ライフサイエンスコーパス: protein kinase inhibitor

1 K inhibitor), but not KT5720 (cAMP-dependent protein kinase inhibitor).

2 nhibitor), but not by KT5720 (cAMP-dependent protein kinase inhibitor).

3 quinazolines represent an important class of protein kinase inhibitor.

4 tive to PKI, the highly specific heat-stable protein kinase inhibitor.

5 PKC inhibitors, but not by a cAMP-dependent protein kinase inhibitor.

6 significantly augmented by mitogen-activated protein kinase inhibitor.

7 s pre-treated with STI-571, a c-Abl-specific protein kinase inhibitor.

8 ptured patch recordings and was blocked by a protein kinase inhibitor.

9 ve been identified as potent ATP-competitive protein kinase inhibitors.

10 ffects of insulin were investigated by using protein kinase inhibitors.

11 optimisation of novel, potent and selective protein kinase inhibitors.

12 eful sites to consider in designing specific protein kinase inhibitors.

13 -inhibitor structure in aiding the design of protein kinase inhibitors.

14 ovide new clues for the design of allosteric protein kinase inhibitors.

15 ha by antioxidants and p38 mitogen-activated protein kinase inhibitors.

16 tein kinase A or cyclic nucleotide-dependent protein kinase inhibitors.

17 ti-inflammatory compounds and cell-permeable protein kinase inhibitors.

18 -complexes of WbdD with two known eukaryotic protein kinase inhibitors.

19 arylimidazole, and triarylpyrrole classes of protein kinase inhibitors.

20 sed successfully to design new highly potent protein kinase inhibitors.

21 regulatory (R) subunits and the heat-stable protein kinase inhibitors.

22 designed, synthesized, and evaluated as RET protein kinase inhibitors.

23 llular calcium and Ca2+/calmodulin-dependent protein kinase inhibitors.

24 +-sensitive and was unaffected by a range of protein kinase inhibitors.

25 kinase inhibitor genistein but not by other protein kinase inhibitors.

26 ance by screening against 160 cell-permeable protein kinase inhibitors.

27 rotein kinases against a library of 80 known protein kinase inhibitors.

28 re needed to identify the next generation of protein kinase inhibitors.

29 e exploited for the development of selective protein kinase inhibitors.

30 mitochondrial inhibitors or flavanoid-based protein kinase inhibitors.

31 was abrogated by selective mitogen-activated protein kinase inhibitors.

32 wo members of different classes of drug-like protein kinase inhibitors.

33 inding were blocked by p38 mitogen-activated protein kinase inhibitors.

34 ection for the rapid identification of novel protein kinase inhibitors.

35 7 when the cells were pre-incubated with the protein kinase inhibitor 1-(5-isoquinolinyl-sulphonyl)-2

36 og 8-(4-chlorophenylthio) (CPT)-cAMP and the protein kinase inhibitors 1-(5-isoquinolinesulfonyl)-2-m

37 y treatment of early G1-phase cells with the protein kinase inhibitor 2-aminopurine (2-AP).

38 re also blocked by the p38 mitogen-activated protein kinase inhibitor 4-(4-fluorophenyl)-2-(4-hydroxy

39 free cdk substrates, were insensitive to the protein kinase inhibitor 5'-fluorosulfonylbenzoyladenosi

40 Inclusion of the protein kinase inhibitor 6-dimethylaminopurine during S

41 Preincubation of ribosomes with a general protein kinase inhibitor, 6-dimethylaminopurine, elimina

42 nd FAK are dose dependently inhibited by the protein kinase inhibitor, AG1879, in cultured human lung

43 amide hydrochloride (H-89) and myristoylated protein kinase inhibitor () amide; cGMP-dependent protei

44 Using protein kinase inhibitors and dominant negative and cons

45 Using protein kinase inhibitors and dominant negative and cons

46 By using selective protein kinase inhibitors and expression of dominant-neg

47 ata provide a new function for plant MPKs as protein kinase inhibitors and suggest a mechanism throug

48 monstrated that certain compounds, including protein kinase inhibitors and their derivatives, act dir

49 i-metabolites have been shown to function as protein kinase inhibitors and to regulate gene expressio

50 substrate (ATP and PKI(5-24)), a fragment of protein kinase inhibitor) and products (ADP and phosphor

51 TGF-beta1 receptor inhibitor, Rho-associated protein kinase inhibitor, and alphav integrin inhibitor

52 mmunophilins, transcription factors, the PKR protein kinase inhibitor, and peroxisomal and mitochondr

53 Treatment with SB203580, a mitogen-activated protein kinase inhibitor, and rolipram, a phosphodiester

54 by protein kinase A regulatory subunits, the protein kinase inhibitor, and the chemical inhibitor H-8

55 by thrombin can be blocked by thrombin and a protein kinase inhibitor, and the effects of thrombin ca

56 sterase 4 inhibitors, p38 mitogen-activating protein kinase inhibitors, and antibodies against IL-1 a

57 ctivity was also inhibited by cAMP-dependent protein kinase inhibitors, and isoPGE2 elevated intracel

58 ckers, it was inhibited by broad-specificity protein kinase inhibitors, and it was not induced by ina

59 -one, bearing pharmacophoric groups of known protein kinase inhibitors, and related benzoxazole and b

60 oM), which is thought to be a cGMP-dependent protein kinase inhibitor; and the anti-inflammatory agen

61 Endogenous protein kinase inhibitors are essential for a wide range

62 Mitogen-activated protein kinase inhibitors are potential therapeutic agen

63 Small molecule protein kinase inhibitors are widely employed as biologi

64 Small molecule protein kinase inhibitors are widely employed as biologi

65 Small-molecule protein kinase inhibitors are widely used to elucidate c

66 t blocked by staurosporine, a broad-spectrum protein kinase inhibitor, arguing against involvement of

67 Despite the success of protein kinase inhibitors as approved therapeutics, drug

68 ine the viability of using mitogen-activated protein kinase inhibitors as immune suppressants.

69 -Gly (DFG)-in/out p38alpha mitogen-activated protein kinase inhibitors as our test cases.

70 0) or indirectly inhibit activation of AP24 (protein kinase inhibitors, basic fibroblast growth facto

71 As a result, the screening of protein kinase inhibitors becomes more rapid, sensitive,

72 t of a real-time, label-free method to study protein kinase inhibitor binding kinetics using surface

73 hitectural similarity to those of eukaryotic protein kinases, inhibitor binding to the BC ATP-binding

74 ty chromatography using the Sepharose-linked protein kinase inhibitor, bisindolylmaleimide (BIM).

75 Although the protein kinase inhibitor bisindoylmaleimide VIII increas

76 The presence of mitogen-activated protein kinase inhibitors blocked the trafficking of SLC

77 Genistein, a tyrosine protein kinase inhibitor, blocked uptake of P. gingivali

78 reatment with specific p38 mitogen-activated protein kinase inhibitors blocks both myotube formation

79 ecreased by a specific p38 mitogen-activated protein kinase inhibitor, but not by a protein kinase C

80 re is great interest in developing selective protein kinase inhibitors by targeting allosteric sites,

81 tasia-mutated (ATM) and ATM and Rad3-related protein kinases inhibitor caffeine.

82 ,5-dione (U-73122) and is attenuated by the protein kinase inhibitor calphostin C or by the intracel

83 trast, staurosporine (100 nM; a nonselective protein kinase inhibitor), calphostin C (1 microM; a sel

84 Protein kinase inhibitors can be effective in treating s

85 tion state-specific antibodies and selective protein kinase inhibitors, Cdk5 was found to be the only

86 A, had no effect; (2) preincubation with the protein kinase inhibitor chelerythrine prevented the PMA

87 The protein kinase inhibitor CKI-7 and unlabeled GTP both bl

88 Cells treated with Nef/protein kinase inhibitor complexes were protected from N

89 imately 90 known X-ray crystal structures of protein kinase-inhibitor complexes obtained from the Pro

90 nhibitor SB203580, but not the AMP-activated protein kinase inhibitor Compound C, attenuates adiponec

91 reviously demonstrated that UCN-01, a potent protein kinase inhibitor currently in phase I clinical t

92 UCN-01, a protein kinase inhibitor currently undergoing clinical t

93 Signaling pathway analysis with protein kinase inhibitors demonstrated that oncogenic re

94 on of protein kinase C by Ca(2+), and use of protein kinase inhibitors demonstrates that this activat

95 t of JEG3 cells with a p38 mitogen-activated protein kinase inhibitor did not influence activation of

96 A G protein inhibitor and protein kinase inhibitors did not block at-RA uncoupling

97 type of cell death because mitogen-activated protein kinase inhibitors did not significantly affect T

98 The novel p38 mitogen-activated protein kinase inhibitor dilmapimod appears well tolerat

99 Using protein kinase inhibitors, dominant negative mutant stud

100 but not in the presence of mitogen-activated protein kinase inhibitors, either alone or in combinatio

101 Several protein kinase inhibitors exhibited a range of inhibitor

102 I also discuss the exploitation of specific protein kinase inhibitors for the study of cell signalli

103 To realize the full potential of targeted protein kinase inhibitors for the treatment of cancer, i

104 role of protein kinases we tested a panel of protein kinase inhibitors for their effect on these step

105 monstrated by application to seven different protein kinase inhibitors: for each inhibitor, relative

106 , there is a unique cellular distribution of protein kinase inhibitor forms, with PKIbeta being essen

107 Hypothemycin is a macrolide protein kinase inhibitor from the fungus Hypomyces subic

108 Similarly, treatment of BFTE cells with the protein kinase inhibitors genistein and staurosporine an

109 resence of staurosporine (a serine/threonine protein kinase inhibitor), genistein (a tyrosine kinase

110 , requires ATP and GTP and is blocked by the protein kinase inhibitor GF-109203X, suggesting a protei

111 -3, 1 mM, six rats), or the serine-threonine protein kinase inhibitor H-7 (1 mM, five rats; 10 mM, fi

112 onditions, application of the broad-spectrum protein kinase inhibitor H-7 (10 microM) had no effect o

113 otein kinase activity, as application of the protein kinase inhibitor H-7 after LTP induction can rev

114 T3 is inhibited by both the serine/threonine protein kinase inhibitor H-7 and the immunosuppressive d

115 inhibitor SQ 22536 nor with the non-specific protein kinase inhibitor H-7.

116 of GSP1, and the cyclic nucleotide-dependent protein kinase inhibitor H-8 inhibited the adhesion-indu

117 enosine and cAMP promoters and also with the protein kinase inhibitor H-8, whereas phorbol myristate

118 eta3AR was insensitive to the cAMP-dependent protein kinase inhibitor H-89 but was abolished by genis

119 of c-fos was abolished by the cAMP-dependent protein kinase inhibitor H-89, suggesting that the trans

120 on of EPSCs was reduced by the non-selective protein kinase inhibitors H-7 (100 microM), H-8 (50 micr

121 Protein kinase inhibitor H7 (100 microM) suppressed quan

122 The serine/threonine protein kinase inhibitor H7 blocked induction of both IL

123 The protein kinase inhibitor H7 blocks influenza virus repli

124 The protein kinase inhibitor H7 suppressed the activation of

125 red-pulse facilitation was unaffected by the protein kinase inhibitors H7 and KN-62.

126 inhibitor, okadaic acid, and inhibited by a protein kinase inhibitor, H7.

127 In initial experiments, the broad-spectrum protein kinase inhibitors, H7 and H89, stabilized REC tu

128 presence of the cyclic nucleotide-dependent protein kinase inhibitor, H8, which (unlike staurosporin

129 cAMP and was inhibited by the cAMP-dependent protein kinase inhibitor H89 and the cystic fibrosis tra

130 ponse can be selectively inhibited using the protein kinase inhibitor H89.

131 ated by experiments using the cAMP-dependent protein kinase inhibitors H89 and PKI.

132 onse was delayed by the H7 infusion, but the protein kinase inhibitor had no effect on performance of

133 osure; incubation with ERK/mitogen-activated protein kinase inhibitor had no effect on UVA-induced cy

134 ariant cells and that H-89, a cAMP-dependent protein kinase inhibitor, has no effect on cAMP-induced

135 Several BRAF protein-kinase inhibitors have been developed through hi

136 lved as a powerful complimentary approach to protein-kinase inhibitor identification.

137 e can be stimulated by cAMP and inhibited by protein kinase inhibitor.Importantly, ex vivo treatment

138 effects of glutamate and APB are blocked by protein kinase inhibitors including Rp-8-pCPT-cGMPS, H-8

139 Treatment of lens organ cultures with protein kinase inhibitors indicated that protein kinase

140 Ser/Thr protein kinase inhibitors inhibited, and protein phospha

141 rthermore, SU5402, an FGF receptor-dependent protein kinase inhibitor, inhibited Pfkp and Ldha expres

142 Rabbits were infused with H7, a general protein kinase inhibitor, into the region of the cerebel

143 ication of the kinase or kinases targeted by protein kinase inhibitors is a critical challenge in val

144 el method for characterizing the kinetics of protein kinase inhibitors is described.

145 The protein kinase inhibitor K252a abolished c-Jun induction

146 calyculin A were counteracted by the general protein kinase inhibitor K252a.

147 TF binding is reduced in the presence of the protein kinase inhibitor K252a.

148 The CDPKs were inhibited by the general protein kinase inhibitors K252a and staurosporine and by

149 The nonselective protein kinase inhibitors K252a and staurosporine provid

150 eatment with caffeine, and its inhibition by protein kinase inhibitors (K252a and staurosporine) and

151 nopus laevis oocytes expressing TaALMT1 with protein kinase inhibitors (K252a and staurosporine) stro

152 Ca(2+)/CaM-dependent protein kinase inhibitor KN-93 also blocked zygote elong

153 nhibitor H-89 or Ca(2+)/calmodulin-activated protein kinase inhibitor KN-93 reduced the nicotine-trig

154 blocked by the calcium/calmodulin-dependent protein kinase inhibitor KN93 and by the p38 mitogen-act

155 brogated by the calcium/calmodulin-dependent protein kinase inhibitor KN93, but not by the CB2 recept

156 rotein kinase activity by the cGMP-dependent protein kinase inhibitor KT5823 or replacement of ATP by

157 The cGMP-dependent protein kinase inhibitor KT5823 reversed the increase in

158 -3,5-cGMP [8-Br-cGMP]), and a cGMP-dependent protein kinase inhibitor (KT5823).

159 ted pathway was selectively inhibited by the protein kinase inhibitor KT5926.

160 an oral small-molecule p38 mitogen-activated protein kinase inhibitor (Losmapimod; GlaxoSmithKline, B

161 ombined treatment with bleomycin and the DNA protein kinase inhibitor LY294002 than the original HCT-

162 mmatory actions of the p38 mitogen-activated protein kinase inhibitor (MAPK), SB203580.

163 so predicted that the endogenous heat-stable protein kinase inhibitor may enhance basal cyclic AMP bu

164 the cellular responses induced by multiplex protein kinase inhibitors may be an emergent property th

165 esponding to the pseudosubstrate sequence of protein kinase inhibitor (myr-PKI), the endogenous inhib

166 of PP-1 was reduced by the cyclin-dependent protein kinase inhibitor, olomoucine, and increased by t

167 The effects of protein kinase inhibitors on EPEC-induced perturbation o

168 e effects of various protein phosphatase and protein kinase inhibitors on these two ionic currents (I

169 The effect of protein kinase inhibitors on transferrin receptor (TR) i

170 hen the cells were treated with a variety of protein kinases inhibitors, only specific inhibitors of

171 d was observed in cells treated with various protein kinase inhibitors or co-expressing a dominant-ne

172 required for dBest1 activation: nonspecific protein kinase inhibitors or intracellular perfusion wit

173 go apoptosis by staurosporine, a nonspecific protein kinase inhibitor, or by culture in suspension wi

174 was induced by staurosporine, a nonspecific protein kinase inhibitor, or by culture in suspension wi

175 d, if PKA activity is inhibited with H-89 or protein kinase inhibitor, or when PKA anchoring is pertu

176 ied by up-regulation of the cyclin-dependent protein kinase inhibitor p21(CIP1).

177 n protein expression of the cyclin-dependent protein kinase inhibitor p21(WAF1/Cip1).

178 iving increasing attention, with some of the protein kinases inhibitors particularly promising.

179 or inhibitor K252a and the mitogen-activated protein kinase inhibitor PD98059 for postoperative days

180 ved in the presence of the mitogen-activated protein kinase inhibitor PD98059.

181 or LY294002 but not by the mitogen-activated protein kinase inhibitor PD98059.

182 l-CaD phosphorylation was attenuated by the protein kinase inhibitor PD98059.

183 nase A inhibitor H-89, the mitogen activated protein kinase inhibitors PD98059 and SB203580, and the

184 can be inhibited with the mitogen-activated protein kinase inhibitors PD98059 or UO126.

185 r), SB203580 (specific p38 mitogen-activated protein kinase inhibitor), PD98059 (specific MEK inhibit

186 re also potentiated by the mitogen-activated protein kinase inhibitor, PD98059 (20 microM).

187 CP-1, HMVEC-Ls were treated with 2 different protein kinase inhibitors: PD98059, a MAP kinase inhibit

188 was not stimulated by cAMP nor inhibited by protein kinase inhibitor peptide (5-24), indicating that

189 ate, Rp-isomer (Rp-cAMPS) or by injection of protein kinase inhibitor peptide (PKI) or mRNA coding fo

190 he binding between the C-subunit and IP20, a protein kinase inhibitor peptide.

191 tibacterial pyridopyrimidines derived from a protein kinase inhibitor pharmacophore.

192 ogically diverse antagonists: staurosporine (protein kinase inhibitor), phorbol 12-myristate 13-aceta

193 sidue peptide inhibitor from the heat-stable protein kinase inhibitor PKI(5-24) and adenosine, was de

194 llular pseudosubstrate inhibitor of PKA, the protein kinase inhibitor PKI, and the PRKX and PKA inhib

195 a-carbonyl backbone flexibility of the 8 kDa protein kinase inhibitor (PKI alpha) peptide of cAMP-dep

196 ne 3'-5'cyclic monophosphothiate, Rp-isomer, protein kinase inhibitor (PKI) (6-22) amide, and myristo

197 The protein kinase inhibitor (PKI) family includes three gen

198 of PKA signaling, members of the endogenous protein kinase inhibitor (PKI) family may be particularl

199 Side effects of this protein kinase inhibitor (PKI) include arthralgia, rash,

200 Protein kinase inhibitor (PKI) is a potent endogenous in

201 Protein kinase inhibitor (PKI) is an endogenous inhibito

202 to understand the physiological roles of the protein kinase inhibitor (PKI) proteins have been hamper

203 l assay that reconstitutes nuclear export of protein kinase inhibitor (PKI) to show that cytosol cont

204 ith the binding of MgATP and the heat stable protein kinase inhibitor (PKI) were probed by mapping th

205 development of an iodopyridopyrimidinone Abl protein kinase inhibitor (PKI), (124)I-SKI-212230 ((124)

206 One of the best-studied examples, protein kinase inhibitor (PKI), binds to the catalytic s

207 substrates as in the case of the heat-stable protein kinase inhibitor (PKI), or they may mimic nucleo

208 ity in the presence of regulatory subunit or protein kinase inhibitor (PKI).

209 Peptide (AIP) and lipophilic (KN-62) protein kinase inhibitors prevented the Ca(2+)/CaM-induc

210 injecting a small molecule derivative of the protein kinase inhibitor protein phosphatase 1 (1NM-PP1)

211 RKIP represents a new class of protein-kinase-inhibitor protein that regulates the acti

212 motif, akin to the mechanism employed by the protein kinase inhibitor proteins.

213 lly, we show that over 70% of small-molecule protein kinase inhibitors published in J. Med. Chem. sin

214 -83583) and a highly specific cGMP-dependent protein kinase inhibitor (RKRARKE) blocked the action of

215 Further studies using the protein kinase inhibitors Ro 31-8220 and staurosporine w

216 rphosphorylation could be inhibited with the protein kinase inhibitor roscovitine.

217 The p38 mitogen-activated protein kinase inhibitors SB-203580 and SB-202190 also i

218 ibited by the specific p38 mitogen-activated protein kinase inhibitor, SB 203580.

219 d was abolished by the p38 mitogen-activated protein kinase inhibitor SB202190 [4-(4-fluorophenyl)-2-

220 and is blocked by the p38 mitogen-activated protein kinase inhibitor SB202190 [4-(4-fluorophenyl)-2-

221 ibitor KN93 and by the p38 mitogen-activated protein kinase inhibitor SB202190.

222 The p38 mitogen-activated protein kinase inhibitors SB202190 and SB203580 blocked

223 edly suppressed by the p38 mitogen-activated protein kinase inhibitor SB203580 but was only minimally

224 ocked by the selective p38 mitogen-activated protein kinase inhibitor SB203580.

225 by treating cells with the mitogen-activated protein kinase inhibitors SB203580 (20 microM) and PD980

226 are diminished by the p38 mitogen-activated protein kinase inhibitors SB203580 and SB202190, but not

227 Using the protein kinase inhibitors SB203580 and U0126, we also sh

228 osphorylation, but the p38 mitogen-activated protein kinase inhibitor, SB203580, did not.

229 -binding adenosine moiety of 1 with a potent protein kinase inhibitor scaffold.

230 class of bis-indoles, represent a promising protein kinase inhibitor scaffold.

231 Staurosporine, a non-selective protein kinase inhibitor, shifted the activation curves

232 the conserved sequence, the cyclin-dependent protein kinase inhibitor Sic1, an SCF(Cdc4) substrate, h

233 ranscription factor and the cyclin-dependent protein kinase inhibitor Sic1.

234 The nonselective protein kinase inhibitor staurosporine (10(-9) to 10(-7)

235 molecular replacement, co-complexed with the protein kinase inhibitor staurosporine (crystals belong

236 s undergo apoptosis after treatment with the protein kinase inhibitor staurosporine (STS).

237 In contrast, the protein kinase inhibitor staurosporine does not affect e

238 The broad-spectrum protein kinase inhibitor staurosporine increases outflow

239 decarboxylase, sodium phenylacetate, and the protein kinase inhibitor staurosporine induced (a) relea

240 The protein kinase inhibitor staurosporine inhibited chromat

241 the phosphatase inhibitor cyclosporine, the protein kinase inhibitor staurosporine or the excitotoxi

242 in II function either with the wide-spectrum protein kinase inhibitor staurosporine or the myosin lig

243 Treatment of wild-type seedlings with the protein kinase inhibitor staurosporine phenocopies the r

244 The protein kinase inhibitor staurosporine prevented Cx43 ph

245 The protein kinase inhibitor staurosporine prevented perijun

246 ssible as LTP but not LTD was blocked by the protein kinase inhibitor staurosporine while LTD but not

247 lso able to inhibit apoptosis induced by the protein kinase inhibitor staurosporine, but is not able

248 nt flagellar adhesion in the presence of the protein kinase inhibitor staurosporine, but not in the p

249 When apoptosis was induced with the protein kinase inhibitor staurosporine, CPP32 was cleave

250 partially reversed by the broad specificity protein kinase inhibitor staurosporine, indicate that tr

251 ), the phospholipase C inhibitor U73122, the protein kinase inhibitor staurosporine, or small interfe

252 The protein kinase inhibitor staurosporine, shown to dephosp

253 on of the B1 isoform could be blocked by the protein kinase inhibitor staurosporine, suggesting that

254 at embryonic cortical neurons exposed to the protein kinase inhibitor staurosporine, the excitatory a

255 owth factors, treatment with the promiscuous protein kinase inhibitor staurosporine, with the protein

256 involved in apoptosis induced by ATP and the protein kinase inhibitor staurosporine.

257 ses, but was enhanced by the addition of the protein kinase inhibitor staurosporine.

258 to apoptosis induced by Fas ligation or the protein kinase inhibitor Staurosporine.

259 rentiating RGC-5 cells using the nonspecific protein kinase inhibitor staurosporine.

260 ished by incubation of cells in non-specific protein kinase inhibitors (staurosporine or H-7) or spec

261 intracellular Ca2+ or cAMP levels, or by the protein kinase inhibitor, staurosporine (0.1-0.5 microM)

262 The broad-spectrum protein kinase inhibitor, staurosporine (300 nm), was wi

263 The protein kinase inhibitor, staurosporine, delayed the ina

264 synthase kinase-3 and p38 mitogen-activated protein kinase inhibitors substantially and synergistica

265 Treatment of pharyngeal cells with protein kinase inhibitors such as genistein and staurosp

266 ession was also inhibited by calphostin-C, a protein kinase inhibitor, suggesting the involvement of

267 findings open the way for the development of protein kinase inhibitors targeting substrate specific d

268 JQ1 affecting the level of c-Myc protein and protein kinase inhibitors targeting the ERK pathway conf

269 tic subunit:ATP:PKI((5)(-)(24)) (heat-stable protein kinase inhibitor) ternary complex in the closed

270 Of the protein kinase inhibitors tested, chelerythrine, 6-dimet

271 tigated the effects of flavopiridol, a novel protein kinase inhibitor that is selective for cyclin-de

272 matinib mesylate, a selective small-molecule protein kinase inhibitor that was first clinically appro

273 eover, staurosporine and K-252a, two Ser/Thr protein kinase inhibitors that blocked WIPK activation,

274 ied protein kinase was sensitive to the same protein kinase inhibitors that diminished NADPH oxidase

275 range of tumor types, to specific, like the protein kinase inhibitors that target molecularly define

276 ation of intracellular [Ca2+] and the use of protein kinase inhibitors, that both protein kinase Calp

277 Application of p38 mitogen-activated protein kinase inhibitor to the burn wound attenuated pu

278 Importantly, when combined with protein kinase inhibitor treatment, Ab stabilization all

279 f mammalian cell cytosolic extracts with the protein kinase inhibitor tyrphostin A25 results in enhan

280 reatment of cells with the mitogen-activated protein kinase inhibitor U0126 prevented the translocati

281 echanisms sensitive to the mitogen-activated protein kinase inhibitor U0126.

282 ibitor hirudin or the MEK (mitogen-activated protein kinase) inhibitor U0126 significantly attenuated

283 zopyran-4-one] or the MAP (mitogen-activated protein) kinase inhibitor U0126 (1,4-diamino-2,3-dicyano

284 eptor kinase (ERK) and p38 mitogen-activated protein kinase inhibitors (U0126 and SB203580) were suff

285 ment of hepatocytes with a mitogen-activated protein kinase inhibitor, U0126 (40 micromol/L) or an in

286 otein interactions was demonstrated with the protein kinase inhibitor UCN-01 in a phosphoserine-depen

287 s additionally inhibited upon treatment with protein kinase inhibitors UCN-01 or SB203580.

288 r LY294002, and the p42/44 mitogen-activated protein kinase inhibitor UO126.

289 The success of the RAF protein kinase inhibitor vemurafenib for the treatment o

290 e microcystin-induced contraction to various protein kinase inhibitors was identical to the sensitivi

291 Selective protein kinase inhibitors were developed on the basis of

292 d the formation of long processes induced by protein kinase inhibitors, were all disrupted by FB1.

293 azolines, an important class of chemicals as protein kinase inhibitors, were investigated.

294 K-252a and staurosporine, two protein-kinase inhibitors, were found to block the oxida

295 sustained STAT5 activation can be blocked by protein kinase inhibitors, which is consistent with the

296 In addition, tozasertib, a small molecule protein kinase inhibitor with activity against DLK, prot

297 nsformation of these cells, and rottlerin, a protein kinase inhibitor with specificity for PKCdelta,

298 Protein kinase inhibitors with enhanced selectivity can

299 Pyrazolo[3,4-d]pyrimidines are potent protein kinase inhibitors with promising antitumor activ

300 e p160 Rho-associated coiled-coil-containing protein kinase inhibitor Y-27632, or by HA 1077.