ライフサイエンスコーパス: p38 MAP kinase

1 all 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

2 number of new scaffold types when applied to p38 MAP kinase.

3 gulated kinase, c-jun N-terminal kinase, and p38 MAP kinase.

4 ix metabolism via activation of NFkappaB and p38 MAP kinase.

5 gh activities that may involve inhibition of p38 MAP kinase.

6 actor alpha from microglia via activation of p38 MAP kinase.

7 protein (HSP27) as downstream regulators of p38 MAP kinase.

8 nly in the absence of chemical inhibitors of p38 MAP kinase.

9 perate by activating their downstream target p38 MAP kinase.

10 n was inhibited by SB203580, an inhibitor of p38 MAP kinase.

11 n activation of the serine/threonine kinase, p38 MAP kinase.

12 growth factor beta (TGFbeta) from activating p38 MAP kinase.

13 ltiple pockets on the proteins Factor Xa and p38 MAP kinase.

14 RK2 but not Jun N-terminal protein kinase or p38 MAP kinase.

15 /EBPepsilon, as being phosphorylated only by p38 MAP kinase.

16 ese pathways interact to converge on Hog1, a p38 MAP kinase.

17 ther mak-1 paralogues and two orthologues of p38 MAP kinase.

18 using a regulatory pathway that may involve p38 MAP kinase.

19 artly mediated by increases in activation of p38 MAP kinase.

20 kinase 2 is phosphorylated and activated by p38 MAP kinase.

21 eries featuring differing selectivity versus p38 MAP kinase.

22 ffectively suppressed the phosphorylation of p38 MAP kinase.

23 sphorylation sites on HBP1 were specific for p38 MAP kinase.

24 ll ligand of the 42 kDa kinase domain of the p38 MAP kinase.

25 tor of the pharmacologically relevant target p38 MAP kinase.

26 ked the TGF-beta1-induced phosphorylation of p38 MAP kinase.

27 gonizes DNMT1 accumulation via activation of p38 MAP kinase.

28 ase Mkp1, which inhibits the Mef2c activator p38 MAP kinase.

29 ects are mediated by transient activation of p38 MAP kinase.

30 that TNF-alpha also led to the activation of p38 MAP kinase.

31 ted by treatment with inhibitors of mTOR and p38 MAP kinase.

32 els and the phosphorylation of Erk, JNK, and p38 MAP kinases.

33 se kinase 6 (MKK6), an upstream activator of p38 MAP kinases.

34 o observed that DSCAM activates both JNK and p38 MAP kinases.

35 fect of PTEN on VEGF, and not the p42/p48 or p38 MAP kinases.

36 relationship between cell transformation and p38 MAP kinase, a major mitogen-activated protein (MAP)

37 (NR2B-containing) NMDARs to the Rac effector p38 MAP kinase, a promoter of LTD.

38 chronic activation in the flight muscles of p38 MAP kinase, a signaling molecule involved in immune

39 Hypoxia enhanced phosphorylation of p38 MAP kinase, a substrate of MKP-1, as well as alpha s

40 ng a known regulator of TTP phosphorylation, p38 MAP kinase, abolishes the effects on cyclin D1 and c

41 alloprotease TNF-alpha-converting enzyme via p38 MAP kinase activation and its concurrent export to t

42 evealed that both the Fgf8-Fgfr1 pathway and p38 MAP kinase activation are partially affected by the

43 s an apoptotic response due to inhibition of p38 MAP kinase activation by the bacterial-produced leth

44 nsport requires p38 MAP kinase activity, but p38 MAP kinase activation does not require ezrin functio

45 Furthermore, TNF-alpha induced increase in p38 MAP kinase activation in astrocytes was inhibited in

46 Here, we have tested the hypothesis that p38 MAP kinase activation in response to arterial shear

47 of these protein kinases in the mechanism of p38 MAP kinase activation in vivo, we examined the effec

48 TNF-alpha-induced Ikk and p38 MAP kinase activation is normal, and the Rip1D138N c

49 vation of ERK1/2 appeared to be selective as p38 MAP kinase activation was not increased by either fe

50 in phosphorylation occurred in parallel with p38 MAP kinase activation, and the latter proceeded norm

51 In conclusion, ATF-1, via p38 MAP kinase activation, functions as a novel regulato

52 ivation, and that cleavage is accelerated by p38 MAP kinase activation.

53 ration of reactive oxygen species (ROS), and p38 MAP kinase activation.

54 gents may prevent NCV deficits by preventing p38 MAP kinase activation.

55 role in stress and conditions that relate to p38 MAP kinase activation.

56 However, it showed no effect on JNK and p38 MAP kinase activities.

57 Our results situate p38 MAP kinase activity as a central regulator of the ph

58 work supports a molecular framework in which p38 MAP kinase activity contributes to cell cycle inhibi

59 he pharmacological and genetic inhibition of p38 MAP kinase activity during infection with the spiroc

60 We investigated the contribution of p38 MAP kinase activity in gamma interferon (IFN-gamma)

61 After showing that TGFbeta upregulated p38 MAP kinase activity in PC3-M cells, we show that inh

62 Our results also demonstrate that although p38 MAP kinase activity is not required for the differen

63 d JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation.

64 We now show that p38 MAP kinase activity regulates the transcriptional ac

65 ion after Na(+)-glucose cotransport requires p38 MAP kinase activity, but p38 MAP kinase activation d

66 g EAG in serum-free media, and EAG increased p38 MAP kinase activity.

67 we suggest that C/EBPepsilon is a target for p38 MAP kinase activity.

68 lian cardiomyocytes to control cell cycle is p38 MAP kinase activity.

69 kinase pathways, and inhibition of mTOR and p38 MAP kinase allowed LC3-II induction in glutamine-dep

70 We demonstrate that p38 MAP kinase and a p38-interacting protein (p38IP) are

71 dothelium can be suppressed by inhibitors of p38 MAP kinase and agents downstream of the kinase that

72 P family function through phosphorylation by p38 MAP kinase and Akt/protein kinase B signaling pathwa

73 ple NGF stimulation to sustain activation of p38 MAP kinase and b-Raf signaling cascades required for

74 Even though the p38 MAP kinase and c-Jun NH(2)-terminal kinases (JNKs) a

75 The data suggest that p38 MAP kinase and ERK act upstream of GSK/beta-catenin

76 e investigated the mechanism of apoptosis by p38 MAP kinase and JNK pathway activation.

77 Hepatitis B virus X protein (pX) activates p38 MAP kinase and JNK pathways and, in response to weak

78 e of the pX-dependent activation of both the p38 MAP kinase and JNK pathways in pX-mediated apoptosis

79 pX-mediated activation of p38 MAP kinase and JNK pathways is sustained, inducing t

80 odulin-dependent protein kinase II (CaMKII), p38 MAP kinase and mitogen-activated protein kinase kina

81 The activation of PAK6 by both p38 MAP kinase and MKK6 suggests that PAK6 plays a role

82 Inactivation of p38 MAP kinase and p53 is required for DN3 thymocytes to

83 A separate pathway recruits p38 MAP kinase and phosphoinositide 3-kinase (PI3-K) sig

84 cer cell line MCF10CA1h and demonstrate that p38 MAP kinase and Rho/ROCK pathways together with Smad2

85 The role of p38 MAP kinase and SHP2 was further defined by transient

86 Both specific inhibitors of p38 MAP kinase and sodium vanadate, a potent protein-tyr

87 nt pathways with Peg IFN-alpha 2a activating p38 MAP kinase and STAT1, leading to increased p53 trans

88 We have now found that both the p38 MAP kinase and the ERK-dependent signal transduction

89 The phosphorylation states of cPLA(2) and p38 MAP kinase and the expression of COX-2 were assessed

90 ROS then enhances LPS-induced activation of p38 MAP kinase and the expression of inflammation-relate

91 he TLR2 ligand correlated with activation of p38 MAP kinase and transforming growth factor (TGF)-beta

92 onRI-induced activation of the Erk, Jnk, and p38 MAP kinases and the release of TNF-alpha.

93 d drug targets, HIV-1 reverse transcriptase, p38 MAP kinase, and cyclin-dependent kinase 2.

94 HSP27 can be regulated by factors other than p38 MAP kinase, and HSP27 is up-regulated during PCa pro

95 level by mechanisms involving suppression of p38 MAP kinase, and modulation of the activity of CDP/cu

96 ted in an increased activation of ERK1/2 and p38 MAP kinase, and the inhibition of the activity of th

97 tosis signal-regulating kinase 1 (ASK1), the p38 MAP kinase, and the neuronal form of nitric oxide sy

98 llular adhesion molecule-1 and activation of p38 MAP kinase, as assessed by enzyme-linked immunosorbe

99 stream phosphorylation and activation of the p38 MAP kinase, as shown by studies using mouse embryoni

100 in kinase 2 (MAPKAPK2), a known substrate of p38 MAP kinase, as well as heat-shock protein 27 (HSP27)

101 Blocking phospholipase C or p38 MAP kinase attenuated, but did not abolish the veloc

102 trast, FSH stimulated the phosphorylation of p38 MAP kinase but PKA-CQR did not.

103 increased the phosphorylation of cPLA(2) and p38 MAP kinase by 4-fold and 3-fold respectively.

104 CLIC4 is required for the activation of p38 map kinase by TGF-beta, a pathway that signals myofi

105 Furthermore, blockade of ERK1/2 or p38 MAP kinases by either specific inhibitors or a domin

106 In addition, p38 MAP kinase can also be activated by an MKK-independe

107 l a presynaptic role of a previously unknown p38 MAP kinase cascade.

108 to sustained activation of the B-Raf/ERK and p38 MAP kinase cascades.

109 show in this study that sodium channels and p38 MAP kinase colocalize in rat brain tissue and that a

110 The effects of a dominant-negative p38 MAP kinase construct on MMP-3 expression were evalua

111 h cytokines was blocked by dominant-negative p38 MAP kinase constructs.

112 Inhibition of interleukin-15 or of p38 MAP kinase controlled such activity.

113 appaB reporter gene as well as ERK, JNK, and p38 MAP kinases correlated with a requirement for serine

114 ith the Wnt-beta-catenin, IGF-1-AKT, Rb-E2F, p38 MAP kinase, cyclin-cdk, p14/19 ARF pathways and the

115 Responses of novel JNK and p38 MAP kinase delta and gamma isoforms also partially a

116 s in a p38 mitogen-activated protein kinase (p38 MAP kinase)-dependent manner, to increase the excita

117 effector mRNAs by DKF-2 proceeded via PMK-1 (p38 Map-kinase)-dependent and -independent pathways.

118 The data also define a pathway of p38 MAP kinase-dependent ezrin activation.

119 t induction of TN-C by IGFBP-3 occurred in a p38 MAP kinase-dependent manner.

120 al inflammation and impairs pLTF by a spinal p38 MAP kinase-dependent mechanism.

121 al inflammation, thereby impairing pLTF by a p38 MAP kinase-dependent mechanism.

122 ction is augmented by a newly appearing cAMP/p38 MAP kinase-dependent signaling cascade.

123 We show that the p38 MAP kinase-dependent, EGFR tyrosine kinase (TK)-inde

124 Rac, and Cdc42 was diminished, but Raf, ERK, p38 MAP kinase, FAK, and Src were unaltered.

125 Three major groups of Map kinases exist: the p38 Map kinase family, the extracellular signal-regulate

126 ataract signaling pathways indicate that the p38 MAP kinase functions upstream of the Src kinase.

127 p38 MAP kinase has received considerable interest in the

128 An enzyme called p38 MAP kinase helps nematodes to adapt to low-oxygen en

129 IH-1 increased phosphorylated (activated) p38 MAP kinase immunofluorescence in identified phrenic

130 o a new class of p38 inhibitors that bind to p38 MAP kinase in a Phe out conformation.

131 that HBP1 could be a relevant substrate for p38 MAP kinase in cell cycle regulation.

132 with stem cell fate, including a hyperactive p38 MAP kinase in FLB1 and a differentially localized Po

133 n of C/EBPalpha is strongly regulated by the p38 MAP kinase in murine alveolar epithelial cells.

134 Activation of p38 MAP kinase in response to TNF-alpha was determined b

135 fy the events that lead to activation of the p38 MAP kinase in response to Type I IFNs.

136 TNF-alpha production and activation of p38 MAP kinase in retinal sections and optic nerve sampl

137 The specific inhibition of p38 MAP kinase in T cells and the administration of a ph

138 , CBD treatment also significantly inhibited p38 MAP kinase in the diabetic retina.

139 kinases also demonstrated the involvement of p38 MAP kinase in the hyaluronan oligosaccharide inducti

140 lts clarify the specific contribution of the p38 MAP kinase in the overall immune response to the spi

141 The authors investigated the involvement of p38 MAP kinase in the TNF-alpha-induced loss of barrier

142 Consistent with this, phosphorylation of p38 MAP kinase induced by Li correlated with its stimula

143 In contrast inhibition of p38 MAP kinase inhibited de novo TGF-beta1 protein synth

144 (ketoprofen; 55 +/- 9%; p < 0.001) or spinal p38 MAP kinase inhibition (58 +/- 2%; p < 0.001).

145 In contrast, p38 MAP kinase inhibition alone fails to rescue heart fu

146 Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to in

147 In addition, p38 MAP kinase inhibition of this cytokine-regulated pat

148 on calponin reduction, MCP-1 inhibition, and p38 MAP kinase inhibition than any individual agonist.

149 ically in the CA1 hippocampus, infusion of a p38 MAP kinase inhibitor into the CA1 hippocampus, or th

150 Compound 1 is a p38 MAP kinase inhibitor potentially useful for the trea

151 The p38 MAP kinase inhibitor SB202190 diminished MMP-3 induc

152 A well-validated p38 MAP kinase inhibitor SB203580 (0.5-5muM) cancelled t

153 tioxidant dexlipotam (R-lipoic acid) nor the p38 MAP kinase inhibitor SB239063 could prevent increase

154 At 3 months after injury, 4 weeks of FGF1/p38 MAP kinase inhibitor therapy results in reduced scar

155 sed on extending the inhibition profile of a p38 MAP kinase inhibitor toward mutant EGFR inhibition.

156 Here we show that FGF1/p38 MAP kinase inhibitor treatment after acute myocardia

157 Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased

158 Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic disseminatio

159 AP kinase or mTOR, but was suppressed by the p38 MAP kinase inhibitor, SB-203580.

160 A p38 MAP kinase inhibitor, SB203580, completely inhibited

161 inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203580.

162 Using a highly selective p38 MAP kinase inhibitor, we demonstrate that it is poss

163 sed by treatment with SB-203580, a selective p38 MAP kinase inhibitor.

164 sults of MAP kinase inhibition by p42/44 and p38 MAP kinase inhibitors and of p42/44 MAP kinase activ

165 disubstituted dibenzosuberone derivatives as p38 MAP kinase inhibitors are described.

166 p38 MAP kinase inhibitors have attracted considerable in

167 by extracellular signal-regulated kinase or p38 MAP kinase inhibitors in a neuronal cell culture.

168 has been applied to the diaryl urea class of p38 map kinase inhibitors.

169 lting in a new structural class of selective p38 MAP kinase inhibitors.

170 ecent stages of development in this class of p38 MAP kinase inhibitors.

171 Gel shift assays indicate that DN-p38 MAP kinase inhibits EGF-induced activator protein-1

172 Additionally, DN-p38 MAP kinase inhibits EGF-induced phosphorylation of c

173 Moreover, our results show that DN-p38 MAP kinase inhibits the phosphorylation of EGF-stimu

174 The p38 MAP kinase is a key player in signaling pathways reg

175 We propose that p38 MAP kinase is activated by V(D)J-mediated DSBs and i

176 We provide evidence that the p38 MAP kinase is constitutively activated or phosphoryl

177 suggest that the activation of ERK, JNK, and p38 MAP kinases is involved in 4-HNE-mediated actin remo

178 /gamma suggests complex interactions between p38 MAP kinase isoforms and their differential uses by T

179 pathway inhibitors on MMP-3 protein levels, p38 MAP kinase isoforms, and phosphorylation levels in h

180 ective inhibitors as protein kinase CK2, not p38, MAP-kinase kinase (MEK)1/2, phosphatidylinositol 3'

181 mad3(-/-) mouse chondrocytes at the level of p38 MAP kinase (MAPK) activation, resulting in reduced A

182 The p38 MAP kinase (MAPK) is phosphorylated and activated by

183 Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pa

184 in suppressive effects on the IFN-activated p38 MAP kinase (MAPK), the function of which is required

185 Our results suggest that the p38 MAP kinase (MAPK)-MK2-Hsp27 signaling axis may targe

186 romoted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcrip

187 These findings suggest p38 MAP kinase-mediated eNOS activation requires ERalpha

188 virulence, and emphasize a central role for p38 MAP kinase-mediated phosphorylation of Hsp27 in acti

189 p38 MAP kinase-mediated PIASxalpha phosphorylation allow

190 We now demonstrate that p38 MAP kinase-mediated responses are critical component

191 nd show that inhibition of interleukin-15 or p38 MAP kinase might have the potential to control coeli

192 ts suggest that a signaling axis composed of p38 MAP kinase-MK2-Hsp27-beta-TrCP may promote AUF1 degr

193 Upstream activators of p38 MAP kinases, MKK3 and MKK6, increased PITX2a and Pit

194 he reactions are sequential or random in the p38 MAP kinase module.

195 athway, either with direct inhibitors of the p38 MAP kinase or a small-molecule therapeutic that also

196 uced phosphorylation of ERK and JNK, but not p38 MAP kinase or NK-kappaB, and resulted in AP-1 activa

197 Inhibition of p38 MAP kinase or phosphatidylinositol 3-kinases did not

198 revealed that overexpression of an inactive p38 MAP kinase or SHP2 mutant partially abrogated HCV-E2

199 as well as decreased phosphorylation of the p38 MAP kinase (p-p38) and diminished expression of mTNF

200 itric oxide synthase (eNOS) activity through p38 MAP kinase (p38 MAPK) activation.

201 phorylation of ERalpha on Ser-118 was due to p38 MAP kinase (p38 MAPK) as, it was inhibited by SB2035

202 taining 14-3-3- and WW-binding domains and a p38 MAP kinase (p38 MAPK) consensus site on Ser-538 (S53

203 In this study, we showed that p38 MAP kinase (p38) is expressed in doublecortin-positi

204 were incubated with selective inhibitors for p38 MAP kinase (p38), Smad3, p42, JNK, RhoA, PI3K, or TG

205 Here, we show that p38 MAP kinase p38delta is required for recruitment of n

206 Here, we demonstrate that in Drosophila, a p38 MAP kinase (p38K)/Mef2/MnSOD pathway is a coregulato

207 ed SPL enzymatic activity and the actions of p38 MAP kinase, p53, p53-inducible death domain protein

208 and functions as a negative regulator of the p38 MAP kinase-p53 signaling pathway.

209 y in PC3-M cells, we show that inhibition of p38 MAP kinase partially blocked TGFbeta-mediated increa

210 hibitor PD98059 but not by inhibitors of the p38 MAP kinase pathway (SB202190) or c-Jun N-terminal pr

211 in 293 cells, VP24 also interferes with the p38 MAP kinase pathway by blocking IFN-beta-stimulated p

212 Specific depletion of various members of the p38 MAP kinase pathway by the use of RNA interference re

213 early response to hypoxia, and inhibition of p38 MAP kinase pathway by variety of approaches abolishe

214 ch cytokine increased phosphorylation of the p38 MAP kinase pathway components and altered TM cell mo

215 We report that RPM-1 negatively regulates a p38 MAP kinase pathway composed of the dual leucine zipp

216 induction of G1 arrest by activation of the p38 MAP kinase pathway has attracted recent attention wi

217 onstrate a critical role for hypoxia-induced p38 MAP kinase pathway in androgen-independent AR activa

218 Although the involvement of the p38 MAP kinase pathway in cellular responses to stress h

219 determine the effects of these cytokines and p38 MAP kinase pathway inhibitors on MMP-3 protein level

220 We demonstrate that activation of the p38 MAP kinase pathway is necessary for the full transcr

221 an activator of twitchin kinase and that the p38 MAP kinase pathway may be involved in the regulation

222 Recent evidence indicates that the p38 Map kinase pathway plays an important role in type I

223 There is accumulating evidence that the p38 MAP kinase pathway plays important roles in Type I i

224 the authors investigated the involvement of p38 MAP kinase pathway proteins in this process.

225 Inhibition of the p38 MAP kinase pathway rescues by 80% the initiation of

226 All three kinases are able to activate the p38 MAP kinase pathway through the specific activation o

227 c elevated glucose in diabetes activates the p38 MAP kinase pathway to increase inflammatory IL-8 gen

228 oteins-the HBP1 transcription factor and the p38 MAP kinase pathway-may now participate together in a

229 e Th1 cytokine through the activation of the p38 MAP kinase pathway.

230 otein that functions upstream of a conserved p38 MAP kinase pathway.

231 entially regulated by STAT complexes and the p38 MAP kinase pathway.

232 Activation of the p38 MAP kinase pathways is crucial for the adaptation of

233 howed normal activation of the Akt, ERK, and p38 MAP kinase pathways when stimulated by the GPCR liga

234 of extracellular signal-regulated kinase and p38 MAP kinase pathways with the chemical inhibitors PD9

235 n was paralleled by inactivation of mTOR and p38 MAP kinase pathways, and inhibition of mTOR and p38

236 or Elk-1 to the ERK and the stress-activated p38 MAP kinase pathways.

237 e mitogen-activated protein (MAP) kinase and p38 MAP kinase pathways.

238 nase, c-Jun NH(2)-terminal kinase (JNK), and p38 MAP kinase pathways.

239 r type 1 and mediates the IkappaB kinase and p38 MAP kinase pathways.

240 tress through its regulation of the mTOR and p38 MAP kinase pathways.

241 rted in MNs which involves the activation of p38 MAP kinase (phospho-p38) and neuronal nitric oxide s

242 p38 MAP kinase phosphorylates the nuclear kinase mitogen

243 fic ligands relaxed its capacity to suppress p38 MAP kinase phosphorylation and promoted T-bet expres

244 agonists correlates with their induction of p38 MAP kinase phosphorylation and with degradation of I

245 hemical inhibitor SC68376 not only abolished p38 MAP kinase phosphorylation but also obliterated apop

246 AFC inhibited the TNF alpha stimulation of p38 MAP kinase phosphorylation in EC.

247 t TGF-beta1 treatment increased the level of p38 MAP kinase phosphorylation in pericytes, and again,

248 A mutation of the p38 MAP kinase phosphorylation site at aa 401 [(S-A)401H

249 TNF alpha stimulation of p38 MAP kinase phosphorylation was also significantly at

250 uced NF-kappa B activation but not decreased p38 MAP kinase phosphorylation.

251 ifferences in the activation of Erk, Jnk and p38 Map kinases, PLCgamma, and Ca(2+) flux do not accoun

252 aring MAPKKK DLK-1, the MAPKK MKK-4, and the p38 MAP kinase PMK-3.

253 In contrast, inhibition of p38 MAP kinase prevented increases in ezrin phosphorylat

254 Pharmacologic inhibition of p38 MAP kinase prevents both hypoxia-mediated ATF-1 phos

255 Active p38 MAP kinase promotes a G2/M cell cycle checkpoint thr

256 Our data indicate that FGF1 and p38 MAP kinase, proteins involved in cardiomyocyte proli

257 These results show that p38 MAP kinase provides critical checkpoints for the pro

258 Rs through RAS-GRF1 occurs via activation of p38 MAP kinase rather than ERK MAP kinase, which has mor

259 scription-specific activity highlighted that p38 MAP kinase regulated HBP1 protein levels but not the

260 protein kinase Sty1, a homolog of mammalian p38 MAP kinase, regulates localization of the Cdc42 pola

261 Activation of TACE by p38 MAP kinase results in the release of TGF-alpha famil

262 The p38 MAP kinase signal transduction pathway is an importa

263 racellular signal-regulated kinase (ERK) and p38 MAP kinase signaling but independent of NF-kappaB.

264 er osmotic stress via CaMKII and a conserved p38 MAP kinase signaling cascade and regulates osmotic a

265 r, our data establish that activation of the p38 MAP kinase signaling cascade plays an important role

266 se interacting proteins), which scaffold JNK/p38 MAP kinase signaling modules, also bind conventional

267 sy-1, which encode components of a conserved p38 MAP kinase signaling pathway involved in nematode de

268 The AT1 receptor-mediated ERK/p38 MAP kinase signaling pathway may be a key mechanism

269 erefore appears to be a new component of the p38 MAP kinase signaling pathway.

270 a occludens-1 (ZO-1) at the BTB site via the p38 MAP kinase signaling pathway.

271 ying intracellular mechanisms, we focused on p38 MAP kinase signaling, which is one of the major down

272 ding from mouse and human platelets requires p38 MAP kinase signaling.

273 ght an unexpected role and connection of the p38 MAP kinase-signaling pathway in cell cycle control,

274 ice that express a dominant negative form of p38 MAP kinase specifically in macrophages, production o

275 Mutation of a consensus p38 MAP kinase target site at serine 165 decreased PAK6

276 extracellular signal-regulated kinase (ERK), p38 MAP kinase, the p38 substrate MAP kinase-activated p

277 gen receptor, neuraminidase, HIV-1 protease, p38 MAP kinase, thrombin) have been assembled such that

278 ing pathway that controls the ability of the p38 MAP kinase to regulate acinar morphogenesis and inva

279 y stimulating ROS production that signal via p38 MAP kinase to the transcription factor SKN-1/NRF1,2,

280 examples of this approach are inhibition of p38 MAP kinase, use of vitamin D to restore interleukin-

281 ovel class of highly selective inhibitors of p38 MAP kinase was discovered from high throughput scree

282 essential for the activation of AP-1 whereas p38 MAP kinase was needed for the activation of C/EBP.

283 Sustained phosphorylation of p38 MAP kinase was observed in MKP-1-null MEFs in respon

284 ERK1/2) but not c-Jun N-terminal kinase-1 or p38 MAP kinase was observed in the mdx muscle compared w

285 uption of different STAT proteins and/or the p38 MAP kinase, we demonstrate that the IFN-dependent ex

286 n the current study, downstream effectors of p38 MAP kinase were sought by first screening for protei

287 In MLK3-overexpressing cells, ERK, JNKs, and p38 MAP kinases were further activated in response to TG

288 provided by recent crystal structures of the p38 MAP kinase, where a 10A movement of the Phe169 side-

289 RAPL can activate JNK but not the ERK or the p38 MAP kinases, whereas its close homolog, TIGIRR, cann

290 Inhibition of p38 MAP kinase, which blocks ezrin phosphorylation, also

291 We show that p38 MAP kinase, which is activated in response to inflam

292 cells requires Epac2-dependent activation of p38 MAP kinase, which posed the important question of ho

293 hol through heterotrimeric G proteins to the p38 MAP kinase, which then activates TCFs in the nucleus

294 inly produced from glial cells and activates p38 MAP kinase, which was significantly inhibited by SNC

295 in kinases, c-Jun amino-terminal kinases and p38 MAP kinases, which are crucial for cell survival and

296 lied to a congeneric series of 16 ligands to p38 MAP kinase whose binding constants span approximatel

297 is in macrophages in which the antiapoptotic p38 MAP kinase (whose activation is prevented by LF) was

298 l urea class of p38alpha inhibitors binds to p38 map kinase with both high affinity and slow binding

299 However, suppression of p38 MAP kinase with chemical inhibitor SC68376 not only

300 t mice, an effect abrogated by inhibition of p38 MAP kinase with SB203580.

301 from activated, differentiated Th1 cells via p38 MAP kinase without disrupting the activation and dif