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1 n2) as the gene most strongly upregulated by celastrol.
2 ced obesity and its therapeutic reduction by celastrol.
3 g the MC4R-independent antiobesity effect of celastrol.
4 wilforol A were prepared en route to racemic celastrol.
5 ns 1A and 1B were significantly increased by celastrol.
6 clic bis-enone during our synthetic study of celastrol.
7 ies have addressed the antitumor activity of celastrol.
8 eatment of PC-3 tumor-bearing nude mice with Celastrol (1-3 mg/kg/d, i.p., 1-31 days) resulted in sig
9                     Further investigation of celastrol (3-hydroxy-24-nor-2-oxo-1 (10),3,5,7-friedelat
10 e transcriptional response in human cells to celastrol, a compound derived from traditional Chinese m
11                                              Celastrol, a compound found in the roots of the Triptery
12                                              Celastrol, a compound reported to increase P. distasonis
13                                              Celastrol, a friedelane-type triterpene with significant
14  mRNA expression profiles similar to that of celastrol, a naturally occurring compound that we previo
15 o drug-screening methods, we discovered that Celastrol, a pentacyclic triterpene extracted from the r
16                                              Celastrol, a pentacyclic triterpene, is the most potent
17                         Here, we report that celastrol, a potent anti-inflammatory pentacyclic triter
18          We describe here characteristics of celastrol, a quinone methide triterpene and an active co
19                                              Celastrol, a TAK1 inhibitor and anti-inflammatory compou
20                                      Whether celastrol, a triterpene from traditional Chinese medicin
21                                              Celastrol activated the yeast Yap1 oxidant defense trans
22                            We show here that celastrol activates Hsf1 in Saccharomyces cerevisiae at
23 ll mice-in this study, we show that systemic celastrol administration substantially reduces food inta
24 n addition to acute block of ion conduction, celastrol also alters the rate of ion channel transport
25                                We found that celastrol also induced reactive oxygen species (ROS) gen
26                                              Celastrol also inhibited cell proliferation, while incre
27                                              Celastrol, an active compound extracted from the root ba
28          In the present study, we found that celastrol, an herb derivative with known anticancer, ant
29                                              Celastrol, an important natural product and Hsp90 inhibi
30 e as a template and discovered 2 new agents, celastrol and 4-hydroxy-2-nonenal, that effectively erad
31 abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced ap
32 ere treated with different concentrations of Celastrol and growth inhibition and target expression we
33 further testing and validation of the use of celastrol and the natural plant extract from Celastrus a
34 anti-arthritic activity of Celastrus-derived celastrol and the underlying mechanisms.
35 Nur77 as a critical intracellular target for celastrol and unravel a mechanism of Nur77-dependent cle
36 comparing the hypothalamic transcriptomes of celastrol and vehicle-treated DIO mice, we identified li
37                                              Celastrol, and for that matter any member of the celastr
38  important precursor for the biosynthesis of celastrol, and it is synthesized through the cyclization
39 f the clinical and mechanistic attributes of celastrol are similar to those of Celastrus extract.
40          We have identified the triterpenoid Celastrol as a potent low-molecular-weight inhibitor of
41         Proteolytic fingerprinting indicates celastrol binds to Hsp90 C-terminal domain to protect it
42 e examined the effects of the IKK inhibitors celastrol, BMS-345541, and parthenolide on bone cell fun
43 iptional activity was generally repressed by celastrol, but one distinct group of genes, enriched for
44 D; ligands that do not bind include C-DIM12, celastrol, camptothecin, IP7e, isoalantolactone, ethyl 2
45                                              Celastrol can activate heat shock gene transcription syn
46        Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL
47                             Our results show Celastrol can significantly inhibit the growth of T/E fu
48 ng on the compounds artemisinin, triptolide, celastrol, capsaicin, and curcumin.
49                                              Celastrol (Cel), a triterpenoid MAE isolated from Tripte
50                          Thus, celastrus and celastrol controlled inflammation-induced bone damage by
51 ritis model of human RA, we demonstrate that celastrol derived from Celastrus has potent anti-arthrit
52               The quinone methide triterpene celastrol, derived from a traditional Chinese medicinal
53                                              Celastrol disrupts Hsp90-Cdc37 complex formation, wherea
54 n vitro and in vivo results demonstrate that celastrol disrupts p23 function by altering its three-di
55 -flavonoid phytochemicals tested, berberine, celastrol, ellagic acid, limonin, oleanolic acid, propyl
56                   These results suggest that celastrols exhibit promise as a new class of pharmacolog
57                 When mice received 0.5 mg/kg Celastrol for 4 times/week, significant growth inhibitio
58 tested celastrus and its bioactive component celastrol for this attribute in the adjuvant-induced art
59 romatic ketone reduction, or reduced form of Celastrol, had significantly decreased the proteasome-in
60                         Furthermore, whether Celastrol has antitumor activity in vivo has never been
61                                     Although Celastrol has been shown to induce leukemia cell apoptos
62                                 In contrast, celastrol has no effects on trafficking of either CD4 or
63            In addition, withaferin A, unlike celastrol, has beneficial effects on glucose metabolism
64                                              Celastrol highlights the therapeutic potential of agents
65 ), the most active being the quinone methide celastrol (IC50 versus TbFPPS approximately 20 microM).
66 hat nucleophiles add to the pharmacophore of celastrol in a remarkable stereospecific manner.
67 e are completely resistant to the effects of celastrol in leptin sensitization and treatment of obesi
68     Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or
69 viously unappreciated mechanism of action of celastrol in the regulation of energy homeostasis and hi
70                                              Celastrol increased LCN2 protein levels in hypothalamus,
71                                      In vivo celastrol increased the HSF1 ChIP signal in hippocampus
72 cells with heat shock or the HSF1 stimulator celastrol increased TTR transcription in parallel with t
73                   In addition, we found that celastrol induced the cell surface expression of both th
74  generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and conseq
75 However, the genes and pathways that mediate celastrol-induced leptin sensitization have not been ful
76               Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-kappaB activation,
77                                              Celastrol inhibits Hsp90 ATPase activity without blockin
78        Here, we show that the small molecule celastrol inhibits the Hsp90 chaperoning machinery by in
79                                              Celastrol interfered with the establishment of the heat-
80                  These results indicate that Celastrol is a leptin sensitizer and a promising agent f
81                                              Celastrol is a leptin-sensitizing agent with profound an
82                        Our results show that Celastrol is a natural proteasome inhibitor that has a g
83                                   Therefore, Celastrol is a promising candidate drug for T/E fusion e
84                                              Celastrol is a well known NF-kB inhibitor, and thus may
85 ivation of two major cell stress pathways by celastrol is conserved.
86                                              Celastrol is known to elicit a cellular stress response
87                    This stereospecificity of celastrol may be important to its protein target selecti
88                      These data suggest that celastrol may represent a new class of Hsp90 inhibitor b
89                                 In addition, celastrol modulated the expression of molecular chaperon
90 f the death receptor abolished the effect of celastrol on TRAIL-induced apoptosis.
91 ylamino-17-demethoxygeldanamycin 17-AGG, and celastrol) or short hairpin RNAs (shRNAs) significantly
92 tion of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in hum
93    Here, we report, for the first time, that Celastrol potently and preferentially inhibits the chymo
94 o inhibitory effects on osteoblast function, celastrol prevented IL1beta-induced TAK1 activation and
95    In this study, transcriptome data of four celastrol-producing plants from Celastraceae were used t
96                                 Furthermore, Celastrol prolongs the survival of mice in a model of an
97                                              Celastrol promotes Nur77 translocation from the nucleus
98 r, the underlying neural mechanisms by which celastrol reduces obesity remain unclear.
99 ds and triterpenoids, such as triptolide and celastrol, respectively.
100 e release may be widely inhibited during the celastrol response.
101 leukin-1 receptor 1 (IL1R1) as a mediator of celastrol's action by using temporally resolved analysis
102                               We report that celastrol's biological effects, including inhibition of
103                       We therefore evaluated Celastrol's effects in vitro and in vivo in VCaP cells,
104                             The mechanism of celastrol's leptin-sensitizing and antiobesity effects h
105 , we conclude that IL1R1 is a gatekeeper for celastrol's metabolic actions.
106                                 Importantly, celastrol steadily increased sympathetic nerve activity
107   From a structure/function examination, the celastrol structure is remarkably specific and activates
108 e treatment of arthritic rats with celastrus/celastrol suppressed inflammatory arthritis and reduced
109                                              Celastrol suppresses food intake, blocks reduction of en
110                          We demonstrate that Celastrol suppresses the proliferative potential of acut
111  of diet-induced obesity, nor the ability of celastrol to promote weight loss and improve obesity-ass
112 nalysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice.
113  dramatic transcriptional effects soon after celastrol treatment at a broad collection of both coding
114      Transcriptional profiling revealed that celastrol treatment induces a battery of oxidant defense
115 al activity and induction of apoptosis after Celastrol treatment.
116 ent inhibition of cell surface expression by celastrol underscores a need to evaluate drug candidates
117                                Unexpectedly, celastrol upregulated proinflammatory cytokines without
118 ability to inhibit growth in vivo, 0.5 mg/kg Celastrol was used to treat mice bearing subcutaneous VC

 
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