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Gene Review

Comt  -  catechol-O-methyltransferase

Mus musculus

Synonyms: Catechol O-methyltransferase, Comt1, D16Wsu103e, D330014B15Rik
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Disease relevance of Comt


Psychiatry related information on Comt

  • Our results provide conclusive evidence for an important sex- and region-specific contribution of COMT in the maintenance of steady-state levels of catecholamines in the brain and suggest a role for COMT in some aspects of emotional and social behavior in mice [6].
  • Catechol-O-methyltransferase (COMT) is one of the major mammalian enzymes involved in the metabolic degradation of catecholamines and is considered a candidate for several psychiatric disorders and symptoms, including the psychopathology associated with the 22q11 microdeletion syndrome [6].
  • METHODS: We measured the effects of d-amphetamine on locomotor activity and on the levels of catecholamines and their metabolites in striatal microdialysis fluid and in striatal, hypothalamic and cortical brain regions of COMT gene disrupted mice [7].

High impact information on Comt

  • By means of homologous recombination in embryonic stem cells, a strain of mice in which the gene encoding the COMT enzyme has been disrupted was produced [6].
  • The conserved linkage between human chromosome 22 and mouse chromosome 16 includes two closely linked loci, Comt and IgI-1 [8].
  • Monoamine oxidase, catechol-O-methyltransferase, and norepinephrine levels in mice with the hereditary obese-hyperglycemic syndrome [9].
  • Inherited differences of brain and erythrocyte soluble catechol-o-methyltransferase activity in two mouse strains [10].
  • The significantly lower COMT activity in the hamster liver and red blood cells suggests that under chronic estrogen treatment at high doses, the concentration of catechol estrogens in these tissues may exceed the capacity of COMT to effectively catalyse their O-methylation into inactive metabolites [11].

Chemical compound and disease context of Comt


Biological context of Comt


Anatomical context of Comt


Associations of Comt with chemical compounds


Other interactions of Comt


Analytical, diagnostic and therapeutic context of Comt


  1. Brain catecholamine metabolism in catechol-O-methyltransferase (COMT)-deficient mice. Huotari, M., Gogos, J.A., Karayiorgou, M., Koponen, O., Forsberg, M., Raasmaja, A., Hyttinen, J., Männistö, P.T. Eur. J. Neurosci. (2002) [Pubmed]
  2. Metabolism of biogenic amines in neuroblastoma and glioma cells in culture. Skaper, S.D., Adelson, G.L., Seegmiller, J.E. J. Neurochem. (1976) [Pubmed]
  3. Dopamine transporter and catechol-O-methyltransferase activities are required for the toxicity of 1-(3',4'-dihydroxybenzyl)-1,2,3, 4-tetrahydroisoquinoline. Kawai, H., Kotake, Y., Ohta, S. Chem. Res. Toxicol. (2000) [Pubmed]
  4. Lack of increased oxidative stress in catechol-O-methyltransferase (COMT)-deficient mice. Forsberg, M.M., Juvonen, R.O., Helisalmi, P., Leppänen, J., Gogos, J.A., Karayiorgou, M., Männistö, P.T. Naunyn Schmiedebergs Arch. Pharmacol. (2004) [Pubmed]
  5. Production, circulation, and excretion of melanin-related metabolites in B16 melanoma-bearing mice. Wakamatsu, K., Ito, S., Fujita, K. Acta Derm. Venereol. (1990) [Pubmed]
  6. Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior. Gogos, J.A., Morgan, M., Luine, V., Santha, M., Ogawa, S., Pfaff, D., Karayiorgou, M. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  7. D-amphetamine responses in catechol-O-methyltransferase (COMT) disrupted mice. Huotari, M., García-Horsman, J.A., Karayiorgou, M., Gogos, J.A., Männistö, P.T. Psychopharmacology (Berl.) (2004) [Pubmed]
  8. Comparative mapping of 9 human chromosome 22q loci in the laboratory mouse. Bućan, M., Gatalica, B., Nolan, P., Chung, A., Leroux, A., Grossman, M.H., Nadeau, J.H., Emanuel, B.S., Budarf, M. Hum. Mol. Genet. (1993) [Pubmed]
  9. Monoamine oxidase, catechol-O-methyltransferase, and norepinephrine levels in mice with the hereditary obese-hyperglycemic syndrome. Feldman, J.M., Henderson, J.H. Diabetes (1978) [Pubmed]
  10. Inherited differences of brain and erythrocyte soluble catechol-o-methyltransferase activity in two mouse strains. Gershon, E.S., Jonas, W.Z. Biol. Psychiatry (1976) [Pubmed]
  11. Variations in catechol O-methyltransferase activity in rodent tissues: possible role in estrogen carcinogenicity. Li, S.A., Purdy, R.H., Li, J.J. Carcinogenesis (1989) [Pubmed]
  12. Favorable effect of catechol-O-methyltransferase inhibition by OR-462 in experimental models of Parkinson's disease. Lindén, I.B., Nissinen, E., Etemadzadeh, E., Kaakkola, S., Männistö, P., Pohto, P. J. Pharmacol. Exp. Ther. (1988) [Pubmed]
  13. Entacapone, a novel catechol-O-methyltransferase inhibitor for Parkinson's disease, does not impair mitochondrial energy production. Nissinen, E., Kaheinen, P., Penttilä, K.E., Kaivola, J., Lindén, I.B. Eur. J. Pharmacol. (1997) [Pubmed]
  14. Catechol-O-methyltransferase decreases levodopa toxicity in vitro. Offen, D., Panet, H., Galili-Mosberg, R., Melamed, E. Clinical neuropharmacology. (2001) [Pubmed]
  15. cDNA cloning, expression and chromosomal localization of the mouse mitochondrial thioredoxin reductase gene(1). Miranda-Vizuete, A., Damdimopoulos, A.E., Spyrou, G. Biochim. Biophys. Acta (1999) [Pubmed]
  16. Reduced natriuretic response to acute sodium loading in COMT gene deleted mice. Odlind, C., Reenilä, I., Männistö, P.T., Juvonen, R., Uhlén, S., Gogos, J.A., Karayiorgou, M., Hansell, P. BMC Physiol. (2002) [Pubmed]
  17. Effects of norlaudanosolinecarboxylic acids on enzymes of catecholamine metabolism. Coscia, C.J., Burke, W.J., Galloway, M.P., Kosloff, A.H., Lasala, J.M., McFarlane, J., Mitchell, J.S., O'Toole, M.M., Roth, B.L. J. Pharmacol. Exp. Ther. (1980) [Pubmed]
  18. Tissue histopathology, clinical chemistry and behaviour of adult Comt-gene-disrupted mice. Haasio, K., Huotari, M., Nissinen, E., Männistö, P.T. Journal of applied toxicology : JAT. (2003) [Pubmed]
  19. Effect of dopamine uptake inhibition on brain catecholamine levels and locomotion in catechol-O-methyltransferase-disrupted mice. Huotari, M., Santha, M., Lucas, L.R., Karayiorgou, M., Gogos, J.A., Männistö, P.T. J. Pharmacol. Exp. Ther. (2002) [Pubmed]
  20. Effects of butylated hydroxyanisole on glutathione S-transferase and catechol O-methyltransferase activities in Syrian golden hamsters. Lam, L.K. Biochem. Pharmacol. (1988) [Pubmed]
  21. Assignment of the catechol-O-methyltransferase gene to human chromosome 22 in somatic cell hybrids. Brahe, C., Bannetta, P., Meera Khan, P., Arwert, F., Serra, A. Hum. Genet. (1986) [Pubmed]
  22. Release and elimination of dopamine in vivo in mice lacking the dopamine transporter: functional consequences. Benoit-Marand, M., Jaber, M., Gonon, F. Eur. J. Neurosci. (2000) [Pubmed]
  23. Neurochemical changes in murine trisomy 16: delay in cholinergic and catecholaminergic systems. Ozand, P.T., Hawkins, R.L., Collins, R.M., Reed, W.D., Baab, P.J., Oster-Granite, M.L. J. Neurochem. (1984) [Pubmed]
  24. Decreased transmethylation of biogenic amines after in vivo elevation of brain S-adenosyl-l-homocysteine. Schatz, R.A., Wilens, T.E., Sellinger, O.Z. J. Neurochem. (1981) [Pubmed]
  25. Curcumin modulates drug metabolizing enzymes in the female Swiss Webster mouse. Valentine, S.P., Le Nedelec, M.J., Menzies, A.R., Scandlyn, M.J., Goodin, M.G., Rosengren, R.J. Life Sci. (2006) [Pubmed]
  26. Synthesis, biological evaluation, and molecular modeling studies of a novel, peripherally selective inhibitor of catechol-O-methyltransferase. Learmonth, D.A., Palma, P.N., Vieira-Coelho, M.A., Soares-da-Silva, P. J. Med. Chem. (2004) [Pubmed]
  27. Epigallocatechin gallate modulates CYP450 isoforms in the female Swiss-Webster mouse. Goodin, M.G., Rosengren, R.J. Toxicol. Sci. (2003) [Pubmed]
  28. Biogenic amine metabolism in Biomphalaria glabrata I. Catechol-O-methyltransferase activity. Guchhait, R.B., Bourgeois, J.G., Bueding, E. Int. J. Neurosci. (1980) [Pubmed]
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