCLUSIONS/SIGNIFICANCE: The COMT Val158Met polymorphism may be a genetic biomarker f

265 Finally, we demonstrate that the COMT rs74745580 "T" mutation is associated with absent s

266 ved locus of control (LOC), here we used the COMT inhibitor tolcapone in a randomized, double-blind,

267 We assessed whether the COMT Val158Met polymorphism was a novel marker in health

268 hronic pain suffering, TMD patients with the COMT (158)Met substitution had higher pain sensitivity a

269 complex interactions of variants within the COMT gene that influence COMT biology and confound concl

270 and female wild-type mice ((+/+)) and their COMT knockout littermates ((+/-) and (-/-)) in the five-

271 of COMT inhibition will differ according to COMT genotype.

272 ructure-activity relationships in binding to COMT and the novel off-target HIBCH.

273 this protein is not bound by the less toxic COMT inhibitor entacapone.

274 s of disease, catechol-O-methyl transferase (COMT(-/-)) and endothelial nitric oxide synthase (Nos3(-

275 en two genes--catechol-O-methyl transferase (COMT) and dysbindin (dys; dystrobrevin-binding protein 1

276 ne clearance--catechol-O-methyl transferase (COMT) and two isoforms of monoamine oxidase--modulated d

277 inhibitors of catechol-O-methyl transferase (COMT) for the treatment of Parkinson's disease.

278 E (APOE) and Catechol-O-methyl transferase (COMT) genotypes on estradiol (E2) levels in men (p=0.003

279 ain penetrant catechol-O-methyl transferase (COMT) inhibitor tolcapone [4, 5], we investigated the ca

280 Catecholamine-0-methyl-transferase (COMT) gene variation effects on prefrontal blood oxygena

281 elevations of catechol-O-methyl-transferase (COMT) or Tbx1, two genes encoded in the two small 22q11.

282 catalysis by catechol-O-methyl-transferase (COMT) predominates over DAT re-uptake.

283 We studied catechol-O-methyl-transferase (COMT)(-/-) mice, which have increased renal dopamine pro

284 alytic enzyme catechol-O-methyl-transferase (COMT), but negligible expression of the dopamine transpo

285 Tyrosinase-COMT are shown to provide highly versatile and regiosele

286 ut those with the Met/Met versus the Val/Val COMT genotype showed less middle temporal gyrus activati

287 e Met-COMT subjects less risk averse but Val-COMT subjects more so.

288 in Met-COMT subjects but enhanced it in Val-COMT subjects.

289 bo group, Met-COMT subjects outperformed Val-COMT subjects on the 2- back, and they were more risk av

290 )Met (Met-COMT) and 33 COMT Val(158)Val (Val-COMT) men were given a single 200-mg dose of the brain-p

291 ee well-studied functional genetic variants (COMT Val158Met, BDNF Val66Met, 5-HTTLPR) associated with

292 We found that dopaminergic augmentation via COMT inhibition increased egalitarian tendencies in part

293 is altered in children with ADHD and whether COMT polymorphism is associated with the altered network

294 We found that this was also the case with COMT, but not for other dopaminergic genes.

295 scalation was limited to incident cases with COMT diplotypes coding for low-activity COMT, signifying

296 gyl lignin in TEs, but cotransformation with COMT improved its formation.

297 6 confirmed that the major interactions with COMT were established via the nitrocatechol ring, allowi

298 d to determine whether the effects seen with COMT deficiency were kidney-specific.

299 nfidence limits (95% CLs) of efficacy within COMT genotypes assuming an additive genetic model.

300 task relevant genetic factors (e.g., for WM: COMT val(158)met, DAT, BDNF val(66)met).

301 al plasticity, we found a significant BDNF x COMT interaction, showing higher plasticity immediately