PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 2547112-7 1989 The reduction in the number of HeLa cells with abnormal metaphase configurations after exposure to 2-OHE2 plus quinalizarin (an inhibitor of catechol-O-methyltransferase) indicated that the production of 2-MeOE2 is necessary for the formation of abnormal spindles in metaphase. 2-hydroxyestradiol 99-105 catechol-O-methyltransferase Homo sapiens 141-169 2542691-5 1989 Sucrose density gradient centrifugation revealed that both 2- and 4-hydroxyestradiol inhibited the binding of estradiol-17 beta to both the 4S and 8S isoforms of the estrogen receptor in a competitive manner, with a Ki = 0.94 nM for 2-hydroxyestradiol and a Ki = 0.48 nM for 4-hydroxyestradiol. 2-hydroxyestradiol 233-251 estrogen receptor 1 Homo sapiens 166-183 2847784-4 1988 Glutathione promoted the loss of 3H from C-4 of either estradiol or 2-hydroxyestradiol but had less effect on this reaction at C-1 and inhibited it at C-6,7. 2-hydroxyestradiol 68-86 complement C4A Rattus norvegicus 41-44 2848987-3 1988 In contrast, Zn2+ inhibited the interaction of 2-hydroxyestradiol with microsomal protein as measured by the release of 3H from C-4 of the labeled steroids but did not influence 2-hydroxylation, except at high concentration. 2-hydroxyestradiol 47-65 complement C4A Rattus norvegicus 128-131 2847784-9 1988 Evidence is also provided for the further hydroxylation of 2-hydroxyestradiol at C-6 (or C-7). 2-hydroxyestradiol 59-77 complement C6 Rattus norvegicus 81-84 2847784-9 1988 Evidence is also provided for the further hydroxylation of 2-hydroxyestradiol at C-6 (or C-7). 2-hydroxyestradiol 59-77 complement C7 Rattus norvegicus 89-92 3032588-12 1987 Studies using the catechol-O-methyltransferase inhibitor, U-0521, and the O-methyl derivative of EPI, metanephrine, suggested that catechol-O-methyltransferase present in GC dramatically reduces the potency of EPI, but is not involved in the synergism between EPI and 2-OH-E2. 2-hydroxyestradiol 268-275 catechol-O-methyltransferase Homo sapiens 131-159 2836172-7 1988 Incubation of cultured porcine GC with 2-OH-E2 caused a time- and dose-dependent increase in the number of specific [125I]iodo-CYP-binding sites. 2-hydroxyestradiol 39-46 peptidylprolyl isomerase G Homo sapiens 127-130 2836172-8 1988 Averaged over eight separate experiments, 4-day treatment with 4 micrograms/ml 2-OH-E2 increased the number of [125I]iodo-CYP-binding sites 3.1 +/- 0.9-fold above the control value (P less than 0.05). 2-hydroxyestradiol 79-86 peptidylprolyl isomerase G Homo sapiens 122-125 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 phenylethanolamine-N-methyltransferase Rattus norvegicus 103-107 2847784-3 1988 The further metabolism of 2-hydroxyestradiol involves activation of the steroid at C-4 and, to a much lesser extent at C-1, by a cytochrome P-450 mediated reaction as indicated by the effects of NADPH, spermine, SKF-525A, and CO in the microsomal system. 2-hydroxyestradiol 26-44 complement C4A Rattus norvegicus 83-86 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 monoamine oxidase A Rattus norvegicus 89-92 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 2820746-1 1987 Chronic administration of the catecholestrogens 2-OH-estrone (2-OH1) and 2-OH-estradiol (2-OHE2), of tamoxifen and its metabolites and of high concentrations of estradiol have been previously shown to inhibit the growth of the estrogen/progesterone receptor-positive transplantable prolactin (PRL)-secreting rat pituitary tumor 7315a. 2-hydroxyestradiol 73-87 prolactin Rattus norvegicus 293-296 2820746-1 1987 Chronic administration of the catecholestrogens 2-OH-estrone (2-OH1) and 2-OH-estradiol (2-OHE2), of tamoxifen and its metabolites and of high concentrations of estradiol have been previously shown to inhibit the growth of the estrogen/progesterone receptor-positive transplantable prolactin (PRL)-secreting rat pituitary tumor 7315a. 2-hydroxyestradiol 89-95 prolactin Rattus norvegicus 293-296 2820746-5 1987 Both 2-OHE2 (100 nM and 1 microM) and 2-OHE2 (1 microM) inhibited PRL release by FCS-cultured tumor cells. 2-hydroxyestradiol 5-11 prolactin Rattus norvegicus 66-69 2820746-5 1987 Both 2-OHE2 (100 nM and 1 microM) and 2-OHE2 (1 microM) inhibited PRL release by FCS-cultured tumor cells. 2-hydroxyestradiol 38-44 prolactin Rattus norvegicus 66-69 2820746-6 1987 In FCSABS-cultured tumor cells, 0.1-10 nM 2-OHE1 and 1 microM 2-OHE2 inhibited PRL release, but 1-100 nM 2-OHE2 stimulated PRL release. 2-hydroxyestradiol 62-68 prolactin Rattus norvegicus 79-82 2820746-6 1987 In FCSABS-cultured tumor cells, 0.1-10 nM 2-OHE1 and 1 microM 2-OHE2 inhibited PRL release, but 1-100 nM 2-OHE2 stimulated PRL release. 2-hydroxyestradiol 105-111 prolactin Rattus norvegicus 123-126 2884573-2 1987 Both catechol oestrogens, 2-hydroxyoestradiol (2OHE2) and 2-hydroxyoesterone (2OHE1), inhibited TH activity in mesenteric artery and vas deferens in a concentration-dependent manner with potencies that were higher than those for noradrenaline but lower than that for dopamine. 2-hydroxyestradiol 47-52 LOC100008895 Oryctolagus cuniculus 96-98 3112468-2 1987 2-OHE1, 2-OHE2, and DES were extensively metabolized by PHS peroxidase activity, E1 and E2 to a lesser extent. 2-hydroxyestradiol 8-14 small nucleolar RNA, H/ACA box 73A Homo sapiens 81-89 3782146-1 1986 The cytochrome P-450-mediated reactions of the synthetic stilbene estrogen (E)-diethylstilbestrol (DES) and of 2-hydroxyestradiol have been investigated in vitro. 2-hydroxyestradiol 111-129 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 4-20 6315964-1 1983 Catechol estrogens, such as 2-hydroxyestriol, 2-hydroxyestradiol, and 2-hydroxyestrone, inhibit human liver dihydropteridine reductase noncompetitively with Ki values ranging from 1.5 to 4.6 X 10(-6)M. Catechol estrogens lose approximately half of their inhibitory potency if the C-2 hydroxyl groups are methylated. 2-hydroxyestradiol 46-64 quinoid dihydropteridine reductase Homo sapiens 108-134 3018374-2 1986 A ratio of about 3.5:1 for the C-4 and C-1 thioether conjugates of 2-OHE2 was observed. 2-hydroxyestradiol 67-73 complement C4A Rattus norvegicus 31-34 3005549-5 1986 Only estrogens and CEs with physiologically significant estrogen receptor binding affinities (17 beta-estradiol, moxestrol, 2-hydroxyestradiol and 4-hydroxyestradiol) decreased the turnover rate of dopamine in the corpus striatum compared to control values. 2-hydroxyestradiol 124-142 estrogen receptor 1 Rattus norvegicus 56-73 6540166-4 1984 The isomeric catechol estrogen 4-hydroxyestrone effectively inhibited the LH surge when given at 0900 h, but not if injected at 1000 or 1200 h. In contrast, the nonestrogenic 2-hydroxyestradiol-17 alpha was effective in blocking the LH surge when given at 0900 or 1000 h. Rats treated with 2OHE2-17 beta at 1000 h responded normally to exogenous LHRH administration in the afternoon, indicating that the action of 2OHE2-17 beta is at the hypothalamic level. 2-hydroxyestradiol 175-193 gonadotropin releasing hormone 1 Rattus norvegicus 346-350 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 3794579-3 1986 The effects of 2-hydroxyoestradiol (2-OHE2) and dopamine on the release of prolactin in vitro by perfused pituitary glands from normal adult female rats at different stages of the oestrous cycle have been investigated. 2-hydroxyestradiol 36-42 prolactin Rattus norvegicus 75-84 3794579-8 1986 The cyclical variation in the suppressive effect of 2-OHE2 on prolactin secretion in the female rat is compatible with a postulated neuroendocrine role for this catecholoestrogen. 2-hydroxyestradiol 52-58 prolactin Rattus norvegicus 62-71 3734774-0 1986 In vivo effects of estrogen and 2-hydroxyestradiol on D-2 dopamine receptor agonist affinity states in rat striatum. 2-hydroxyestradiol 32-50 dopamine receptor D2 Rattus norvegicus 54-75 3734774-2 1986 In an attempt to characterize further the molecular mechanism(s) which underlie this biphasic response, we studied the effects of estrogen and one of its metabolites (2-hydroxyestradiol) on striatal D-2 dopamine receptor agonist affinity states. 2-hydroxyestradiol 167-185 dopamine receptor D2 Rattus norvegicus 199-220 3970543-3 1985 2-Hydroxyestradiol is also the principal metabolite in reconstitution experiments in which P-450 1 exhibits the greatest Vmax, ca. 2-hydroxyestradiol 0-18 cytochrome P450 2C5 Oryctolagus cuniculus 91-98 6196675-11 1983 2-OHE2, however, was a much weaker competitor for AFP than either of the other two compounds. 2-hydroxyestradiol 0-6 alpha-fetoprotein Rattus norvegicus 50-53 6640024-7 1983 The release of PGE-A and PGF in the presence of 44 microM of 2-OH-E2 was stimulated by about 60% and 37%. 2-hydroxyestradiol 61-68 placenta growth factor Oryctolagus cuniculus 15-28 6838618-1 1983 The ability of 2-Hydroxyestradiol, a catecholestrogen, and 17 beta Estradiol to interact with the dopamine inhibition of prolactin and with dopamine receptors has been tested on dispersed human prolactin-secreting cells obtained from ten pituitary adenomas. 2-hydroxyestradiol 15-33 prolactin Homo sapiens 121-130 6763895-0 1982 Effect of the catecholestrogen 2-hydroxyestradiol on the renin-angiotensin system in the rat. 2-hydroxyestradiol 31-49 renin Rattus norvegicus 57-62 6275286-1 1981 Temporal alterations in plasma prolactin levels caused by the administration of 2-hydroxyestradiol and 2-hydroxyestrone (100 microgram/kg) into the right atrium of freely-moving conscious male rats were examined. 2-hydroxyestradiol 80-98 prolactin Rattus norvegicus 31-40 6293764-6 1982 However, when thrombin was used to stimulate release, estradiol enhanced, while 2-hydroxyestradiol inhibited, PGI2 formation. 2-hydroxyestradiol 80-98 coagulation factor II, thrombin Homo sapiens 14-22 7054211-3 1982 The infusion of 130 microgram/h purified 2-OHE2 elevated its plasma concentration to 155 pg/ml, consistent with a plasma MCR (MCRp) of approximately 20,000 liters/day. 2-hydroxyestradiol 41-47 nuclear receptor subfamily 3 group C member 2 Homo sapiens 121-124 7054211-3 1982 The infusion of 130 microgram/h purified 2-OHE2 elevated its plasma concentration to 155 pg/ml, consistent with a plasma MCR (MCRp) of approximately 20,000 liters/day. 2-hydroxyestradiol 41-47 nuclear receptor subfamily 3 group C member 2 Homo sapiens 126-130 7054211-5 1982 The MCRp, of 2-OHE2 is approximately half that of 2-hydroxyestrone (2-OHE1), but much higher than those of other steroids. 2-hydroxyestradiol 13-19 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-8 6127206-0 1982 The catechol estrogen, 2-hydroxyestradiol-17 alpha, is formed from estradiol-17 alpha by hypothalamic tissue in vitro and inhibits tyrosine hydroxylase. 2-hydroxyestradiol 23-41 tyrosine hydroxylase Rattus norvegicus 131-151 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 tyrosine hydroxylase Rattus norvegicus 71-91 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 6817001-0 1982 The effect of estrogen priming of hypogonadal women on the release of gonadotropins and prolactin in response to 2-hydroxyestradiol. 2-hydroxyestradiol 113-131 prolactin Homo sapiens 88-97 6817001-1 1982 We have previously shown that the administration of a 2-hydroxyestradiol (20H-E2) infusion (250 microgram/h x 4 h) to hypogonadal women resulted in a selective increase in the levels of circulating prolactin (PRL) without changes in LH or FSH. 2-hydroxyestradiol 54-72 prolactin Homo sapiens 198-207 6817001-1 1982 We have previously shown that the administration of a 2-hydroxyestradiol (20H-E2) infusion (250 microgram/h x 4 h) to hypogonadal women resulted in a selective increase in the levels of circulating prolactin (PRL) without changes in LH or FSH. 2-hydroxyestradiol 54-72 prolactin Homo sapiens 209-212 6276130-8 1982 The results suggest that 2-OHE1 plays no discernible role in PRL release in either sex, but that 2-OHE2 might play a role in the tonic release of PRL in the male and in the preovulatory release of PRL in the female. 2-hydroxyestradiol 97-103 prolactin Rattus norvegicus 146-149 6276130-8 1982 The results suggest that 2-OHE1 plays no discernible role in PRL release in either sex, but that 2-OHE2 might play a role in the tonic release of PRL in the male and in the preovulatory release of PRL in the female. 2-hydroxyestradiol 97-103 prolactin Rattus norvegicus 146-149 6275286-3 1981 A pulsatile elevation of plasma prolactin occurred approximately 4 h after the injection of 2-hydroxyestradiol and a small increase was also observed when it was administered to rats bearing a Silastic capsule containing estradiol. 2-hydroxyestradiol 92-110 prolactin Rattus norvegicus 32-41 6275286-6 1981 A longer latent period was required to produce an elevation in plasma prolactin levels by 2-hydroxyestradiol than by estradiol. 2-hydroxyestradiol 90-108 prolactin Rattus norvegicus 70-79 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 6252068-1 1980 The response of serum prolactin to the catechol estrogens, 2-hydroxyestrone (2-OH E1) and 2-hydroxyestradiol (2-OH E2) and their primary estrogens, estrone (E1) and estradiol (E2), was studied in 35-day-old male rats. 2-hydroxyestradiol 90-108 prolactin Rattus norvegicus 22-31 6252068-1 1980 The response of serum prolactin to the catechol estrogens, 2-hydroxyestrone (2-OH E1) and 2-hydroxyestradiol (2-OH E2) and their primary estrogens, estrone (E1) and estradiol (E2), was studied in 35-day-old male rats. 2-hydroxyestradiol 110-117 prolactin Rattus norvegicus 22-31 32558920-24 2020 The pro-angiogenic EM 2-OHE2 increased the angiogenic potential and VEGF levels of GCs from PCOS women compared to the basal condition (P < 0.05). 2-hydroxyestradiol 22-28 vascular endothelial growth factor A Homo sapiens 68-72 671023-0 1978 The catechol estrogen, 2-hydroxyestradiol, inhibits catechol-O-methyltransferase activity in neuroblastoma cells. 2-hydroxyestradiol 23-41 catechol-O-methyltransferase Homo sapiens 52-80 33247592-13 2021 While 2-OHE2 inhibited apoptosis and BAX mRNA expression, 4-OHE2 induced proliferation and decreased apoptosis (P<0.05). 2-hydroxyestradiol 6-12 BCL2 associated X, apoptosis regulator Homo sapiens 37-40 32781018-9 2020 Cytochrome P450 1A1 and P450 1B1 catalyze the oxidative metabolism of estradiol to catechol estrogens (2-hydroxy estradiol and 4-hydroxy estradiol), respectively. 2-hydroxyestradiol 103-122 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-19 32781018-9 2020 Cytochrome P450 1A1 and P450 1B1 catalyze the oxidative metabolism of estradiol to catechol estrogens (2-hydroxy estradiol and 4-hydroxy estradiol), respectively. 2-hydroxyestradiol 103-122 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 24-32 29948193-6 2018 CTh findings showed lower grey matter volumes for ECs in the left anterior insula, precuneus, inferior parietal cortex, and right pars triangularis than for LCs, and in the right superior parietal gyrus than for ICs. 2-hydroxyestradiol 50-53 V-set and immunoglobulin domain containing 2 Homo sapiens 0-3 30680817-1 2019 Human cytochrome P450 1B1 (CYP1B1)-mediated formation of 4-hydroxyestradiol (4-OHE2) from 17beta-estradiol plays an important role in the progression of human breast cancer, while the biotransformation of 17beta-estradiol to 2-hydroxyestradiol mediated by cytochrome P450 1A1 (CYP1A1) is considered as a less harmful pathway. 2-hydroxyestradiol 225-243 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 6-25 30680817-1 2019 Human cytochrome P450 1B1 (CYP1B1)-mediated formation of 4-hydroxyestradiol (4-OHE2) from 17beta-estradiol plays an important role in the progression of human breast cancer, while the biotransformation of 17beta-estradiol to 2-hydroxyestradiol mediated by cytochrome P450 1A1 (CYP1A1) is considered as a less harmful pathway. 2-hydroxyestradiol 225-243 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 27-33 30680817-1 2019 Human cytochrome P450 1B1 (CYP1B1)-mediated formation of 4-hydroxyestradiol (4-OHE2) from 17beta-estradiol plays an important role in the progression of human breast cancer, while the biotransformation of 17beta-estradiol to 2-hydroxyestradiol mediated by cytochrome P450 1A1 (CYP1A1) is considered as a less harmful pathway. 2-hydroxyestradiol 225-243 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 256-275 30680817-1 2019 Human cytochrome P450 1B1 (CYP1B1)-mediated formation of 4-hydroxyestradiol (4-OHE2) from 17beta-estradiol plays an important role in the progression of human breast cancer, while the biotransformation of 17beta-estradiol to 2-hydroxyestradiol mediated by cytochrome P450 1A1 (CYP1A1) is considered as a less harmful pathway. 2-hydroxyestradiol 225-243 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 277-283 31493422-1 2019 Cytochrome P450 1B1 (CYP1B1) is a key enzyme that catalyzes the metabolism of 17beta-estradiol (E2) into catechol estrogens, such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). 2-hydroxyestradiol 133-151 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 0-19 31493422-1 2019 Cytochrome P450 1B1 (CYP1B1) is a key enzyme that catalyzes the metabolism of 17beta-estradiol (E2) into catechol estrogens, such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). 2-hydroxyestradiol 133-151 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 21-27 31493422-1 2019 Cytochrome P450 1B1 (CYP1B1) is a key enzyme that catalyzes the metabolism of 17beta-estradiol (E2) into catechol estrogens, such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). 2-hydroxyestradiol 153-159 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 0-19 31493422-1 2019 Cytochrome P450 1B1 (CYP1B1) is a key enzyme that catalyzes the metabolism of 17beta-estradiol (E2) into catechol estrogens, such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). 2-hydroxyestradiol 153-159 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 21-27 31147316-14 2019 CYP1A1 and CYP1A2 are responsible for hydroxylation of estradiol (E2) at the C-2 position, resulting in the formation of 2-OHE2, which is proposed to be a detoxification pathway. 2-hydroxyestradiol 121-127 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-6 31147316-14 2019 CYP1A1 and CYP1A2 are responsible for hydroxylation of estradiol (E2) at the C-2 position, resulting in the formation of 2-OHE2, which is proposed to be a detoxification pathway. 2-hydroxyestradiol 121-127 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 11-17 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 126-132 mitogen-activated protein kinase 3 Homo sapiens 34-40 29102625-9 2018 It also increases ovarian synthesis of the catecholestrogen, 2-hydroxy-estradiol-17beta (2-OHE2) which inhibits the GPER/Gs/adenylyl cyclase pathway. 2-hydroxyestradiol 61-87 G protein-coupled estrogen receptor 1 Mus musculus 116-120 29102625-9 2018 It also increases ovarian synthesis of the catecholestrogen, 2-hydroxy-estradiol-17beta (2-OHE2) which inhibits the GPER/Gs/adenylyl cyclase pathway. 2-hydroxyestradiol 89-95 G protein-coupled estrogen receptor 1 Mus musculus 116-120 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 113-119 mitogen-activated protein kinase 3 Homo sapiens 34-40 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 126-132 mitogen-activated protein kinase 1 Homo sapiens 42-45 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 113-119 mitogen-activated protein kinase 1 Homo sapiens 42-45 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 126-132 mitogen-activated protein kinase 8 Homo sapiens 50-53 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 113-119 mitogen-activated protein kinase 8 Homo sapiens 50-53 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 126-132 dihydrolipoamide branched chain transacylase E2 Homo sapiens 219-226 28437005-2 2017 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary for 2-OHE2 - and 4-OHE2 -induced P-UAEC proliferation, as well as proliferation induced by the parent hormone E2 beta and other beta-AR signalling hormones (i.e. catecholamines). 2-hydroxyestradiol 113-119 dihydrolipoamide branched chain transacylase E2 Homo sapiens 219-226 28437005-3 2017 Conversely, although 2-OHE2 and 4-OHE2 rapidly activate phosphatidylinositol 3-kinase (PI3K), its activation is not involved in catecholoestradiol-induced P-UAEC proliferation. 2-hydroxyestradiol 21-27 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 56-85 28437005-3 2017 Conversely, although 2-OHE2 and 4-OHE2 rapidly activate phosphatidylinositol 3-kinase (PI3K), its activation is not involved in catecholoestradiol-induced P-UAEC proliferation. 2-hydroxyestradiol 32-38 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 56-85 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 0-6 mitogen-activated protein kinase 3 Homo sapiens 57-63 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 0-6 mitogen-activated protein kinase 1 Homo sapiens 70-73 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 0-6 mitogen-activated protein kinase 8 Homo sapiens 78-81 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 11-17 mitogen-activated protein kinase 3 Homo sapiens 57-63 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 11-17 mitogen-activated protein kinase 1 Homo sapiens 70-73 28437005-11 2017 2-OHE2 and 4-OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and rapid monophasic AKT phosphorylation. 2-hydroxyestradiol 11-17 mitogen-activated protein kinase 8 Homo sapiens 78-81 28461606-1 2017 Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). 2-hydroxyestradiol 48-66 catechol-O-methyltransferase Homo sapiens 0-28 28461606-1 2017 Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). 2-hydroxyestradiol 48-66 catechol-O-methyltransferase Homo sapiens 30-34 28461606-1 2017 Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). 2-hydroxyestradiol 48-66 angiotensinogen Homo sapiens 258-272 28461606-1 2017 Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). 2-hydroxyestradiol 48-66 angiotensinogen Homo sapiens 274-280 28007532-9 2017 It also increases ovarian synthesis of the catecholestrogen, 2-hydroxy-estradiol-17beta (2-OHE2) which inhibits the GPER/Gs/adenylyl cyclase pathway. 2-hydroxyestradiol 61-87 G protein-coupled estrogen receptor 1 Mus musculus 116-120 28007532-9 2017 It also increases ovarian synthesis of the catecholestrogen, 2-hydroxy-estradiol-17beta (2-OHE2) which inhibits the GPER/Gs/adenylyl cyclase pathway. 2-hydroxyestradiol 89-95 G protein-coupled estrogen receptor 1 Mus musculus 116-120 28072767-5 2017 RESULTS: In addition to having lower urinary E1 levels, CYP3A7*1C carriers had significantly lower levels of four of the 2-hydroxylation pathway EMs that we measured (2-hydroxyestrone, P=1.1 x 10-12; 2-hydroxyestradiol, P=2.7 x 10-7; 2-methoxyestrone, P=1.9 x 10-12; and 2-methoxyestradiol, P=0.0009). 2-hydroxyestradiol 200-218 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 56-62 27312859-11 2016 These results suggest that in neonatal rat osteoblasts, the anti-estrogenic effect of I3C is mediated by 2-OHE2 through ER-alpha. 2-hydroxyestradiol 105-111 estrogen receptor 1 Rattus norvegicus 120-128 25588877-7 2015 However, G0S2 prevented ECs from serum-free starvation stress- and hydrogen peroxide (H2O2)-induced apoptosis. 2-hydroxyestradiol 24-27 G0/G1 switch 2 Homo sapiens 9-13 25814058-9 2015 Yeast microsomes containing bsCYP1A1 and 1B1 and hCYP1A1, 1A2, and 1B1 metabolized E2 to 2-OHE2 and 4-OHE2, whereas bsCYP1A2 showed no such activity. 2-hydroxyestradiol 89-95 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 49-61 25814058-9 2015 Yeast microsomes containing bsCYP1A1 and 1B1 and hCYP1A1, 1A2, and 1B1 metabolized E2 to 2-OHE2 and 4-OHE2, whereas bsCYP1A2 showed no such activity. 2-hydroxyestradiol 100-106 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 49-61 26732685-7 2016 Inhibition of COMT blocked the conversion of 2-OE to 2-ME and the antimitogenic effects of 2-OE but not 2-ME. 2-hydroxyestradiol 45-49 catechol-O-methyltransferase Mus musculus 14-18 26732685-7 2016 Inhibition of COMT blocked the conversion of 2-OE to 2-ME and the antimitogenic effects of 2-OE but not 2-ME. 2-hydroxyestradiol 91-95 catechol-O-methyltransferase Mus musculus 14-18 24528081-2 2014 17beta-estradiol (E2), the main steroidal estrogen present in women, is metabolized via two major pathways: formation of the 2-hydroxyestradiol (2-OH E2) and 4-hydroxyestradiol (4-OH E2) through the action of Cytochrome P450 (CYP) 1A1 and 1B1, respectively. 2-hydroxyestradiol 125-143 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 209-242 25609836-0 2015 The catecholestrogen, 2-hydroxyestradiol-17beta, acts as a G protein-coupled estrogen receptor 1 (GPER/GPR30) antagonist to promote the resumption of meiosis in zebrafish oocytes. 2-hydroxyestradiol 22-47 G protein-coupled estrogen receptor 1 Danio rerio 59-96 25609836-0 2015 The catecholestrogen, 2-hydroxyestradiol-17beta, acts as a G protein-coupled estrogen receptor 1 (GPER/GPR30) antagonist to promote the resumption of meiosis in zebrafish oocytes. 2-hydroxyestradiol 22-47 G protein-coupled estrogen receptor 1 Danio rerio 98-102 25609836-0 2015 The catecholestrogen, 2-hydroxyestradiol-17beta, acts as a G protein-coupled estrogen receptor 1 (GPER/GPR30) antagonist to promote the resumption of meiosis in zebrafish oocytes. 2-hydroxyestradiol 22-47 G protein-coupled estrogen receptor 1 Danio rerio 103-108 25609836-3 2015 We tested the hypothesis that 2-OHE2 is produced in zebrafish ovaries and promotes the resumption of oocyte meiosis through its action as a GPER antagonist. 2-hydroxyestradiol 30-36 G protein-coupled estrogen receptor 1 Danio rerio 140-144 25609836-6 2015 Expression of cyp1a, cyp1b1, and cyp1c mRNAs was increased by gonadotropin treatment, further implicating these Cyp1s in 2-OHE2 synthesis prior to OM. 2-hydroxyestradiol 121-127 cytochrome P450, family 1, subfamily A Danio rerio 14-19 25609836-6 2015 Expression of cyp1a, cyp1b1, and cyp1c mRNAs was increased by gonadotropin treatment, further implicating these Cyp1s in 2-OHE2 synthesis prior to OM. 2-hydroxyestradiol 121-127 peptidylprolyl isomerase Aa (cyclophilin A) Danio rerio 112-116 25609836-8 2015 2-OHE2 treatment significantly increased spontaneous OM in defolliculated zebrafish oocytes and reversed the inhibition of OM by E2 and the GPER agonist G-1. 2-hydroxyestradiol 0-6 G protein-coupled estrogen receptor 1 Danio rerio 140-144 25609836-9 2015 2-OHE2 was an effective competitor of [(3)H]-E2 binding to recombinant zebrafish GPER expressed in HEK-293 cells. 2-hydroxyestradiol 0-6 G protein-coupled estrogen receptor 1 Danio rerio 81-85 25609836-10 2015 2-OHE2 also antagonized estrogen actions through GPER on cAMP production in zebrafish oocytes, resulting in a reduction in cAMP levels. 2-hydroxyestradiol 0-6 G protein-coupled estrogen receptor 1 Homo sapiens 49-53 25609836-11 2015 Stimulation of OM by 2-OHE2 was blocked by pretreatment of defolliculated oocytes with the GPER antibody. 2-hydroxyestradiol 21-27 G protein-coupled estrogen receptor 1 Danio rerio 91-95 25609836-12 2015 Collectively, the results suggest that 2-OHE2 functions as a GPER antagonist and promotes OM in zebrafish through blocking GPER-dependent E2 inhibition of the resumption of OM. 2-hydroxyestradiol 39-45 G protein-coupled estrogen receptor 1 Danio rerio 61-65 25609836-12 2015 Collectively, the results suggest that 2-OHE2 functions as a GPER antagonist and promotes OM in zebrafish through blocking GPER-dependent E2 inhibition of the resumption of OM. 2-hydroxyestradiol 39-45 G protein-coupled estrogen receptor 1 Danio rerio 123-127 25257533-5 2014 More specifically, ERalpha represses the expression of the CYP1A1 gene, which encodes an enzyme that converts 17beta-estradiol into 2-hydroxyestradiol. 2-hydroxyestradiol 132-150 estrogen receptor 1 Homo sapiens 19-26 25257533-5 2014 More specifically, ERalpha represses the expression of the CYP1A1 gene, which encodes an enzyme that converts 17beta-estradiol into 2-hydroxyestradiol. 2-hydroxyestradiol 132-150 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 59-65 24528081-2 2014 17beta-estradiol (E2), the main steroidal estrogen present in women, is metabolized via two major pathways: formation of the 2-hydroxyestradiol (2-OH E2) and 4-hydroxyestradiol (4-OH E2) through the action of Cytochrome P450 (CYP) 1A1 and 1B1, respectively. 2-hydroxyestradiol 145-152 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 209-242 23685341-3 2013 Exposure to 2-OHE2, 4-OHE2 or E2 resulted in a significant increase in the protein abundance of cyclin D1 and c-myc. 2-hydroxyestradiol 12-18 cyclin D1 Homo sapiens 96-105 24144187-3 2013 Herein, the interaction of Ngb with the quinones generated by oxidation of catecholamines (dopamine, norepinephrine) and catechol estrogens (2-hydroxyestradiol and 4-hydroxyestradiol), which have been implicated in neurodegenerative pathologies like Parkinson"s and Alzheimer"s diseases, has been investigated. 2-hydroxyestradiol 141-159 neuroglobin Homo sapiens 27-30 23685341-6 2013 Reduced abundance of estrogen receptor-beta (ERbeta) and its downstream tumor suppressor FOXO-1 were observed in cells exposed to E2, 2-OHE2 and, to a greater extent, 4-OHE2. 2-hydroxyestradiol 134-140 estrogen receptor 2 Homo sapiens 21-43 23685341-6 2013 Reduced abundance of estrogen receptor-beta (ERbeta) and its downstream tumor suppressor FOXO-1 were observed in cells exposed to E2, 2-OHE2 and, to a greater extent, 4-OHE2. 2-hydroxyestradiol 134-140 estrogen receptor 2 Homo sapiens 45-51 24424856-1 2014 The effects of tetrahydrocannabinol (THC) and endogenous cannabinoids (endocannabinoids, ECs) are both mediated by activation of the cannabinoid receptors CB1 and CB2. 2-hydroxyestradiol 89-92 cannabinoid receptor 1 Homo sapiens 155-158 24424856-1 2014 The effects of tetrahydrocannabinol (THC) and endogenous cannabinoids (endocannabinoids, ECs) are both mediated by activation of the cannabinoid receptors CB1 and CB2. 2-hydroxyestradiol 89-92 cannabinoid receptor 2 Homo sapiens 163-166 23685341-3 2013 Exposure to 2-OHE2, 4-OHE2 or E2 resulted in a significant increase in the protein abundance of cyclin D1 and c-myc. 2-hydroxyestradiol 12-18 MYC proto-oncogene, bHLH transcription factor Homo sapiens 110-115 23685341-6 2013 Reduced abundance of estrogen receptor-beta (ERbeta) and its downstream tumor suppressor FOXO-1 were observed in cells exposed to E2, 2-OHE2 and, to a greater extent, 4-OHE2. 2-hydroxyestradiol 134-140 forkhead box O1 Homo sapiens 89-95 23665934-8 2013 In this setting, the addition of paraquat, TCDD, DMBA, 2OHE2 or 4OHE2 significantly augmented ROS generation in BRCA1-KD MCF10A cells. 2-hydroxyestradiol 55-60 BRCA1 DNA repair associated Homo sapiens 112-117 23665934-8 2013 In this setting, the addition of paraquat, TCDD, DMBA, 2OHE2 or 4OHE2 significantly augmented ROS generation in BRCA1-KD MCF10A cells. 2-hydroxyestradiol 64-69 BRCA1 DNA repair associated Homo sapiens 112-117 22178088-4 2012 2-Methoxyestradiol (2-ME) is formed by the action of catechol-O-methyltransferase (COMT) on 2-hydroxyestradiol. 2-hydroxyestradiol 92-110 catechol-O-methyltransferase Homo sapiens 53-81 22914890-9 2012 The high-dose OCP, PCB, and M group increased the production of 2-OH-E2 and 6alpha-OH-E2, while only the PCB and M groups increased the 2-OH-CE/methoxyestrogen ratio. 2-hydroxyestradiol 64-71 pyruvate carboxylase Rattus norvegicus 19-22 22658921-1 2012 The enzyme catechol-O-methyltransferase (COMT) is part of the metabolic pathway of 17beta-estradiol, converting 2-hydroxyestradiol to 2-methoxyestradiol. 2-hydroxyestradiol 112-130 catechol-O-methyltransferase Mus musculus 11-39 22658921-1 2012 The enzyme catechol-O-methyltransferase (COMT) is part of the metabolic pathway of 17beta-estradiol, converting 2-hydroxyestradiol to 2-methoxyestradiol. 2-hydroxyestradiol 112-130 catechol-O-methyltransferase Mus musculus 41-45 22178088-4 2012 2-Methoxyestradiol (2-ME) is formed by the action of catechol-O-methyltransferase (COMT) on 2-hydroxyestradiol. 2-hydroxyestradiol 92-110 catechol-O-methyltransferase Homo sapiens 83-87 21824401-9 2011 In particular, the metabolic ratio of 2-hydroxyestrone to 2-hydroxy-17beta-estradiol, which could reveal the enzyme activity of 17beta-hydroxysteroid dehydrogenase, showed gender differences in PTC patients (P < 1 x 10-7). 2-hydroxyestradiol 58-84 hydroxysteroid 17-beta dehydrogenase 7 Homo sapiens 128-163 22329816-11 2012 Phospho-ERK1/2 protein expression in cells stimulated with E2, 2-OH-E2 and 4-OH-E2 was not significantly different from the control. 2-hydroxyestradiol 63-70 mitogen-activated protein kinase 3 Homo sapiens 8-14 22329816-11 2012 Phospho-ERK1/2 protein expression in cells stimulated with E2, 2-OH-E2 and 4-OH-E2 was not significantly different from the control. 2-hydroxyestradiol 75-82 mitogen-activated protein kinase 3 Homo sapiens 8-14 19020775-5 2008 Kinetic analysis showed that these new COMT variants had essentially the same kinetic characteristics and catalytic activity as the wild-type COMTs for the O-methylation of 2-hydroxyestradiol and 4-hydroxyestradiol in vitro, but they have asignificantly reduced thermostability at 37 degrees C. In addition, the mutant enzymes have different binding affinities for S-adenosyl-L-methionine compared with the wild-type COMTs. 2-hydroxyestradiol 173-191 catechol-O-methyltransferase Homo sapiens 39-43 21793624-0 2011 The ability of hydroxylated estrogens (2-OH-E2 and 4-OH-E2) to increase of SHBG gene, protein expression and intracellular levels in MCF-7 cells line. 2-hydroxyestradiol 39-46 sex hormone binding globulin Homo sapiens 75-79 21793624-0 2011 The ability of hydroxylated estrogens (2-OH-E2 and 4-OH-E2) to increase of SHBG gene, protein expression and intracellular levels in MCF-7 cells line. 2-hydroxyestradiol 51-58 sex hormone binding globulin Homo sapiens 75-79 21793624-2 2011 This study was conducted to elucidate the effects of hydroxylated estrogen (E2) metabolites (2-OH-E2 and 4-OH-E2) on sex hormone binding globulin (SHBG) mRNA and protein expression as well as on intracellular and extracellular SHBG levels. 2-hydroxyestradiol 93-100 sex hormone binding globulin Homo sapiens 117-145 21793624-2 2011 This study was conducted to elucidate the effects of hydroxylated estrogen (E2) metabolites (2-OH-E2 and 4-OH-E2) on sex hormone binding globulin (SHBG) mRNA and protein expression as well as on intracellular and extracellular SHBG levels. 2-hydroxyestradiol 93-100 sex hormone binding globulin Homo sapiens 147-151 21793624-2 2011 This study was conducted to elucidate the effects of hydroxylated estrogen (E2) metabolites (2-OH-E2 and 4-OH-E2) on sex hormone binding globulin (SHBG) mRNA and protein expression as well as on intracellular and extracellular SHBG levels. 2-hydroxyestradiol 93-100 sex hormone binding globulin Homo sapiens 227-231 21793624-2 2011 This study was conducted to elucidate the effects of hydroxylated estrogen (E2) metabolites (2-OH-E2 and 4-OH-E2) on sex hormone binding globulin (SHBG) mRNA and protein expression as well as on intracellular and extracellular SHBG levels. 2-hydroxyestradiol 105-112 sex hormone binding globulin Homo sapiens 117-145 21793624-2 2011 This study was conducted to elucidate the effects of hydroxylated estrogen (E2) metabolites (2-OH-E2 and 4-OH-E2) on sex hormone binding globulin (SHBG) mRNA and protein expression as well as on intracellular and extracellular SHBG levels. 2-hydroxyestradiol 105-112 sex hormone binding globulin Homo sapiens 147-151 21793624-6 2011 Both metabolites increased SHBG mRNA expression, the rank order of potency being E2 > 4-OH-E2 > 2-OH-E2. 2-hydroxyestradiol 89-96 sex hormone binding globulin Homo sapiens 27-31 21793624-6 2011 Both metabolites increased SHBG mRNA expression, the rank order of potency being E2 > 4-OH-E2 > 2-OH-E2. 2-hydroxyestradiol 102-109 sex hormone binding globulin Homo sapiens 27-31 21344307-0 2011 2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1. 2-hydroxyestradiol 8-13 tumor protein p53 Homo sapiens 141-144 21344307-0 2011 2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1. 2-hydroxyestradiol 8-13 checkpoint kinase 1 Homo sapiens 149-153 20881610-4 2010 Estradiol is metabolized to 2-hydroxyestradiol (2HE) by CYP1A1/CYP1B1, and 2HE is converted to 2-methoxyestradiol (2ME) by catechol-O-methyl transferase. 2-hydroxyestradiol 28-46 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 56-62 20881610-4 2010 Estradiol is metabolized to 2-hydroxyestradiol (2HE) by CYP1A1/CYP1B1, and 2HE is converted to 2-methoxyestradiol (2ME) by catechol-O-methyl transferase. 2-hydroxyestradiol 28-46 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 63-69 20881610-4 2010 Estradiol is metabolized to 2-hydroxyestradiol (2HE) by CYP1A1/CYP1B1, and 2HE is converted to 2-methoxyestradiol (2ME) by catechol-O-methyl transferase. 2-hydroxyestradiol 48-51 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 56-62 20881610-4 2010 Estradiol is metabolized to 2-hydroxyestradiol (2HE) by CYP1A1/CYP1B1, and 2HE is converted to 2-methoxyestradiol (2ME) by catechol-O-methyl transferase. 2-hydroxyestradiol 48-51 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 63-69 20237589-6 2010 Moreover, E2, 2-HOE, and 2-MeOH antagonized the contraction induced by the vasospasm agonist endothelin-1 (0.1 micromol/L) by approximately 36%. 2-hydroxyestradiol 14-19 endothelin 1 Homo sapiens 93-105 20534756-1 2010 CONTEXT: Antimitogenic effects of estradiol on vascular smooth muscle cells (VSMCs) may be cardioprotective, and these effects are mediated by estrogen receptor-alpha-dependent and -independent mechanisms, with the latter involving the conversion of estradiol to 2-hydroxyestradiol/2-methoxyestradiol by CYP450. 2-hydroxyestradiol 263-281 estrogen receptor 1 Homo sapiens 143-166 19077667-5 2009 Kinetic analysis showed that these new COMT variants had essentially the same kinetic characteristics and catalytic activity as the wild-type COMTs for the O-methylation of 2-hydroxyestradiol and 4-hydroxyestradiol in vitro, but they have a significantly reduced thermostability at 37 degrees C. 2-hydroxyestradiol 173-191 catechol-O-methyltransferase Homo sapiens 39-43 18456490-5 2008 Cyp1A1 and Cyp1B1 are responsible for the metabolism of E(2) to generate 2-hydroxyestradiol (2-OHE(2)) and 4-hydroxyestradiol (4-OHE(2)), respectively. 2-hydroxyestradiol 73-91 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-6 18256205-8 2008 Of the seven compounds tested, only vorozole exhibited inhibition of CYP1B1 activity with IC(50) values of 17 and 21 microM for 4-hydroxy estradiol and 2-hydroxy estradiol, respectively. 2-hydroxyestradiol 152-171 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 69-75 18761407-6 2008 The high fat/low fiber group had significantly higher urinary total estrogens, estriol-3-glucuronide, 2-hydroxyestradiol, 16alpha-hydroxyestrone, and a higher 2-hydroxyestrone/4-hydroxyestrone ratio. 2-hydroxyestradiol 102-120 FAT atypical cadherin 1 Homo sapiens 9-12 18761407-7 2008 Total fat intake correlated significantly with plasma estrone, estradiol, urinary 2-hydroxyestrone, 2-hydroxyestradiol, 2-hydroxyestrone/4-hydroxyestrone ratio, and total urinary estrogens, even after adjustment for total fiber intake. 2-hydroxyestradiol 100-118 FAT atypical cadherin 1 Homo sapiens 6-9 18301880-9 2008 In OVX females, E2 supplement alone or cotreatment with E2 and 50 mg/kg amitraz produced 1.3- to several-fold increases of 2- and 4-OH-E2 formation and 2beta- and 16alpha-OH-testosterone production. 2-hydroxyestradiol 130-137 dihydrolipoamide S-succinyltransferase Rattus norvegicus 56-65 18456490-5 2008 Cyp1A1 and Cyp1B1 are responsible for the metabolism of E(2) to generate 2-hydroxyestradiol (2-OHE(2)) and 4-hydroxyestradiol (4-OHE(2)), respectively. 2-hydroxyestradiol 73-91 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 11-17 18197555-2 2008 EGCG has an IC(50) value of 70 nM for inhibiting human liver COMT-mediated O-methylation of 2-hydroxyestradiol, which was 210-760 times more potent than catechin, epigallocatechin and epicatechin. 2-hydroxyestradiol 92-110 catechol-O-methyltransferase Homo sapiens 61-65 16893557-2 2006 Here, we present results from kinetic studies characterizing the formation of 4-OHE2 and 2-hydroxyestradiol (2-OHE2) by rat CYP1B1 using 17beta-estradiol (E2) as a substrate. 2-hydroxyestradiol 89-107 cytochrome P450, family 1, subfamily b, polypeptide 1 Rattus norvegicus 124-130 17234793-4 2007 CYP1B1 oxidized E2 to the catechol 4-OHE2 and the labile quinone 4-hydroxyestradiol-quinone to produce 4-OHE2-N7-Gua and 4-OHE2-N3-Ade in a time- and concentration-dependent manner. 2-hydroxyestradiol 35-41 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 0-6 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 16893557-2 2006 Here, we present results from kinetic studies characterizing the formation of 4-OHE2 and 2-hydroxyestradiol (2-OHE2) by rat CYP1B1 using 17beta-estradiol (E2) as a substrate. 2-hydroxyestradiol 109-115 cytochrome P450, family 1, subfamily b, polypeptide 1 Rattus norvegicus 124-130 16893557-4 2006 For rat CYP1B1, the apparent Km values for the formation of 4-OHE2 and 2-OHE2 were 0.61+/-0.23 and 1.84+/-0.73 microM; the turnover numbers (Kcat) were 0.23+/-0.02 and 0.46+/-0.05 pmol/min/pmol P450; and the catalytic efficiencies (Kcat/Km) were 0.37 and 0.25, respectively. 2-hydroxyestradiol 71-77 cytochrome P450, family 1, subfamily b, polypeptide 1 Rattus norvegicus 8-14 16893557-5 2006 For human CYP1B1, the apparent Km values for the formation of 4-OHE2 and 2-OHE2 were 1.22+/-0.25 and 1.10+/-0.26; the turnover numbers were 1.23+/-0.06 and 0.33+/-0.02; and the catalytic efficiencies were 1.0 and 0.30, respectively. 2-hydroxyestradiol 73-79 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 10-16 16790556-4 2006 Kinetic studies using HLM, CYP3A4, and CYP1A2 showed similar affinities (Km) for E2 with respect to 2-OHE2 production. 2-hydroxyestradiol 100-106 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 39-45 16411670-7 2006 Similar results were obtained with lactoperoxidase or tyrosinase-catalyzed oxidation of 4-OHE2 and 2-OHE2, whereas with activation by PHS or microsomes, a relatively higher amount of the depurinating adduct from E2-2,3-Q was detected. 2-hydroxyestradiol 99-105 tyrosinase Rattus norvegicus 54-64 16675129-14 2006 Treatment of MCF-10F cells, which are estrogen receptor-alpha-negative immortalized human breast epithelial cells, with E2, 4-OHE2 or 2-OHE2 induces their neoplastic transformation in vitro, even in the presence of the antiestrogen ICI-182,780. 2-hydroxyestradiol 124-130 estrogen receptor 1 Homo sapiens 38-61 16675129-14 2006 Treatment of MCF-10F cells, which are estrogen receptor-alpha-negative immortalized human breast epithelial cells, with E2, 4-OHE2 or 2-OHE2 induces their neoplastic transformation in vitro, even in the presence of the antiestrogen ICI-182,780. 2-hydroxyestradiol 134-140 estrogen receptor 1 Homo sapiens 38-61 16287077-9 2006 Cells treated with E2 or 4-OHE2 at doses of 0.007 nM and 70 nM and 2-OHE2 only at a higher dose (3.6 microM) exhibited a 5 bp deletion in p53 exon 4. 2-hydroxyestradiol 67-73 tumor protein p53 Homo sapiens 138-141 15050414-5 2004 Estradiol (E2) is usually metabolized by CYP1A1/1A2 and CYP3A4 to the 2-hydroxy estradiol (2-OHE2) and 4-hydroxy estradiol (4-OHE2) in human liver. 2-hydroxyestradiol 70-89 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 41-47 16112414-4 2005 A major metabolite of estradiol, 2-hydroxyestradiol, is mainly catalyzed by CYP1A2 and CYP3A4 in liver, and by CYP1A1 in extrahepatic tissues. 2-hydroxyestradiol 33-51 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 76-82 16112414-4 2005 A major metabolite of estradiol, 2-hydroxyestradiol, is mainly catalyzed by CYP1A2 and CYP3A4 in liver, and by CYP1A1 in extrahepatic tissues. 2-hydroxyestradiol 33-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 16112414-4 2005 A major metabolite of estradiol, 2-hydroxyestradiol, is mainly catalyzed by CYP1A2 and CYP3A4 in liver, and by CYP1A1 in extrahepatic tissues. 2-hydroxyestradiol 33-51 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 111-117 15342355-8 2005 We remark that, in human spermatozoa, bicarbonate acts primarily through activation of sAC to stimulate tyrosine phosphorylation of AKAP3 and sperm motility because both effects are blunted by the sAC inhibitor 2OH-estradiol. 2-hydroxyestradiol 211-224 A-kinase anchoring protein 3 Homo sapiens 132-137 15507517-9 2005 OR486 and quercetin (COMT inhibitor) blocked the conversion of 2-hydroxyestradiol to 2-methoxyestradiol in CFs. 2-hydroxyestradiol 63-81 catechol-O-methyltransferase Homo sapiens 21-25 15142886-4 2004 It also reduced the formation of 2-hydroxyestradiol and 4-hydroxyestradiol from 17beta-estradiol by recombinant human CYP1A1 and CYP1B1, respectively. 2-hydroxyestradiol 33-51 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 118-124 15142886-4 2004 It also reduced the formation of 2-hydroxyestradiol and 4-hydroxyestradiol from 17beta-estradiol by recombinant human CYP1A1 and CYP1B1, respectively. 2-hydroxyestradiol 33-51 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 129-135 15126566-7 2004 Up-regulation of ERalpha by AS-OLIGOs did not increase the antimitogenic effects of estradiol on HASMCs; the estradiol metabolites 2-hydroxyestradiol and 2-methoxyestradiol were more potent inhibitors of HASMC growth, compared with estradiol; and blockade of metabolism of estradiol to hydroxyestradiols and methoxyestradiols abrogated the inhibitory effects of estradiol on HASMC growth. 2-hydroxyestradiol 131-149 estrogen receptor 1 Homo sapiens 17-24 15805301-6 2005 Catalytic efficiencies for the formation of the major metabolites, 2-OH-E2 and 2-OH-E1, by CYP1A1.2 were 5.7- and 12-fold higher, respectively, compared with the wild-type enzyme. 2-hydroxyestradiol 67-74 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 91-97 15513894-2 2004 2-Hydroxyestradiol (2-OHE2), a major oxidized metabolite of E2 formed preferentially by cytochrome P-450 1A1, reacts with DNA to form stable adducts and exerts genotoxicity. 2-hydroxyestradiol 0-18 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 88-108 15513894-2 2004 2-Hydroxyestradiol (2-OHE2), a major oxidized metabolite of E2 formed preferentially by cytochrome P-450 1A1, reacts with DNA to form stable adducts and exerts genotoxicity. 2-hydroxyestradiol 20-26 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 88-108 15050414-5 2004 Estradiol (E2) is usually metabolized by CYP1A1/1A2 and CYP3A4 to the 2-hydroxy estradiol (2-OHE2) and 4-hydroxy estradiol (4-OHE2) in human liver. 2-hydroxyestradiol 70-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 15050414-5 2004 Estradiol (E2) is usually metabolized by CYP1A1/1A2 and CYP3A4 to the 2-hydroxy estradiol (2-OHE2) and 4-hydroxy estradiol (4-OHE2) in human liver. 2-hydroxyestradiol 91-97 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 41-47 15050414-5 2004 Estradiol (E2) is usually metabolized by CYP1A1/1A2 and CYP3A4 to the 2-hydroxy estradiol (2-OHE2) and 4-hydroxy estradiol (4-OHE2) in human liver. 2-hydroxyestradiol 91-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 15050414-8 2004 In the present study, we have demonstrated that one of the catechol estrogen metabolites of E2, 4-OHE2, induces HIF-1alpha and VEGF-A expression at protein level in two human ovarian cancer cell lines, OVCAR-3 and A2780-CP70 cells, in dose- and time-dependent manners, whereas the other catechol estrogen metabolite of E2, 2-OHE2, does not alter HIF-1alpha and VEGF-A expression. 2-hydroxyestradiol 323-329 hypoxia inducible factor 1 subunit alpha Homo sapiens 112-122 14871858-5 2004 Intrinsic clearances indicated that UGT1A1 had a preference for the glucuronidation of 2-hydroxyestradiol, a metabolite associated with antiproliferative activity. 2-hydroxyestradiol 87-105 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 36-42 14871858-11 2004 These observations suggest that lower expression of UGT1A1 decreases the risk of endometrial cancer by reducing the excretion of 2-hydroxyestradiol, the antiproliferative metabolite of E(2), in the endometrium. 2-hydroxyestradiol 129-147 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 52-58 12810639-5 2003 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2. 2-hydroxyestradiol 124-130 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 80-86 12865317-7 2003 CYP3A4 had strong activity for the formation of 2-hydroxyestradiol, followed by 4-hydroxyestradiol and an unknown polar metabolite, and small amounts of 16alpha- and 16beta-hydroxyestrogens were also formed. 2-hydroxyestradiol 48-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 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 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 129-135 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-19 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 129-135 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 21-27 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 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 129-135 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 38-44 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 129-135 dihydrolipoamide branched chain transacylase E2 Homo sapiens 102-104 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 140-146 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-19 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 140-146 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 21-27 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 140-146 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 38-44 12810639-1 2003 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quinones, which may lead to DNA damage. 2-hydroxyestradiol 140-146 dihydrolipoamide branched chain transacylase E2 Homo sapiens 102-104 12810639-5 2003 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2. 2-hydroxyestradiol 64-70 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 5-11 12810639-5 2003 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2. 2-hydroxyestradiol 64-70 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 16-22 12810639-5 2003 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2. 2-hydroxyestradiol 124-130 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 5-11 12810639-5 2003 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2. 2-hydroxyestradiol 124-130 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 16-22 12376470-2 2002 The two major pathways of estrogen metabolism, to the carcinogenic 4-hydroxyestradiol (4-OHE2) and to the non-carcinogenic 2-hydroxyestradiol (2-OHE2), are mediated by cytochromes P450 CYP1B1 and CYP1A1, respectively. 2-hydroxyestradiol 123-141 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 185-191 12376470-2 2002 The two major pathways of estrogen metabolism, to the carcinogenic 4-hydroxyestradiol (4-OHE2) and to the non-carcinogenic 2-hydroxyestradiol (2-OHE2), are mediated by cytochromes P450 CYP1B1 and CYP1A1, respectively. 2-hydroxyestradiol 123-141 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 196-202 12376470-2 2002 The two major pathways of estrogen metabolism, to the carcinogenic 4-hydroxyestradiol (4-OHE2) and to the non-carcinogenic 2-hydroxyestradiol (2-OHE2), are mediated by cytochromes P450 CYP1B1 and CYP1A1, respectively. 2-hydroxyestradiol 143-149 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 185-191 12376470-2 2002 The two major pathways of estrogen metabolism, to the carcinogenic 4-hydroxyestradiol (4-OHE2) and to the non-carcinogenic 2-hydroxyestradiol (2-OHE2), are mediated by cytochromes P450 CYP1B1 and CYP1A1, respectively. 2-hydroxyestradiol 143-149 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 196-202 12151356-2 2002 NADPH-dependent oxidation of E(2) by liver microsomes from ACI and Sprague-Dawley rats produced several metabolites of which 2-hydroxyestradiol (2-OH-E(2)), estrone (E(1)), and 2-hydroxyestrone (2-OH-E(1)) were predominant. 2-hydroxyestradiol 125-143 dihydrolipoamide S-succinyltransferase Rattus norvegicus 29-33 12151356-2 2002 NADPH-dependent oxidation of E(2) by liver microsomes from ACI and Sprague-Dawley rats produced several metabolites of which 2-hydroxyestradiol (2-OH-E(2)), estrone (E(1)), and 2-hydroxyestrone (2-OH-E(1)) were predominant. 2-hydroxyestradiol 125-143 dihydrolipoamide S-succinyltransferase Rattus norvegicus 150-154 12151356-2 2002 NADPH-dependent oxidation of E(2) by liver microsomes from ACI and Sprague-Dawley rats produced several metabolites of which 2-hydroxyestradiol (2-OH-E(2)), estrone (E(1)), and 2-hydroxyestrone (2-OH-E(1)) were predominant. 2-hydroxyestradiol 125-143 carboxylesterase 1C Rattus norvegicus 200-204 12084525-5 2002 This report is the first to identify ECs as a new source of BNP. 2-hydroxyestradiol 37-40 natriuretic peptide B Homo sapiens 60-63 12579301-2 2003 Mechanistically, hyperhomocysteinemia may exert its pathogenic effects largely through metabolic accumulation of intracellular S-adenosyl-L-homocysteine, a strong non-competitive inhibitor of the catechol-O-methyltransferase-mediated methylation metabolism of endogenous and exogenous catechol estrogens (mainly 2-hydroxyestradiol and 4-hydroxyestradiol). 2-hydroxyestradiol 312-330 catechol-O-methyltransferase Homo sapiens 196-224 12228253-7 2002 By contrast, the low affinity of SHBG for 2-hydroxyestradiol can be attributed to intra-molecular hydrogen bonding between the hydroxyls in the aromatic steroid ring A, which generates a steric clash with the amido group of Asn(82). 2-hydroxyestradiol 42-60 sex hormone binding globulin Homo sapiens 33-37 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 11906176-5 2002 We determined apparent K(m) values for 10 recombinant human SULT isoforms, as well as the three most common allozymes for SULT1A1 and SULT1A2, with 2-OHE1, 2-OHE2, 4-OHE1, and 4-OHE2, and with the endogenous estrogens, estrone (E1) and 17beta-estradiol (E2), as substrates. 2-hydroxyestradiol 156-162 sulfotransferase family 1A member 1 Homo sapiens 122-129 11906176-7 2002 SULT1E1 had the lowest apparent K(m) values, 0.31, 0.18, 0.27, and 0.22 microM for 4-OHE1, 4-OHE2, 2-OHE1, and 2-OHE2, respectively. 2-hydroxyestradiol 111-117 sulfotransferase family 1E member 1 Homo sapiens 0-7 11844241-7 2002 RESULTS: In all tissues, ECs in the majority of vessels were immunopositive for CD31 with two distinct antibodies. 2-hydroxyestradiol 25-28 platelet and endothelial cell adhesion molecule 1 Homo sapiens 80-84 11882582-8 2002 The abrogating effects of quercetin and OR486 on the metabolism and antimitogenic effects of 2-hydroxyestradiol were mimicked by 20 micromol/L norepinephrine and isoproterenol, substrates for COMT. 2-hydroxyestradiol 93-111 catechol-O-methyltransferase Homo sapiens 192-196 11882583-9 2002 The growth inhibitory effects of 2-hydroxyestradiol were abrogated by quercetin and OR486 (two structurally dissimilar catechol-O-methyltransferase inhibitors), but not by ICI182780. 2-hydroxyestradiol 33-51 catechol-O-methyltransferase Homo sapiens 119-147 11701460-1 2001 Catechol-O-methyltransferase (COMT)-mediated methylation of 2-hydroxyestradiol (endogenous estradiol metabolite) to 2-methoxyestradiol (angiogenesis inhibitor) may be responsible for the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells (VSMCs). 2-hydroxyestradiol 60-78 catechol-O-methyltransferase Homo sapiens 30-34 11701460-1 2001 Catechol-O-methyltransferase (COMT)-mediated methylation of 2-hydroxyestradiol (endogenous estradiol metabolite) to 2-methoxyestradiol (angiogenesis inhibitor) may be responsible for the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells (VSMCs). 2-hydroxyestradiol 212-230 catechol-O-methyltransferase Homo sapiens 0-28 11701460-1 2001 Catechol-O-methyltransferase (COMT)-mediated methylation of 2-hydroxyestradiol (endogenous estradiol metabolite) to 2-methoxyestradiol (angiogenesis inhibitor) may be responsible for the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells (VSMCs). 2-hydroxyestradiol 60-78 catechol-O-methyltransferase Homo sapiens 0-28 11701460-1 2001 Catechol-O-methyltransferase (COMT)-mediated methylation of 2-hydroxyestradiol (endogenous estradiol metabolite) to 2-methoxyestradiol (angiogenesis inhibitor) may be responsible for the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells (VSMCs). 2-hydroxyestradiol 212-230 catechol-O-methyltransferase Homo sapiens 30-34 11701460-3 2001 We hypothesize that catecholamines may abrogate the vasoprotective effects of 2-hydroxyestradiol by competing for COMT and inhibiting 2-methoxyestradiol formation. 2-hydroxyestradiol 78-96 catechol-O-methyltransferase Homo sapiens 114-118 11559542-5 2001 COMT activity was assessed by determining the methylation of 2-OHE2, 4-OHE2, 2-OHE1, and 4-OHE1, using gas chromatography/mass spectrometry for quantitation of the respective methoxy products. 2-hydroxyestradiol 61-67 catechol-O-methyltransferase Homo sapiens 0-4 11606384-11 2001 This study is the first to show that O-methylation of 2-OH E2 by COMT is protective against oxidative DNA damage caused by 2-OH E2, a major oxidative metabolite of E2. 2-hydroxyestradiol 54-61 catechol-O-methyltransferase Homo sapiens 65-69 11606384-11 2001 This study is the first to show that O-methylation of 2-OH E2 by COMT is protective against oxidative DNA damage caused by 2-OH E2, a major oxidative metabolite of E2. 2-hydroxyestradiol 123-130 catechol-O-methyltransferase Homo sapiens 65-69 11559542-5 2001 COMT activity was assessed by determining the methylation of 2-OHE2, 4-OHE2, 2-OHE1, and 4-OHE1, using gas chromatography/mass spectrometry for quantitation of the respective methoxy products. 2-hydroxyestradiol 69-75 catechol-O-methyltransferase Homo sapiens 0-4 11741520-8 2001 This result suggests that in human liver microsomes CYP1A2 and CYP3A4 play an important role in 2-hydroxy estradiol formation. 2-hydroxyestradiol 96-115 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 52-58 11454902-10 2001 The activity of testosterone 6beta-hydroxylation (a selective probe for CYP3A4/5 activity) strongly correlated with the rate of formation of 2-OH-E2, 4-OH-E2, and several other hydroxyestrogen metabolites by both male and female liver microsomes. 2-hydroxyestradiol 141-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 11454902-10 2001 The activity of testosterone 6beta-hydroxylation (a selective probe for CYP3A4/5 activity) strongly correlated with the rate of formation of 2-OH-E2, 4-OH-E2, and several other hydroxyestrogen metabolites by both male and female liver microsomes. 2-hydroxyestradiol 150-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 11457662-11 2001 Using microsome preparation (from HK293 cell expressing monkey UGT1A01), the apparent K(m) values were 13, 5 and 6 microM for the conjugation of estradiol, 2-hydroxyestradiol and 2-hydroxyestrone, respectively, and were very similar to the values obtained with human UGT1A1. 2-hydroxyestradiol 156-174 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 267-273 11358677-4 2001 Using [35S]-phosphosadenosine phosphosulfate (PAPS) as cofactor, we showed that hEST1 efficiently metabolizes the transformation of 2-OH-E2 and 2-OH-E1. 2-hydroxyestradiol 132-139 sulfotransferase family 1E member 1 Homo sapiens 80-85 11741520-8 2001 This result suggests that in human liver microsomes CYP1A2 and CYP3A4 play an important role in 2-hydroxy estradiol formation. 2-hydroxyestradiol 96-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 11067738-4 2000 Among the nine enzymes (CYP1A1, 1A2, 2A6, 2C8, 2C9, 2C19, 2D6, 2E1, and 3A4) tested, CYP3A4 having a V(max)/K(m) (ml/min/nmol P450) value of 0.32 for production of 2-OH-E2 was shown to be the most suitable enzyme as the reagent. 2-hydroxyestradiol 164-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 11706521-1 2001 BACKGROUND: Catechol-O-methyltransferase (COMT) inactivates the estradiol metabolites, 2-hydroxy estradiol and 4-hydroxy estradiol. 2-hydroxyestradiol 87-106 catechol-O-methyltransferase Homo sapiens 12-40 11706521-1 2001 BACKGROUND: Catechol-O-methyltransferase (COMT) inactivates the estradiol metabolites, 2-hydroxy estradiol and 4-hydroxy estradiol. 2-hydroxyestradiol 87-106 catechol-O-methyltransferase Homo sapiens 42-46 11230349-4 2001 Treatment of porcine coronary artery endothelial cells for 4 to 24 hours with 0.001 to 1 micromol/L of estradiol, 2-hydroxyestradiol, or 2-methoxyestradiol concentration-dependently inhibited basal as well as serum-induced (2.5%), TNFalpha-induced (10 ng/mL), angiotensin II-induced (100 nmol/L), and thrombin-induced (4 U/mL) endothelin-1 synthesis. 2-hydroxyestradiol 114-132 tumor necrosis factor Mus musculus 231-239 11230349-4 2001 Treatment of porcine coronary artery endothelial cells for 4 to 24 hours with 0.001 to 1 micromol/L of estradiol, 2-hydroxyestradiol, or 2-methoxyestradiol concentration-dependently inhibited basal as well as serum-induced (2.5%), TNFalpha-induced (10 ng/mL), angiotensin II-induced (100 nmol/L), and thrombin-induced (4 U/mL) endothelin-1 synthesis. 2-hydroxyestradiol 114-132 endothelin 1 Mus musculus 327-339 11230349-7 2001 The inhibitory effects of 2-hydroxyestradiol and 2-methoxyestradiol on endothelin-1 release and mitogen-activated protein kinase activity were not blocked by ICI182780 (50 micromol/L), an estrogen receptor antagonist. 2-hydroxyestradiol 26-44 endothelin 1 Mus musculus 71-83 11230349-8 2001 Our findings indicate that the estradiol metabolites 2-hydroxyestradiol and 2-methoxyestradiol potently inhibit endothelin-1 synthesis by means of an estrogen receptor-independent mechanism. 2-hydroxyestradiol 53-71 endothelin 1 Mus musculus 112-124 8437370-1 1993 Effects of estradiol (E2) and catechol-estrogens (CEs: 2-OHE2 and 4-OHE2) on uterine ornithine decarboxylase (ODC) activity have been compared in immature rats. 2-hydroxyestradiol 66-72 ornithine decarboxylase 1 Rattus norvegicus 85-108 9827019-5 1998 Conversely, somatostatin (1 microM), adrenalin (1 microM), clonidine (2 microM), dexamethasone (0.4 microM), and 2-hydroxyestradiol (5 microM) decreased significantly the glucose-induced insulin release. 2-hydroxyestradiol 113-131 insulin Homo sapiens 187-194 9780030-6 1998 Estrogens, except for 2-OH-E2, partially prevented the inactivation of alcohol dehydrogenase (ADH) induced by ferrylMb. 2-hydroxyestradiol 22-29 aldo-keto reductase family 1 member A1 Homo sapiens 71-92 9018099-3 1996 We investigated the effects of 2-hydroxy-17beta-estradiol, a cell proliferator, and 2-methoxy-17beta-estradiol, a potent inhibitor of cell growth, on the levels and activity of p34(cdc2) and on the levels of PCNA, as well as on protein phosphorylation in MCF-7 cells. 2-hydroxyestradiol 31-57 general transcription factor IIH subunit 3 Homo sapiens 177-180 9018099-4 1996 2-Hydroxyestradiol increased p34(cdc2) activity at G1/S and elevated PCNA levels during S-phase. 2-hydroxyestradiol 0-18 general transcription factor IIH subunit 3 Homo sapiens 29-32 9018099-4 1996 2-Hydroxyestradiol increased p34(cdc2) activity at G1/S and elevated PCNA levels during S-phase. 2-hydroxyestradiol 0-18 cyclin dependent kinase 1 Homo sapiens 33-37 9018099-4 1996 2-Hydroxyestradiol increased p34(cdc2) activity at G1/S and elevated PCNA levels during S-phase. 2-hydroxyestradiol 0-18 proliferating cell nuclear antigen Homo sapiens 69-73 8274412-6 1993 The PR level, was slightly increased by treatment with 2-hydroxyestradiol (10%), whereas treatment with 4-hydroxyestradiol increased the PR level at 28%, compared to estradiol (100%). 2-hydroxyestradiol 55-73 progesterone receptor Homo sapiens 4-6 8386306-9 1993 At pH 7.5, the highest rates of catechol-O-methyltransferase-mediated methylation were observed with the catechol metabolites of 2-fluoroestradiol, 2-fluoro-4-hydroxyestradiol and 2-hydroxyestradiol (3780 and 2960 pmol/mg of protein/min, respectively). 2-hydroxyestradiol 180-198 catechol O-methyltransferase Mesocricetus auratus 32-60 1315925-9 1992 Purified rat liver cytochrome P450c also oxidized 2-hydroxyestradiol to 2,3-estradiol quinone. 2-hydroxyestradiol 50-68 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 19-35 2160607-4 1990 Since the methylation of 4-hydroxyestradiol by catechol-O-methyltransferase is inhibited by 2-hydroxyestradiol, it is proposed that a build up of 4-hydroxyestrogens precedes estrogen-induced cancer. 2-hydroxyestradiol 92-110 catechol-O-methyltransferase Homo sapiens 47-75 2174335-0 1990 2-hydroxyestradiol enhanced progesterone production by porcine granulosa cells: dependence on de novo cholesterol synthesis and stimulation of cholesterol side-chain cleavage activity and cytochrome P450scc messenger ribonucleic acid levels. 2-hydroxyestradiol 0-18 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 188-206 2174335-9 1990 2-OH-E2 also increased basal (by 2 to 3-fold) and FSH-stimulated (to 3.5-fold of FSH-treated controls) levels of mRNA for cytochrome P450scc. 2-hydroxyestradiol 0-7 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 122-140 2174335-10 1990 Collectively, our studies support the hypothesis that 2-OH-E2-enhanced progesterone biosynthesis by porcine granulosa cells is dependent on de novo cholesterol synthesis and is associated with increased levels of the mRNA encoding cytochrome P-450scc, which leads to increases in basal and gonadotropin-induced SCC activity. 2-hydroxyestradiol 54-61 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 231-250 2155347-5 1990 Uterine cytosolic COMT utilized 2-hydroxyestradiol (2-OH-OE2) as the preferred substrate as compared to 4-hydroxyoestradiol (4-OH-OE2). 2-hydroxyestradiol 32-50 catechol O-methyltransferase Oryctolagus cuniculus 18-22 35164068-0 2022 2-Hydroxyestradiol Overcomes Mesenchymal Stem Cells-Mediated Platinum Chemoresistance in Ovarian Cancer Cells in an ERK-Independent Fashion. 2-hydroxyestradiol 0-18 mitogen-activated protein kinase 1 Homo sapiens 116-119