ライフサイエンスコーパス: Wy-14,643

1 and mice treated with the PPARalpha agonist-WY-14,643.

2 e PDK4 message comparable to that induced by WY-14,643.

3 ollowing oral administration of the fibrate, Wy-14,643.

4 treated with the specific PPARalpha agonist WY-14,643.

5 H OX) is the source of oxidants increased by Wy-14,643.

6 by the PPARalpha activators fenofibrate and Wy-14,643.

7 oxicity despite activation of PPARalpha with Wy-14,643.

8 fat-free diet with the PPARalpha-activator, WY 14, 643.

9 n cell proliferation due to a single dose of Wy-14,643 (100 mg/kg) were prevented completely when rat

10 ted by activation of PPARalpha by the ligand Wy-14,643 ([4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]

11 WY-14,643, 5,8,11,14-eicosatetraynoic acid, LY-171883, a

12 dent carcinogen and peroxisome proliferator, WY-14,643 (500 ppm, 1 month).

13 of rats with the specific PPARalpha agonist WY-14,643 (8 days) did not affect the trophic response o

14 2,3-xylidino)-2-pyrimidinylthio acetic acid (Wy-14,643), a potent peroxisome proliferator, caused rap

15 s induced in the liver of rats that were fed Wy-14,643, a peroxisome proliferator and inducer of rode

16 Pbp(DeltaLiv) mice, chronically exposed to Wy-14,643, a PPARalpha ligand, revealed a striking proli

17 treated mice injected with tumor cells with Wy-14,643, a PPARalpha-selective ligand.

18 It was further found that feeding rats WY-14,643, a selective agonist for the peroxisome prolif

19 In livers of wild-type mice, Wy-14,643 activated NF-kappaB, followed by an increase i

20 ults are consistent with the hypothesis that Wy-14,643 activates NADPH OX, which leads to NF-kappaB-m

21 Wy-14,643 activation of PPARalpha induced hepatic FGF21,

22 y we determined the effect of clofibrate and Wy-14,643, activators of PPARalpha, on hyperproliferativ

23 ly weak, nonthiazolidinedione PPAR activator WY 14,643 also inhibited leptin expression, but was appr

24 nd the prototypical peroxisome proliferator, WY-14, 643, also enhanced COX-2 expression.

25 ator-activated receptor (PPAR) alpha ligands Wy-14,643 and ciprofibrate increase the Cidea mRNA level

26 Both Wy-14,643 and ciprofibrate occupied the ligand binding p

27 genic mice with the peroxisome proliferators Wy-14,643 and clofibric acid resulted in a less than two

28 effective against the stimulatory effects of WY-14,643 and fatty acids.

29 ctivated receptor-alpha (PPAR-alpha) agonist WY-14,643 and the glucocorticoid dexamethasone increased

30 of WY 14,643 from the oxidized (hAR*NADP(+)*WY 14,643) and reduced (hAR*NADPH*WY 14,643) ternary com

31 Ralpha is increased by treatment with the PP Wy-14,643 as well as the PKC activator phorbol myristol

32 ns demonstrate how fibrate molecules such as WY 14,643, besides being valued as agonists for PPAR, al

33 report here that synthetic PPARalpha ligands Wy-14,643, ciprofibrate, clofibrate, and others induce t

34 e (ACOX::CAT) with peroxisome proliferators, WY 14,643, clofibrate, di(2-ethylhexyl) phtalhate, and a

35 ) wild-type mice fed either ciprofibrate- or Wy-14, 643-containing diets.

36 Finally, when mice were fed a Wy-14,643-containing (0.1%) diet for 7 days, the increas

37 The down-regulation of the P450 2C11 by WY-14,643 could be reproduced in cultured rat hepatocyte

38 Treatment with the fibrate Wy 14,643 decreased apoA-I serum levels and hepatic mRNA

39 pressing mouse model, which is responsive to Wy-14,643 effects on beta-oxidation and serum triglyceri

40 The peroxisome proliferator, WY 14,643 exhibits a pure non-competitive inhibition pat

41 Kd values for the dissociation of WY 14,643 from the oxidized (hAR*NADP(+)*WY 14,643) and

42 D-1 mice treated with dietary fenofibrate or Wy-14,643 had fivefold-higher lipopolysaccharide (LPS)-i

43 reover, when Kupffer cells were treated with Wy-14,643 in vitro, superoxide production was increased

44 as markedly induced by the PPARalpha agonist Wy-14,643 in wild-type mice but not in Ppara-null mice.

45 iver weight and cell proliferation caused by Wy-14,643 in wild-type mice was blocked in p47phox-null

46 treatment with the potent PPARalpha agonist Wy-14,643 in wild-type mice.

47 2,3-xylidino)-2-pyrimidinyl)thioacetic acid (WY-14,643) in +/dw mice.

48 The PPAR activator, WY-14,643 increased COX-2 expression.

49 ute exposure to the potent Pparalpha agonist Wy-14,643, indicating a role for Pparalpha in regulating

50 rmore, LPS markedly decreased both basal and Wy-14,643-induced expression of acyl-CoA synthetase, a w

51 In these Pbp(DeltaLiv) mice, none of the Wy-14,643-induced hepatic adenomas and hepatocellular ca

52 ssential partner of PPARalpha, in modulating WY-14,643-induced hepatocyte proliferation and cholestas

53 RXRalpha deficiency protected the mice from WY-14,643-induced liver injury.

54 In addition, inhibitors of PKC decreased Wy-14,643-induced PPARalpha activity in a variety of rep

55 a, -delta, and -zeta affected both basal and Wy-14,643-induced PPARalpha activity.

56 al role of hepatocyte RXRalpha in regulating WY-14,643-mediated cell cycle progression as well as bil

57 WY-14,643-mediated induction of the small heterodimer pa

58 peritoneal macrophage studies indicate that Wy-14,643 modestly decreased TNF expression in vitro.

59 in immortalized mouse liver cells by the PPs Wy-14, 643, monoethylhexyl phthalate, ciprofibrate ethyl

60 ructurally diverse synthetic ligands such as Wy-14,643 or by unmetabolized endogenous ligands resulti

61 dation enzymes, with the experimental ligand Wy-14,643 or the clinically used fibrate drug fenofibrat

62 hat incubation of quiescent ML457 cells with Wy-14,643 resulted in the appearance of two tyrosine-pho

63 The ternary complex structure of hAR*NADP(+)*WY 14,643 reveals the first structural evidence of a fib

64 AR*NADP(+)*WY 14,643) and reduced (hAR*NADPH*WY 14,643) ternary complexes are comparable to each othe

65 a PPARalpha ligand, such as ciprofibrate or Wy-14,643, the SRC-1(-/-) mice displayed typical pleiotr

66 These results show that Wy-14,643, through PPARalpha, post-transcriptionally dow

67 Administration of the fibrate Wy 14,643 to wild-type mice results in marked depression

68 teomic approach to analyze liver proteins of Wy-14,643-treated and AOX(-/-) mice.

69 resence of heme and arachidonic acid, and 2) WY-14,643-treated cells were depleted of intracellular G

70 PPARalpha-deficient mice were unaffected by Wy 14,643 treatment.

71 WY-14,643 treatment also induced cholestasis and liver i

72 Wy-14,643 treatment decreased HNF4alpha protein levels i

73 Wy-14,643 treatment did not inhibit let-7C or induce c-m

74 WY-14,643 treatment induced hepatomegaly in wild type (W

75 Furthermore, neither WY-14,643 treatment nor RXRalpha deficiency affected apo

76 Wy-14,643 treatment stimulated STAT3 ubiquitination lead

77 f ERK phosphorylation and junB expression by Wy-14,643 was also seen in rat hepatocytes.

78 s whose mRNA levels are modulated by the PPC WY-14,643 (WY) in rat liver.

79 ll mice pretreated with the PPAR pan-agonist WY-14,643 (WY) were protected from damage to cadmium and

80 ic acid (AGN194,204) or the PPAR pan-agonist WY-14,643 (WY; pirinixic acid) and compared with the pro