EC Number   |
General Information |
Reference |
|---|
   2.1.1.6 | malfunction |
knockdown of COMT expression in endometrial glandular cells results in increased estrogenic milieu and increased estrogen-induced cell proliferation, and increases the propensity of estrogen or catecholestrogens to induce reactive oxygen species, microsatellite instability, and neoplastic transformation of endometrial glandular cells |
704065 |
| 2.1.1.6 | malfunction |
lack of S-COMT does not affect the levels of L-DOPA in plasma or peripheral tissues, whereas in the full COMT-knock-out mice, these levels are increased. The total COMT activity in the S-COMT-deficient mice is 22-47% of that in the wild type mice. In S-COMT-deficient mice, MB-COMT in the liver and the duodenum is able to O-methylate about one-half of exogenous L-Dopa |
702948 |
| 2.1.1.6 | metabolism |
concerted action of cytosolic sulfotransferase SULT1A3 and COMT in dopamine metabolism |
705926 |
| 2.1.1.6 | physiological function |
catechol-O-methyltransferase COMT2 is essential for auditory function |
706484 |
| 2.1.1.6 | physiological function |
COMT gene expression plays a critical role in modulating the hormonal and carcinogenic effects of estrogen and catecholestrogens and, consequently, modifies the risk for estrogen-induced endometrial cancer |
704065 |
| 2.1.1.6 | physiological function |
COMT over expression stabilizes microtubules, ameliorates 17beta-estradiol-induced proliferation, inhibits estrogen receptor alpha and progesterone receptor signaling, and reduces hypoxia-inducible factor-1alpha and tissue necrosis factor-alpha-induced aromatase (CYP19) expression in human uterine leiomyoma cells |
706440 |
| 2.1.1.6 | physiological function |
exposure to catechol enhances hemin-induced hemoglobin accumulation and induces mRNA expression of erythroid-specific genes in K-562 cells. Treatment with catechol causes a time- and concentration-dependent increase in guaiacol concentration in the medium of cultured K-562 cells. Knock down of COMT expression significantly reduces the production of guaiacol, and the sensitivity of K562 cells to cytotoxicity of catechol significantly increases. Knockdown of COMT expression also eliminates catechol-enhanced erythroid differentiation of K-562 cells. The pretreatment with S-adenosyl-L-methionine or S-adenosyl-L-homocysteine induces a significant increase in hemin-induced hemoglobin synthesis in K-562 cells and the mRNA expression of erythroid specific genes |
735306 |
| 2.1.1.6 | physiological function |
inhibition of catechol O-methyltransferase by inhibitor tropolone results in a decrease of the total amount of sulfated metabolites of dopamine, epinephrine, isoproterenol, and isoetharine. The sequential methylation and sulfation of dopamine, epinephrine, isoproterenol, and isoetharine is mediated by, respectively, the COMT and the cytosolic sulfotransferase SULT1A3 |
733309 |
| 2.1.1.6 | physiological function |
knockdown of isoform CTOMT1 results in significantly reduced fruit guaiacol emissions. CTOMT1 overexpression results in slightly increased fruit guaiacol emission. Upon supply with exogenously applied catechol, guaiacol production increases in both wild-type and transgenic fruit discs, although to a much greater extent in CTOMT1 overexpressing discs |
734911 |
