ライフサイエンスコーパス: celastrol

1 wilforol A were prepared en route to racemic celastrol.

2 ns 1A and 1B were significantly increased by celastrol.

3 clic bis-enone during our synthetic study of celastrol.

4 ies have addressed the antitumor activity of celastrol.

5 eatment of PC-3 tumor-bearing nude mice with Celastrol (1-3 mg/kg/d, i.p., 1-31 days) resulted in sig

6 Further investigation of celastrol (3-hydroxy-24-nor-2-oxo-1 (10),3,5,7-friedelat

7 e transcriptional response in human cells to celastrol, a compound derived from traditional Chinese m

8 mRNA expression profiles similar to that of celastrol, a naturally occurring compound that we previo

9 o drug-screening methods, we discovered that Celastrol, a pentacyclic triterpene extracted from the r

10 Here, we report that celastrol, a potent anti-inflammatory pentacyclic triter

11 We describe here characteristics of celastrol, a quinone methide triterpene and an active co

12 Celastrol, a TAK1 inhibitor and anti-inflammatory compou

13 Whether celastrol, a triterpene from traditional Chinese medicin

14 Celastrol activated the yeast Yap1 oxidant defense trans

15 We show here that celastrol activates Hsf1 in Saccharomyces cerevisiae at

16 n addition to acute block of ion conduction, celastrol also alters the rate of ion channel transport

17 We found that celastrol also induced reactive oxygen species (ROS) gen

18 Celastrol also inhibited cell proliferation, while incre

19 Celastrol, an active compound extracted from the root ba

20 In the present study, we found that celastrol, an herb derivative with known anticancer, ant

21 Celastrol, an important natural product and Hsp90 inhibi

22 e as a template and discovered 2 new agents, celastrol and 4-hydroxy-2-nonenal, that effectively erad

23 abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced ap

24 ere treated with different concentrations of Celastrol and growth inhibition and target expression we

25 further testing and validation of the use of celastrol and the natural plant extract from Celastrus a

26 anti-arthritic activity of Celastrus-derived celastrol and the underlying mechanisms.

27 Nur77 as a critical intracellular target for celastrol and unravel a mechanism of Nur77-dependent cle

28 Celastrol, and for that matter any member of the celastr

29 f the clinical and mechanistic attributes of celastrol are similar to those of Celastrus extract.

30 We have identified the triterpenoid Celastrol as a potent low-molecular-weight inhibitor of

31 Proteolytic fingerprinting indicates celastrol binds to Hsp90 C-terminal domain to protect it

32 e examined the effects of the IKK inhibitors celastrol, BMS-345541, and parthenolide on bone cell fun

33 iptional activity was generally repressed by celastrol, but one distinct group of genes, enriched for

34 Celastrol can activate heat shock gene transcription syn

35 Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL

36 Our results show Celastrol can significantly inhibit the growth of T/E fu

37 ng on the compounds artemisinin, triptolide, celastrol, capsaicin, and curcumin.

38 Celastrol (Cel), a triterpenoid MAE isolated from Tripte

39 Thus, celastrus and celastrol controlled inflammation-induced bone damage by

40 ritis model of human RA, we demonstrate that celastrol derived from Celastrus has potent anti-arthrit

41 The quinone methide triterpene celastrol, derived from a traditional Chinese medicinal

42 Celastrol disrupts Hsp90-Cdc37 complex formation, wherea

43 n vitro and in vivo results demonstrate that celastrol disrupts p23 function by altering its three-di

44 -flavonoid phytochemicals tested, berberine, celastrol, ellagic acid, limonin, oleanolic acid, propyl

45 These results suggest that celastrols exhibit promise as a new class of pharmacolog

46 When mice received 0.5 mg/kg Celastrol for 4 times/week, significant growth inhibitio

47 tested celastrus and its bioactive component celastrol for this attribute in the adjuvant-induced art

48 romatic ketone reduction, or reduced form of Celastrol, had significantly decreased the proteasome-in

49 Furthermore, whether Celastrol has antitumor activity in vivo has never been

50 Although Celastrol has been shown to induce leukemia cell apoptos

51 In contrast, celastrol has no effects on trafficking of either CD4 or

52 In addition, withaferin A, unlike celastrol, has beneficial effects on glucose metabolism

53 Celastrol highlights the therapeutic potential of agents

54 ), the most active being the quinone methide celastrol (IC50 versus TbFPPS approximately 20 microM).

55 hat nucleophiles add to the pharmacophore of celastrol in a remarkable stereospecific manner.

56 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or

57 In vivo celastrol increased the HSF1 ChIP signal in hippocampus

58 cells with heat shock or the HSF1 stimulator celastrol increased TTR transcription in parallel with t

59 In addition, we found that celastrol induced the cell surface expression of both th

60 generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and conseq

61 Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-kappaB activation,

62 Celastrol inhibits Hsp90 ATPase activity without blockin

63 Here, we show that the small molecule celastrol inhibits the Hsp90 chaperoning machinery by in

64 Celastrol interfered with the establishment of the heat-

65 These results indicate that Celastrol is a leptin sensitizer and a promising agent f

66 Our results show that Celastrol is a natural proteasome inhibitor that has a g

67 Therefore, Celastrol is a promising candidate drug for T/E fusion e

68 Celastrol is a well known NF-kB inhibitor, and thus may

69 ivation of two major cell stress pathways by celastrol is conserved.

70 Celastrol is known to elicit a cellular stress response

71 This stereospecificity of celastrol may be important to its protein target selecti

72 These data suggest that celastrol may represent a new class of Hsp90 inhibitor b

73 In addition, celastrol modulated the expression of molecular chaperon

74 f the death receptor abolished the effect of celastrol on TRAIL-induced apoptosis.

75 tion of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in hum

76 Here, we report, for the first time, that Celastrol potently and preferentially inhibits the chymo

77 o inhibitory effects on osteoblast function, celastrol prevented IL1beta-induced TAK1 activation and

78 Furthermore, Celastrol prolongs the survival of mice in a model of an

79 Celastrol promotes Nur77 translocation from the nucleus

80 ds and triterpenoids, such as triptolide and celastrol, respectively.

81 e release may be widely inhibited during the celastrol response.

82 We report that celastrol's biological effects, including inhibition of

83 We therefore evaluated Celastrol's effects in vitro and in vivo in VCaP cells,

84 From a structure/function examination, the celastrol structure is remarkably specific and activates

85 e treatment of arthritic rats with celastrus/celastrol suppressed inflammatory arthritis and reduced

86 Celastrol suppresses food intake, blocks reduction of en

87 We demonstrate that Celastrol suppresses the proliferative potential of acut

88 dramatic transcriptional effects soon after celastrol treatment at a broad collection of both coding

89 Transcriptional profiling revealed that celastrol treatment induces a battery of oxidant defense

90 al activity and induction of apoptosis after Celastrol treatment.

91 ent inhibition of cell surface expression by celastrol underscores a need to evaluate drug candidates

92 ability to inhibit growth in vivo, 0.5 mg/kg Celastrol was used to treat mice bearing subcutaneous VC