PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
6136632-7	1983	The evidence for catecholestrogen action upon COMT, an outside membrane enzyme involved in the process of catecholamine degradation, supports the idea of a catechol action for 2-OHE2.	2-hydroxyestradiol	176-182	catechol-O-methyltransferase	Rattus norvegicus	46-50	
12771046-7	2003	In the kidney, the catechol-O-methyltransferase inhibitor quercetin and norepinephrine (10 micromol/L) reduced methylation of 2-hydroxyestradiol by approximately 90% and 41%, respectively.	2-hydroxyestradiol	126-144	catechol-O-methyltransferase	Rattus norvegicus	19-47	
12771046-9	2003	Our results indicate that a robust 2-hydroxyestradiol methylation pathway exists in the kidney and heart, but not in the mesentery, and that this pathway is mediated by catechol-O-methyltransferase.	2-hydroxyestradiol	35-53	catechol-O-methyltransferase	Rattus norvegicus	169-197	
11967239-1	2002	Methylation of 2-hydroxyestradiol to 2-methoxyestradiol by catechol-O-methyl transferase (COMT) mediates the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells.	2-hydroxyestradiol	15-33	catechol-O-methyltransferase	Rattus norvegicus	59-88	
11967239-1	2002	Methylation of 2-hydroxyestradiol to 2-methoxyestradiol by catechol-O-methyl transferase (COMT) mediates the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells.	2-hydroxyestradiol	15-33	catechol-O-methyltransferase	Rattus norvegicus	90-94	
11967239-1	2002	Methylation of 2-hydroxyestradiol to 2-methoxyestradiol by catechol-O-methyl transferase (COMT) mediates the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells.	2-hydroxyestradiol	134-152	catechol-O-methyltransferase	Rattus norvegicus	59-88	
11967239-1	2002	Methylation of 2-hydroxyestradiol to 2-methoxyestradiol by catechol-O-methyl transferase (COMT) mediates the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells.	2-hydroxyestradiol	134-152	catechol-O-methyltransferase	Rattus norvegicus	90-94	
11967239-3	2002	Because catecholamines are substrates for COMT, which is expressed in GMCs, we hypothesize that catecholamines may abrogate the antimitogenic effects of 2-hydroxyestradiol on GMCs by competing for COMT and inhibiting 2-methoxyestradiol formation.	2-hydroxyestradiol	153-171	catechol-O-methyltransferase	Rattus norvegicus	42-46	
11967239-3	2002	Because catecholamines are substrates for COMT, which is expressed in GMCs, we hypothesize that catecholamines may abrogate the antimitogenic effects of 2-hydroxyestradiol on GMCs by competing for COMT and inhibiting 2-methoxyestradiol formation.	2-hydroxyestradiol	153-171	catechol-O-methyltransferase	Rattus norvegicus	197-201	
11967239-12	2002	Moreover, catecholamines may abrogate the renoprotective effects of 2-hydroxyestradiol in the glomeruli by inhibiting COMT and 2-methoxyestradiol formation.	2-hydroxyestradiol	68-86	catechol-O-methyltransferase	Rattus norvegicus	118-122	
3343893-9	1988	Finally, administration of HE caused non-significant changes in NE and E contents and in MAO, COMT and PNMT activities.	2-hydroxyestradiol	27-29	catechol-O-methyltransferase	Rattus norvegicus	94-98	
6252315-1	1980	Incubations of 2-hydroxyestradiol (I), 2-hydroxyestradiol 17 beta-sulfate (II), and 2-hydroxyestradiol 17 beta-glucuronide (III) with purified rat liver catechol O-methyltransferase were carried out at pH 7.2 in the presence of Mg2+ and (3H-Me)-S-adenosyl-L-methionine.	2-hydroxyestradiol	15-33	catechol-O-methyltransferase	Rattus norvegicus	153-181	
6127206-4	1982	In addition, 2-OHE2-17 alpha was shown to inhibit purified rat adrenal tyrosine hydroxylase with a potency comparable to that of 2-OHE2-17 beta, a finding similar to that reported by others with respect to catechol-o-methyltransferase.	2-hydroxyestradiol	13-19	catechol-O-methyltransferase	Rattus norvegicus	206-234	
17699737-6	2007	O-methylation of 2-hydroxyestradiol was up to 4-fold higher in oviductal protein extracts from cyclic rats than from pregnant rats and was blocked by OR486, which is a selective inhibitor of COMT.	2-hydroxyestradiol	17-35	catechol-O-methyltransferase	Rattus norvegicus	191-195