ライフサイエンスコーパス: catechol estrogen

1 ally stable analogs of 4-hydroxyestradiol, a catechol estrogen.

2 Phase II metabolic inactivation pathway for catechol estrogens.

3 olism of catecholamine neurotransmitters and catechol estrogens.

4 chol-O-methyltransferase (COMT), inactivates catechol estrogens.

5 Like catechol estrogens, 16alpha-hydroxylated estrogens are h

6 eptor affinity and pS2 gene induction to the catechol estrogen 2-hydroxyestradiol and may prove usefu

7 Catechol estrogens (2- or 4-hydroxyestradiol and 2- or 4

8 ive metabolism of 17beta-estradiol (E(2)) to catechol estrogens (2-OHE(2) and 4-OHE(2)) and highly re

9 tive metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and 4-OHE2) and estrogen quin

10 ass spectrometry to measure E2, the 2- and 4-catechol estrogens (2-OHE2, 4-OHE2), and the depurinatin

11 of 17beta-estradiol (E2) and estrone (E1) to catechol estrogens (2-OHE2, 4-OHE2, 2-OHE1, and 4-OHE1)

12 s (CE) of estrone (E1) and estradiol (E2) to catechol estrogen-3,4-quinones (CE-3, 4-Q) results in el

13 In addition to 17beta-E2, the catechol estrogen 4-hydroxyestradiol (4OHE2) has been sh

14 ed similar estrogen receptor affinity as the catechol estrogen, 4-hydroxyestradiol, and may prove use

15 YP1B1 O-demethylated the methoxyestrogens to catechol estrogens according to Michaelis-Menten kinetic

16 e associated with significant differences in catechol estrogen and methoxy estrogen levels and, there

17 fections, including roles for metabolites of catechol estrogen and oxysterols of parasite origin as i

18 igations on the potential biological role of catechol estrogens and also enable further examination o

19 The concentration gap between catechol estrogens and GSH-estrogen conjugates may resul

20 mediate ERalpha/beta-independent effects of catechol estrogens and their metabolites.

21 etry to measure the parent hormone E(2), the catechol estrogens, and the GSH conjugates.

22 ese helminth infections, including roles for catechol estrogen- and oxysterol-metabolites of parasite

23 Catechol estrogens are implicated as possible causative

24 nic activity in vivo; on the other hand, the catechol estrogens are prone to further oxidative metabo

25 Catechol estrogens are reactive to DNA and form several

26 Catechol estrogens are steroid metabolites that elicit p

27 n of methoxyestrogens both yielded identical catechol estrogens as products, we used deuterated E2 (E

28 Specific catechol estrogen binding was competitively inhibited by

29 TP, and we solved the crystal structure of a catechol estrogen bound to a soluble adenylyl cyclase fr

30 ing was competitively inhibited by unlabeled catechol estrogens, but not by 17beta-E2 or the estrogen

31 that oxidation of the carcinogenic 4-hydroxy catechol estrogens (CE) of estrone (E1) and estradiol (E

32 We show here that catechol estrogens directly inhibit soluble adenylyl cyc

33 DNA damage caused by catechol estrogens has been shown to play an etiologic r

34 leads to a chelating interaction between the catechol estrogen hydroxyl groups and the catalytic magn

35 We examined the carcinogenic potential of catechol estrogen in an experimental model previously re

36 atalytic efficiencies differ with respect to catechol estrogen inactivation.

37 Catechol estrogen inhibition is non-competitive with res

38 The catechol estrogen is bound to a newly identified, conser

39 Catechol estrogens may mediate estrogen-induced carcinog

40 f labeled catechol estrogen, suggesting that catechol estrogen metabolites were responsible for the s

41 e compelling evidence for the interaction of catechol estrogen metabolites with a novel binding prote

42 beta-estradiol (E2) through the formation of catechol estrogen metabolites, 2-OH-E2 and 4-OH-E2, and

43 P1 but overall yielded only one-tenth of the catechol estrogen production.

44 can be metabolized to reactive quinones, the catechol estrogen quinones (CEQs) modify DNA by redox cy

45 Catechol estrogen quinones, on the other hand, are suffi

46 nts revealed extensive metabolism of labeled catechol estrogen, suggesting that catechol estrogen met

47 gen-induced cancers because COMT inactivates catechol estrogens that have cancer-promoting activities

48 s a means to increase estrogen metabolism to catechol estrogens, then treated with estradiol (E2) +/-

49 nsferase (COMT) catalyzes the methylation of catechol estrogens to methoxy estrogens, which simultane

50 thyltransferase catalyzes the methylation of catechol estrogens to methoxyestrogens (2-MeOE2, 2-OH-3-

51 could be mediating the biological effects of catechol estrogens using enzymatically synthesized, radi

52 yme (reductant) and, unlike redox cycling of catechol estrogens, without the production of reactive o