ライフサイエンスコーパス: SB203580

1 y reversed by a specific p38 MAPK inhibitor (SB203580).

2 ylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580).

3 ors of ERK (U0126), JNK (SP600125), and p38 (SB203580).

4 ylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580).

5 r (PD98059) but not by a p38-MAPK inhibitor (SB203580).

6 g Cox-2 and interleukin-8, was attenuated by SB203580.

7 oxidative stress was blocked by SP600125 or SB203580.

8 of these effects were blocked by SP600125 or SB203580.

9 her siRNA targeting p38 or to treatment with SB203580.

10 duction, and this was blocked by SP600125 or SB203580.

11 gen-activated protein (MAP) kinase inhibitor SB203580.

12 ha t2 or p38 alpha, and to the p38 inhibitor SB203580.

13 s obviously attenuated by p38-MAPK inhibitor SB203580.

14 resence and absence of a p38 MAPK inhibitor, SB203580.

15 sely mimicked that of the p38 MAPK inhibitor SB203580.

16 A 2-15-fold; these effects were abrogated by SB203580.

17 gG aPL and this effect was also inhibited by SB203580.

18 by 8-bromo-cAMP and was inhibited by H89 or SB203580.

19 rogated by inhibition of p38 MAP kinase with SB203580.

20 s decreased; these effects were prevented by SB203580.

21 ated NF-kappaB when p38 MAPK is inhibited by SB203580.

22 eated with aPL and thrombin, with or without SB203580.

23 ent with protein kinase inhibitors UCN-01 or SB203580.

24 t was completely abrogated by treatment with SB203580.

25 n-activated protein kinase inhibitor (MAPK), SB203580.

26 he absence and presence of the p38 inhibitor SB203580.

27 fluoromethyl ketone or the p38MAPK inhibitor SB203580.

28 pharmacologically by blocking p38 MAPK using SB203580.

29 toxin and a selective p38 kinase inhibitor, SB203580.

30 y was reduced by the p38-selective inhibitor SB203580.

31 8 mitogen-activated protein kinase inhibitor SB203580.

32 PD98059, LY294002, NAC, curcumin, EGCG, and SB203580.

33 or treating cells with a p38 MAPK inhibitor, SB203580.

34 atase inhibitors and the p38(MAPK) inhibitor SB203580.

35 e energy source or by the p38 MAPK inhibitor SB203580.

36 , ERK1/2 inhibitor PD98059, or p38 inhibitor SB203580.

37 can be blocked by inhibition of p38MAPK with SB203580.

38 d with heat-killed L. major plus CpG without SB203580.

39 K(ir)3.1-ir was blocked by the p38 inhibitor SB203580.

40 te, but not by the p38 map kinase inhibitor, SB203580.

41 ha expression was blocked by minocycline and SB203580.

42 xpression was blocked by minocycline but not SB203580.

43 rlift culture and partially was inhibited by SB203580.

44 ctivity and was blocked by the p38 inhibitor SB203580.

45 NMDA (2-200 nmol), SB203580 (0.2-10 nmol, an inhibitor of p38 MAP kinase),

46 A well-validated p38 MAP kinase inhibitor SB203580 (0.5-5muM) cancelled the effect of TGF-beta1 in

47 However, SB203580 (1 micromol/L) did not prevent the phosphorylat

48 mice, the p38-MAPK catalytic site inhibitor SB203580 (1 micromol/L) diminished phosphorylation durin

49 ogen-activated protein kinase inhibition via SB203580 (10 mg/kg).

50 50 muM), STAT3 (S31-201, 10 muM), p38 MAPK (SB203580, 10 muM), and ERK1/2 (U0126, 10 muM) resulted i

51 tion and find that inhibition of p38 MAPK by SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-

52 -nitrophenyl)-5-(4-pyridyl)-1H-imidazole] or SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-

53 SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-

54 was rescued in the presence of an inhibitor (SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-

55 ctivation, we administered the p38 inhibitor SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-

56 ly, intrathecal infusion of a p38 inhibitor (SB203580, 4 mg/d) was effective only if it was started b

57 gen-activated protein (MAP) kinase inhibitor SB203580 (5 microM) and the c-Jun NH2-terminal kinase (J

58 U0126, and the MAPK (p38 isoform) inhibitor, SB203580 (9+/-1 and 15+/-1 vs. -1+/-1 and -1+/-1 vs. 5+/

59 rakis(4-benzoic acid)porphyrin chloride) and SB203580 (a known suppressor ofUcp1expression) decreased

60 ocarbamate (PDTC, an NF-kappaB inhibitor) or SB203580 (a MAPK inhibitor) showed significantly improve

61 d AG490 (a Janus kinase 2 [JAK2] inhibitor), SB203580 (a p38 inhibitor), and PD98059 (a MEK1 inhibito

62 2 transcription by bacteria was inhibited by SB203580 (a specific inhibitor of p38 MAPK) and by a dom

63 up-regulation was significantly inhibited by SB203580 (a specific inhibitor of p38 MAPK) and by MG132

64 emonstrate that BIRB796, in combination with SB203580, a compound that inhibits p38alpha and p38beta,

65 of either the p38 kinase-specific inhibitor SB203580, a dominant negative p38 mutant, the SAPK/JNK i

66 Treatment with SB203580, a mitogen-activated protein kinase inhibitor,

67 However, SB203580, a p38 inhibitor, did not prevent relocalizatio

68 SB203580, a p38 inhibitor, prevented p38 activation and

69 tol-3 (PI3) kinase, respectively, but not by SB203580, a p38 kinase inhibitor.

70 eta type I receptor (TbetarI) inhibitor, and SB203580, a p38 MAPK inhibitor, impede Tgfbeta2 inductio

71 This induction was blocked by SB203580, a p38 MAPK inhibitor, which also decreased the

72 SB203580, a p38 MAPK pathway inhibitor, and JNK inhibito

73 tagonist of bone morphogenetic protein-4, or SB203580, a phospho-p38 inhibitor.

74 ls, and treatment of SHP-2 mutant cells with SB203580, a selective inhibitor for p38 kinase, partiall

75 Interestingly, SB203580, a selective inhibitor of p38 MAPK, blocked STI

76 We show here that SB203580, a selective inhibitor of the p38 MAPK, and PD0

77 Treatment of melanoma cells with SB203580, a selective inhibitor of the p38 mitogen-activ

78 Treatment of cardiomyocytes with SB203580, a selective p38 MAPK inhibitor, significantly

79 SB203580, a specific inhibitor of p38 MAPK, partially su

80 SB203580, a specific inhibitor of p38 MAPK, reduced TNF-

81 d several chemical inhibitors and found that SB203580, a specific inhibitor of p38MAPK, significantly

82 NK inhibitor SP600125, but not p38 inhibitor SB203580, ablated this response.

83 Furthermore, addition of the p38 inhibitor SB203580 abolished abnormal epidermal differentiation wi

84 0126, but not the p38-MAPK pathway inhibitor SB203580, abolished the effect of Q79R-Shp2 on cushion o

85 Inhibition of p38 with SB203580 abrogated adiponectin-induced IFN-gamma product

86 Only the p38 MAPK inhibitor, SB203580, abrogated ESAT-6-mediated inhibition of IFN-ga

87 Neither SP600125 nor SB203580 affected CYP2E1 activity or protein levels.

88 NO production was not the mechanism by which SB203580 afforded protection against the BSO plus CYP2E1

89 hibition of p44/42 ERKs (PD98059), p38 MAPK (SB203580), Akt, and PI3K (LY294002), individually or com

90 SB203580 also inhibited LPS-induced production of IL-1be

91 SB203580 an inhibitor of p38MAPK specifically induced ca

92 lsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580), an inhibitor of p38 kinase, had little effect

93 responses are maintained in the presence of SB203580, an agent that inhibits p38 alpha and beta, fur

94 ell invasion, which in turn was inhibited by SB203580, an inhibitor of p38 MAP kinase.

95 acellular calcium and is highly sensitive to SB203580, an inhibitor of p38 MAPK as well as a related

96 SB203580, an inhibitor of p38 MAPK, suppressed HGF-induc

97 death in MKP-1-deficient MEFs was rescued by SB203580, an inhibitor of p38 MAPK.

98 h were enhanced by inhibition with 10 microM SB203580 and 10 muM PD98059, respectively.

99 se MKK3/6 and inhibited by the p38 inhibitor SB203580 and a latter phase that was coincident with MKK

100 but is diminished by the p38-MAPK inhibitors SB203580 and A304000 (P > 0.99).

101 n of phospho-p38 by two specific inhibitors, SB203580 and BIRB796, led to a significant decrease in a

102 In rabbit hearts SB203580 and chelerythrine reduced Hsp70i message levels

103 NER in cells treated with p38 MAPK inhibitor SB203580 and found that p38 MAPK is required for the pro

104 lon with chelerythrine, p38 MAP kinase, with SB203580 and JUN kinase with curcumin abolished the card

105 (pY418)Src-ir; this increase was blocked by SB203580 and not evident in KOR(S369A)-GFP expressing At

106 AP kinase (p38 MAPK) as, it was inhibited by SB203580 and overexpression of dominant-negative p38alph

107 ing pathways by pretreatment with inhibitors SB203580 and PD98059 and subsequent stimulation with HGF

108 imulated p38 MAPK and ERK1/2 activation, and SB203580 and PD98059 blunted IL-17-mediated NF-kappaB an

109 MAP) kinase (MAPK) pharmacologic antagonists SB203580 and PD98059.

110 nhibition of p38 and NF-kappaB activation by SB203580 and pyrrolidine dithiocarbamate, respectively,

111 ce of selective inhibitors of MAPK pathways (SB203580 and SB202190 for p38, SP600125 for JNK, and U01

112 Inhibition of p38 MAPK activity by SB203580 and SB202190 resulted in decreased iPLA2 activi

113 e blocked by the specific inhibitors of p38, SB203580 and SB202190, or a dominant negative p38.

114 e suppressed by the p38alpha/beta inhibitors SB203580 and SB202590 or by expression of a p38alpha siR

115 Results from SB203580 and siRNA experiments suggest the stress kinase

116 Using specific kinase inhibitors (SB203580 and SP600125), we showed the central role of p3

117 rotein kinase (MAPK) inhibitors SB202190 and SB203580 and the general protein synthesis inhibitor cyc

118 The p38 and ERK pathway inhibitors SB203580 and U0126 reversed the repressive effect of IL-

119 Using the protein kinase inhibitors SB203580 and U0126, we also show that the ERK and p38 pa

120 heterologous desensitization was blocked by SB203580 and was not evident in cells expressing KOR(S36

121 -1/2 inhibitor (PD98059) or a p38 inhibitor (SB203580) and an anti-CTGF antibody to analyze the signa

122 harmacological inhibitors of p38 MAPK (i.e., SB203580) and c-Jun N-terminal kinase (JNK, SP600125), s

123 g mitogen-activated protein kinase (p38MAPK; SB203580) and RNAi silencing of SNAI1.

124 ffeine), one induced dark-like phase shifts (SB203580), and two did not induce phase shifts at all (U

125 th MEK inhibitor U0126, p38 kinase inhibitor SB203580, and JNK inhibitor SP600125 significantly atten

126 aurosporine, genistein, bisindolylmaleimide, SB203580, and PD98059).

127 of Wisconsin solution containing the p38IH, SB203580, and Pefabloc (n=6) or vehicle (dimethyl sulfox

128 SB431542, the p38 antagonist SB203580, and siRNA-mediated reduction of Smad2 and p38a

129 nt, was attenuated in the presence of U0126, SB203580, and SP600125 in a dose-dependent manner and wa

130 rs PD98059 and U0126, the p38 MAPK inhibitor SB203580, and the c-Jun NH2-terminal kinase inhibitor SP

131 The p38 MAPK antagonist SB203580, and their inactive analog SB202474, also atten

132 lls rapidly induces PKB/Akt activation in an SB203580- and suramin-sensitive manner, suggesting p38 M

133 ly available p38 catalytic inhibitors (e.g., SB203580) are poorly effective and cause toxicity.

134 in kinase (p38 MAPK) with either SB202190 or SB203580 as well as overexpression of a dominant negativ

135 Pretreatment with the p38 inhibitor SB203580 attenuated 23% of LPS-regulated genes and 18% o

136 umab stimulated sustained p38 activation and SB203580 attenuated the TSP-1 upregulation induced by tr

137 hibitors (BIRB796, Tarceva, NU6102, Gleevec, SB203580, balanol, H89, PP1).

138 nd drug-resistant p38alpha-MAPK, lacking the SB203580 binding site, was phosphorylated when H9c2 myob

139 The p38 MAPK inhibitor SB203580 blocked AICAR-induced increase in VEGF mRNA and

140 Inhibition of p38 by SB203580 blocked migration of epithelial cells almost co

141 However, the p38 MAPK inhibitor SB203580 blocked platelet aggregation and phosphorylatio

142 ERK1/2 inhibition with PD98059 or p38 with SB203580 blocked the effect of LXA4 on wound healing.

143 n of p38alpha with a p38-specific inhibitor (SB203580) blocked LITAF nuclear translocation and reduce

144 the hepatocytes with the p38 MAPK inhibitor, SB203580, blocked the arachidonic acid inhibition of G6P

145 SB203580 both inhibited the initiation of ETE and altere

146 ylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580) but not by the specific inhibitor 2'-amino-3'-

147 inhibitors specific for MEK (U0126) and p38 (SB203580), but not JNK (SP600125).

148 mitogen-activated protein kinase (MAPK) with SB203580, but not by inhibition of PI3 kinase with wortm

149 Pretreatment with the p38MAPK inhibitor SB203580, but not the AMP-activated protein kinase inhib

150 Treating the cells with p38 MAPK inhibitor SB203580, but not with MEK inhibitor PD98058, reduced CC

151 hrine reduced Hsp70i message levels, whereas SB203580, chelerythrine, and curcumin reversed the subce

152 Furthermore, pretreatment of platelets with SB203580 completely abrogated the aPL-mediated enhanced

153 in vivo administration of p38 MAPK inhibitor SB203580 completely blocked cocaine-induced NET up-regul

154 inhibitor RO318220 and p38 kinase inhibitor SB203580 completely blocked heregulin-beta1-mediated act

155 A p38 MAP kinase inhibitor, SB203580, completely inhibited DDR1b-mediated HLA-DR exp

156 Signal transduction pathway inhibitors (SB203580, curcumin, and PD98059) implicated p38 and JNK,

157 Furthermore, SB203580 decreased the arachidonic acid-mediated Ser(307

158 ed with the p38 alpha and p38 beta inhibitor SB203580 demonstrated significant inhibition of otitis m

159 our data showing that the p38MAPK inhibitor SB203580 dephosphorylates integrin beta1 and that bindin

160 SB203580 did not act through inhibition of AKT (PKB) as

161 SB203580 did not prevent the loss of GSH nor lower the i

162 SB203580 did not reverse ESAT-6-mediated inhibition of I

163 regulated kinase (ERK, PD98059) or p38 MAPK (SB203580) did not affect IL-1 beta-mediated suppression

164 mitogen-activated protein kinase inhibitor, SB203580, did not.

165 ctivity, with its pharmacological antagonist SB203580, downregulated MMP-9 and MT1-MMP/MMP-14 express

166 a higher dose of LPS, the p38 MAPK inhibitor SB203580 dramatically increased MCP-1 release and neutro

167 ation with heat-killed L. major plus CpG and SB203580 elicited complete protection against infection

168 Furthermore, blockade of p38 by SB203580 enhanced M. tuberculosis-induced AP-1 binding t

169 Additionally, SB203580 enhanced transcription factor binding to the ol

170 Inhibitors of p38 (SB203580), ERK (UO1026), JNK (SP600125), and NF-kappaB (

171 of p38 MAPK by the small molecule inhibitor SB203580 expanded ES-derived hematopoietic progenitors b

172 This increase was reversed by minocycline or SB203580 exposure.

173 (PD98059 for MAP/ERK, SP600125 for JNK, and SB203580 for p38).

174 ptor antagonist, and the chemical inhibitors SB203580, for p38, and SP600125, for JNKs, were used in

175 and lowered NO levels, reactions blocked by SB203580; however, protection by SB203580 was the same i

176 -stimulated migration was not compromised by SB203580 in endothelial cells expressing the uPA transge

177 mulations predicted an IC50 of 1-1.2 mum for SB203580 in hepatocytes.

178 d to BBB impairment and this was reversed by SB203580 in naive mice.

179 f p38 with the pyridinyl imidazole inhibitor SB203580 in naive NZB/W mice reproduced in vivo the effe

180 nd, UM101, that was at least as effective as SB203580 in stabilizing endothelial barrier function, re

181 armacological inhibitors PD98059, U0126, and SB203580 in T98G LGI1-null cells inhibits MMP1 and MMP3

182 en-activated protein kinase (MAPK) inhibitor SB203580 in the predominantly slow-twitch soleus muscle.

183 The molecular hierarchies targeted by SB203580 include the combinatorial interaction of NF-kap

184 Most interestingly, the occurrence of SB203580-induced migratory inhibition coincided with a r

185 kinase path was simultaneously inhibited by SB203580 (ineffective alone).

186 , the pyridinyl imidazole drugs SB202190 and SB203580 inhibited 17,20 lyase but not 17alpha-hydroxyla

187 ion of both p38 MAP kinase and PKB, 1 microm SB203580 inhibited activation of p38 MAP kinase, but not

188 Although 100 microm SB203580 inhibited cell swelling- and 8-chlorophenylthio

189 specific proteins; however, only S31-201 and SB203580 inhibited collagen biosynthesis.

190 Whereas SB203580 inhibited endotoxin-induced NF-kappaB activatio

191 Blockage of p38 by SB203580 inhibited p53 phosphorylation and induction of

192 F7 cells with Rituximab or the p38 inhibitor SB203580 inhibited the constitutive p38 MAPK activity an

193 COLO-357 cells, PD98059, and U0126, but not SB203580, inhibited EGF-stimulated mitogenesis, whereas

194 revealed that UM101 inhibited only 28 of 61 SB203580-inhibited genes and 7 of 15 SB203580-inhibited

195 8 of 61 SB203580-inhibited genes and 7 of 15 SB203580-inhibited transcription factors, but spared the

196 romotion of ER-mitochondria interaction, and SB203580 inhibition of p38 MAPK increased ER-mitochondri

197 blockade of p38 MAPK signaling pathway with SB203580 inhibits IFN-gamma- and LPS-induced p19 mRNA ex

198 A p38 kinase inhibitor, SB203580, instead blocked TSP-1 expression and a p38 act

199 hyperalgesia was blocked by minocycline and SB203580 intrathecally.

200 ell type (G9c), we observed that SB203580 or SB203580-iodo efficiently inhibited the salvage synthesi

201 Incubation of K562 cells with SB203580, SB203580-iodo, or SB202474, an analogue of SB203580 that

202 ibitors for ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125), or PI3K (LY294002) were

203 PD98059, LY294002, NAC, curcumin, EGCG, and SB203580 markedly inhibited TGM-2 expression induced by

204 Neither SB203580 nor LY294002 inhibited HGF-induced ERK1/2 activ

205 ype (DN) JNK, but not the p38 MAPK inhibitor SB203580 nor the protein kinase C inhibitor GF109203X, p

206 ioned place preference (CPP), mice receiving SB203580 on cocaine challenge day or on postconditioning

207 production, suggesting a specific effect of SB203580 on IFN-gamma production.

208 Topical treatment with LY294002 and SB203580 on the cornea after cryotreatment blocked the p

209 However, SB203580 only inhibited the binding of MMP-1-specific CR

210 Rac, and inhibition of p38 MAPK with either SB203580 or adenoviral dominant negative p38alpha also b

211 Treatment with SB203580 or adenoviral overexpression of dominant negati

212 were both blunted by p38 inhibitors, either SB203580 or curcumin.

213 Inhibition of p38 MAPK by either SB203580 or dominant-negative construct blocked inductio

214 However, inhibition of p38 with SB203580 or ERK with either U0126 or a transfected domin

215 Pharmacological inhibition of p38 MAPK with SB203580 or expression of a p38 kinase-deficient mutant

216 en-activated protein kinase (MAPK) inhibitor SB203580 or in a submerged manner for different duration

217 but was not affected by 10 microM of either SB203580 or JNK inhibitor 1.

218 Inhibition of either p38 with SB203580 or JNK with SP600125 reduced superoxide product

219 Using SB203580 or p38alpha(-/-) cells, we showed that p38alpha

220 Administration of resveratrol and SB203580 or resveratrol and SP600125 together significan

221 Blockade of p38 phosphorylation with SB203580 or SB202190 in turn abolished [Ca(2+)](e)-media

222 -dependent cell type (G9c), we observed that SB203580 or SB203580-iodo efficiently inhibited the salv

223 esterol, whereas inhibition of p38 MAPK with SB203580 or siRNA reduced the LDL loading-induced intrac

224 y was prevented by blockade of p38 MAPK with SB203580 or siRNA.

225 A-sensitive swelling, which was prevented by SB203580 or SP600125.

226 and IGF-I secretion were partly inhibited by SB203580 or U1026 and abolished by the combination of th

227 thylsulfonylphenyl)-5-(4-pyridyl) imidazole (SB203580) or by overexpression of a dominant negative mu

228 tained in the presence of inhibitors of p38 (SB203580) or mitogen-activated protein/ERK kinase 1 sign

229 signaling pathway with either p38 inhibitor (SB203580) or shPTHrP may result in improving/restoring t

230 injections of minocycline, the p38 inhibitor SB203580, or saline.

231 ERK1/2) inhibitor, UO126, the p38 inhibitor, SB203580, or the phosphatidylinositol-3 kinase inhibitor

232 trast, inhibition of the p38 MAPK pathway by SB203580, or through overexpression of a dominant-negati

233 yed in rats given injections of minocycline, SB203580, or vehicle.

234 antly, inhibition of the p38 MAPK pathway by SB203580 overcomes the block in deriving ES cells from b

235 SB203580 (p38 MAPK inhibitor) prevented IL-1beta-induced

236 The p38 MAPK inhibitor SB203580 partially inhibited both AICAR- and hypoxia-sti

237 SB203580 partially rescued RGCs, whereas LY294002 enhanc

238 However, inhibition of the p38 pathway by SB203580 partially suppressed ADP- and 2-MeSADP-induced

239 plus MCAO to compare with MCAO alone or with SB203580 plus isoflurane preconditioning plus MCAO) and

240 preconditioning plus MCAO, and 30 +/- 6% for SB203580 plus isoflurane preconditioning plus MCAO, n =

241 8 activities because the selective inhibitor SB203580 prevented both phosphorylation of the pathway a

242 Inhibition of p38 with SB203580 prevented the antiproliferative response, while

243 nd treatment of cells with the p38 inhibitor SB203580 prevented this increase in p21 stability.

244 NK) inhibitor SP600125 or p38 MAPK inhibitor SB203580 prevented this liver injury.

245 by ethanol treatment and the p38 inhibitor, SB203580, prevented both the ethanol-induced increase in

246 However, the p38 MAPK inhibitor, SB203580, prevented NMDA dilator impairment significantl

247 as a large-scale application of the method, SB203580, purvalanol B, and imatinib were screened again

248 For five of the inhibitors (SB203580, purvalanol B, imatinib, H89, and hymenialdisin

249 n, whereas a chemical inhibitor of p38 MAPK (SB203580) reduced the phosphorylation of GSK3beta, decre

250 duced in mice treated with the p38 inhibitor SB203580, relative to vehicle-treated counterparts.

251 or p38 with specific inhibitors (AG1478 and SB203580, respectively) blocked RPTC dedifferentiation.

252 r the JNK or p38 MAPK pathways (SP600125 and SB203580, respectively).

253 rs farnesylthiosalicylic acid, PD-98059, and SB203580, respectively.

254 Inhibiting p38 (by inhibitor SB203580) restored the morphology, phenotype, and Ag pre

255 her ERK1/2 or p38 MAPK inhibitor (PD98059 or SB203580) resulted in an additive inhibition of IFN-gamm

256 and a pharmacological inhibitor of p38 MAPK, SB203580, resulted in the attenuation of PGD(2) levels.

257 Experiments using the p38 inhibitor SB203580 revealed that endogenous p38 participates in NP

258 ver, antagonism of p38 MAPK by the inhibitor SB203580 reversed apoptosis inhibition in live or heat-k

259 of p38 MAPK, and inhibition of p38 MAPK with SB203580 reversed ESAT-6 inhibition of M. tuberculosis-s

260 PD98059, but not SB203580, reversed the inhibitory effect of GH on chlori

261 or without the inhibitors of p38 (10 microM SB203580/SB202190) or ERK (50 microM PD98059) to delinea

262 Incubation of K562 cells with SB203580, SB203580-iodo, or SB202474, an analogue of SB2

263 togen-activated protein kinase inhibition by SB203580 selectively decreased (3.8 +/- 0.1 versus 1.4 +

264 ization of eIF4E and eIF4GI, it promoted the SB203580-sensitive association of eIF4GI and hsp25, an e

265 tal muscle through PI 3-kinase-sensitive and SB203580-sensitive mechanisms.

266 8alpha MAPK, and inhibition of p38alpha with SB203580 significantly prevented H/R-induced cell death.

267 Inhibition of the p38 pathway using 5 microm SB203580 significantly reduced glucose-mediated IL-8 mRN

268 Two inhibitors of p38 MAPK, SB202190 and SB203580, significantly attenuated PAO1-dependent expres

269 The p38 MAPK inhibitor, SB203580, significantly reduced p47(phox) phosphorylatio

270 ase inhibitor apocynin, p38 kinase inhibitor SB203580, simvastatin, or Rho-kinase inhibitor Y-27632,

271 d pharmacological inhibitor (PD98059, U0126, SB203580, SP600125) approaches positioned MEK1/ERK1-2, b

272 bition of erk, p38, jnk, and akt with U0126, SB203580, SP600125, and Akt inhibitor, respectively, doc

273 owed that a minimum of a 10-h treatment with SB203580 (specific p38 MAPK inhibitor) was needed to blo

274 itor) but not by losartan (AT(1) inhibitor), SB203580 (specific p38 mitogen-activated protein kinase

275 Post-treatment with SB203580 starting on day 1 or on day 10 after surgery al

276 ort that p38 kinase inhibitors, SB202190 and SB203580, stimulated U6 promoter activity and this stimu

277 ways with the chemical inhibitors PD98059 or SB203580 suggested that activation of these signaling pa

278 of p38 mitogen-activated protein kinase with SB203580 suppressed apoptosis and caspase-3 activation i

279 The p38-specific inhibitor SB203580 suppressed p38 activity and MMP-1 mRNA and prot

280 11, JNK inhibitor JNKi II, and p38 inhibitor SB203580 suppressed the synergistic effect of IL-6 and I

281 h p.i., with no effect on virus titers (only SB203580 tested).

282 , SB203580-iodo, or SB202474, an analogue of SB203580 that does not inhibit p38 MAPK activity, inhibi

283 ylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580) (the percentages of infarct volumes in the ips

284 Addition of SB203580, the MAPK p38 pathway inhibitor, partially inhi

285 this targeting are linked to the ability of SB203580 to inhibit p38 MAPK-controlled pathways.

286 Lymphoma growth was also inhibited in SB203580-treated NOD-SCID mice.

287 Furthermore, SB203580 treatment potently repressed [Ca(2+)](e)-mediat

288 e inhibitors wortmannin and LY294002 or with SB203580 uncovered an insulin-stimulated NKCC activity a

289 lsulfonylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580) via the intrathecal route, starting before the

290 tive oxygen production; hence, protection by SB203580 was downstream of the elevated oxidative stress

291 PGE(2), but only the inhibition of MMP-1 by SB203580 was reversed by PGE(2) or dibutyryl cAMP.

292 blocked by SB203580; however, protection by SB203580 was the same in the absence or presence of an i

293 n-activated protein kinase (MAPK) inhibitor, SB203580, was delivered with PDGF-AA in naive animals.

294 intraperitoneal injection of p38 inhibitor (SB203580), we demonstrated that the induction of C/EBPal

295 ors for MAP kinase kinase (PD98059) and p38 (SB203580), we show that ERK1/2 exhibited differential ef

296 catechin-3 gallate (EGCG), and p38 inhibitor SB203580 were added to find the possible regulatory mech

297 ential new targets; the predicted targets of SB203580 were compared with those identified in recent p

298 tivated protein kinase inhibitors (U0126 and SB203580) were sufficient to block Nup hyperphosphorylat

299 presence or absence of a p38 MAPK inhibitor, SB203580, were examined.

300 vation; however, direct inhibition of p38 by SB203580, which selectively inhibits the activity of the