2.1.1.6: catechol O-methyltransferase
This is an abbreviated version!
For detailed information about catechol O-methyltransferase, go to the full flat file.
Word Map on EC 2.1.1.6
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2.1.1.6
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dopamine
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val158met
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catechols
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parkinson
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monoamine
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dopaminergic
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schizophrenia
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prefrontal
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levodopa
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estrogen
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val
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o-methylation
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psychiatric
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norepinephrine
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entacapone
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l-dopa
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tolcapone
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serotonin
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noradrenaline
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dyskinesia
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neurotransmitter
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striatal
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psycho
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dopac
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carbidopa
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verbal
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3,4-dihydroxyphenylacetic
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extraneuronal
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5-httlpr
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low-activity
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parkinsonian
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homovanillic
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normetanephrine
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benserazide
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antiparkinsonian
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synthesis
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endophenotype
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dsm-iv
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3h-noradrenaline
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2-methoxyestradiol
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analysis
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tropolone
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updrs
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slc6a4
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dihydroxyphenylacetic
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amantadine
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pargyline
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oxidase-b
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phenylethanolamine-n-methyltransferase
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metanephrine
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selegiline
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medicine
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antisocial
- 2.1.1.6
- dopamine
-
val158met
- catechols
- parkinson
-
monoamine
-
dopaminergic
-
schizophrenia
-
prefrontal
- levodopa
- estrogen
- val
-
o-methylation
-
psychiatric
- norepinephrine
- entacapone
- l-dopa
- tolcapone
- serotonin
- noradrenaline
- dyskinesia
-
neurotransmitter
- striatal
-
psycho
-
dopac
- carbidopa
-
verbal
-
3,4-dihydroxyphenylacetic
-
extraneuronal
-
5-httlpr
-
low-activity
-
parkinsonian
-
homovanillic
- normetanephrine
- benserazide
-
antiparkinsonian
- synthesis
-
endophenotype
-
dsm-iv
-
3h-noradrenaline
- 2-methoxyestradiol
- analysis
- tropolone
-
updrs
-
slc6a4
-
dihydroxyphenylacetic
- amantadine
- pargyline
-
oxidase-b
-
phenylethanolamine-n-methyltransferase
- metanephrine
- selegiline
- medicine
-
antisocial
Reaction
Synonyms
catechol methyltransferase, catechol-O-methyl transferase, catechol-O-methyl transferase, membrane bound, catechol-O-methyl transferase, soluble, catechol-O-methyltransferase, catechol-O-transferase, catecholamine O-methyltransferase, COMT, COMT I, COMT II, COMT-mb, COMT-s, COMT1, COMT2, CTOMT1, L-COMT, MB-COMT, methyltransferase, catechol, S-COMT, SCOMT
ECTree
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Source Tissue
Source Tissue on EC 2.1.1.6 - catechol O-methyltransferase
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membrane-bound COMT activities in the cerebral cortex are significantly reduced in high-salt loaded Dahl salt-sensitive rats compared with normal-salt loaded Dahl salt-sensitive rats
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leukocyte exposure to morphine down-regulates catechol-O-methyl transferase and CYP2D6 by approximately 50% compared with control values. Exposure of white blood cells to 0.001 mM S-nitroso-N-acetyl-DL-penicillamine, a nitric oxide donor, reduces the expression of CYP2D6 and COMT. Prior naloxone (0.001 mM) or N-nitro-L-arginine methyl ester (0.1 mM) addition abrogates down-regulating activity of morphine, demonstrating morphine is initiating its actions via stimulating constitutive NO synthase derived NO release via the mu3 opiate receptor splice variant
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Val158Met polymorphism within COMT and PvuII polymorphism within ESR1, alone or together with physical activity may, at least partly, modulate muscle mass and performance phenotypes in older women. COMT Val158Met polymorphism is associated with muscle mass in that subjects with the LL genotype have significantly larger muscles than heterozygotes. Furthermore, within are observed than within other sedentary subjects or subjects with more active life-style
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COMT is not located in dopaminergic nigrostriatal projection neurons
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additional information
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postmortem dorsolateral prefrontal cortex tissue predominantly expresses the membrane-bound isoform. Females have lower COMT activity than males
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catechol-O-methyltransferase Val158Met modulation of prefrontal-parietal-striatal brain systems during arithmetic and temporal transformations in working memory
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COMT Val158Met polymorphism is related to structural brain differences in healthy adults. Val158 allele homozygotes exhibit significantly smaller temporal lobe and hippocampal volumes, with a trend for smaller amygdala volumes
genetic variations of COMT can contribute to brain morphological abnormalities described in early phases of schizophrenia. Low-activity allele of catechol-O-methyltransferase is associated with increased lateral ventricles in patients with first episode non-affective psychosis
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significant contribution of COMT in modulating the dynamics of dopamine overflow in the prefrontal cortex. Evoked dopamine overflow shows that removal of dopamine is twofold slower in the prefrontal cortex of mice lacking COMT than in wild-type mice, indicating that half of the dopamine decline in this brain region results from COMT-mediated enzymatic degradation. Lack of COMT does not influence dopamine overflow/decline in the dorsal striatum
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highest activity in hippocampus. In all brain areas membrane-bound enzyme activity is lower than soluble enzyme activity
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membrane-bound COMT activities in the cerebral cortex are significantly reduced in high-salt loaded Dahl salt-sensitive rats compared with normal-salt loaded Dahl salt-sensitive rats
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paranigral lipopolysaccharide infusion to rats results in intense microglial activation around the lesion area followed by a delayed injury in nigrostriatal pathway in 2 weeks. Simultaneously, catechol-O-methyltransferase activity in the substantia nigra is gradually increased up to 213%. Soluble COMT and membrane bound COMT proteins are increased by 255% and 86%, respectively. Increased catechol-O-methyltransferase immunoreactivity is located primarily into the activated microglial cells in the lesion area
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COMT is not present in presynaptic dopaminergic and noradrenergic neurons
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norepinephrine stimulates alpha2-adrenoceptor of the cells to increase the MB-COMT activity, but not the level of MB-COMT mRNA transcription
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high-salt loading significantly suppresses the activities of membrane-bound COMT and increases the urinary norepinephrine level in Dahl salt-sensitive rats
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441507, 441508, 441511, 441512, 441523, 441527, 441538, 657883, 658268, 658520, 658525, 686075, 703190, 705398, 734846
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441507, 441508, 441509, 441511, 441514, 441515, 441516, 441517, 441520, 441521, 441522, 441527, 441531, 441533, 441537, 441541, 441543, 658520, 658656, 687048, 719299, 720182, 733709
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S-COMT isoforms are highly expressed in liver, liver displays a very weak expression of L-COMT isoforms
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levels of staining for the COMT protein in myometrium are highest on day 1 and lowest on days 8 and 13, but high levels returned by days 16 and 19 of pregnancy. Modulation of COMT activity may play a role in the regulation of myometrial contractility and cervical ripening during pregnancy
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modulation of COMT activity may play a role in the regulation of myometrial contractility and cervical ripening during pregnancy
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isoform COMT2 is not expressed in the central nervous system
additional information
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sexual dimorphism and activity of the two COMT isoforms seems to be tissue specific and more prominent in peripheral tissues than in the brain
additional information
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both of the L-COMT isoforms are found in all of the tissues examined except the heart, which expresses only the most acidic form, and the kidney, which expresses only the most basic form