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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
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
16 n addition to acute block of ion conduction, celastrol also alters the rate of ion channel transport
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
27 Nur77 as a critical intracellular target for celastrol and unravel a mechanism of Nur77-dependent cle
29 f the clinical and mechanistic attributes of celastrol are similar to those of Celastrus extract.
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
40 ritis model of human RA, we demonstrate that celastrol derived from Celastrus has potent anti-arthrit
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
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
54 ), the most active being the quinone methide celastrol (IC50 versus TbFPPS approximately 20 microM).
56 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or
58 cells with heat shock or the HSF1 stimulator celastrol increased TTR transcription in parallel with t
60 generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and conseq
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
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
88 dramatic transcriptional effects soon after celastrol treatment at a broad collection of both coding
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
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