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 olism of catecholamine neurotransmitters and catechol estrogens.

3 ting insulin secretion than any other tested catechol estrogens.

4 Phase II metabolic inactivation pathway for catechol estrogens.

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

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

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

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

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

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

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

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

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

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

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

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

17 Catechol estrogens also generated sustained elevations i

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

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

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

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

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

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

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

25 Catechol estrogens are implicated as possible causative

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

27 Catechol estrogens are reactive to DNA and form several

28 Catechol estrogens are steroid metabolites that elicit p

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

30 Specific catechol estrogen binding was competitively inhibited by

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

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

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

34 s to target optimal conditions for detecting catechol estrogens (CEs)-adducted human serum albumin (H

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

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

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

38 We show that catechol estrogens, hydroxylated at positions C2 and C4

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

40 atalytic efficiencies differ with respect to catechol estrogen inactivation.

41 Catechol estrogen inhibition is non-competitive with res

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

43 Catechol estrogens may mediate estrogen-induced carcinog

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

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

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

47 fects of major natural estrogen metabolites, catechol estrogens, on insulin secretion in pancreatic b

48 In insulin-secreting cells, catechol estrogens produced rapid activation of calcium

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

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

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

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

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

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

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

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

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

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