ライフサイエンスコーパス: p38 mitogen-activated protein kinase

1 on, it also inhibited the phosphorylation of p38 mitogen-activated protein kinase.

2 tokinemia seems to involve hyperinduction of p38 mitogen-activated protein kinase.

3 ical inhibitors of nuclear factor-kappaB and p38 mitogen-activated protein kinase.

4 howed exaggerated phosphorylation of Syk and p38 mitogen-activated protein kinase.

5 -terminal kinase, but not by an inhibitor of p38 mitogen-activated protein kinase.

6 gher levels of the IL-1 receptor and phospho-p38 mitogen-activated protein kinase.

7 r hypertrophy and phosphorylation of Akt and p38 mitogen-activated protein kinase.

8 hrough a signaling pathway involving Src and p38 mitogen-activated protein kinase.

9 s and regulates downstream engagement of the p38 mitogen-activated protein kinase.

10 ternalization of GRP78 and the activation of p38 mitogen-activated protein kinase.

11 apparently involved increased activation of p38 mitogen-activated protein kinase.

12 1 collagen associated with the activation of p38 mitogen-activated protein kinase.

13 ecific phosphorylation and activation of the p38 mitogen-activated protein kinase.

14 the activities of both protein kinase A and p38 mitogen-activated protein kinase.

15 l changes involving actin polymerization and p38 mitogen-activated protein kinase.

16 he phosphoinositide-3-kinase/Akt pathway and p38 mitogen-activated protein kinase.

17 protein kinases such as protein kinase A and p38 mitogen-activated protein kinase.

18 kinases 1 and 2, c-Jun N-terminal kinase and p38 mitogen-activated protein kinase.

19 ollagen 3a1 expression via the activation of p38 mitogen-activated protein kinase.

20 growth factor and an increase in myocardial p38 mitogen-activated protein kinase activation in femal

21 p38 mitogen-activated protein kinase activation plays an

22 ion of signaling via various TLRs, prolonged p38 mitogen-activated protein kinase activation, and ind

23 order zone fibrosis, augmented NF-kappaB and p38 mitogen-activated protein kinase activation, higher

24 nd inhibition of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation, which a

25 gh extracellular signal-regulated kinase and p38 mitogen-activated protein kinase activation.

26 ation of HuR, controlled by TGF-beta-induced p38 mitogen-activated protein kinase activation.

27 by TGF-beta1 was dependent on both SMAD3 and p38 mitogen-activated protein kinase activation.

28 earance receptor, nprc, was increased as was p38 mitogen-activated protein kinase activation.

29 sed phosphorylation as a result of a loss of p38 mitogen-activated protein kinase activity and increa

30 TRAF6 mediates the activation of JNK1/2, p38 mitogen-activated protein kinase, adenosine monophos

31 reased activation of EGF receptor (EGFR) and p38 mitogen-activated protein kinase, all of which could

32 s a result of activation of several kinases (p38 mitogen-activated protein kinase alpha, p38 mitogen-

33 as well as decreased phosphorylated JNK and p38 mitogen-activated protein kinase-alpha, in the Ad.Tr

34 Messenger RNA expression levels of p38 mitogen activated protein kinase and nuclear factor

35 The phosphorylation state of p38 mitogen activated protein kinase and nuclear factor

36 ers, which was associated with activation of p38 mitogen-activated protein kinase and Abeta internali

37 At sublytic concentrations, INY activates p38 mitogen-activated protein kinase and allows entry of

38 iated with an increase in phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-termina

39 MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-termina

40 m, interstitial fibrosis, and phosphorylated p38 mitogen-activated protein kinase and decreases in le

41 GCH1 overexpression decreases phosphorylated p38 mitogen-activated protein kinase and elevates tetrah

42 We also found evidence of increased p38 mitogen-activated protein kinase and glycogen syntha

43 d p62 levels and downstream on activation of p38 mitogen-activated protein kinase and inactivation of

44 cancer stem-like cells (CSCs) by activating p38 mitogen-activated protein kinase and increasing expr

45 ing, leading to sustained phosphorylation of p38 mitogen-activated protein kinase and induction of p3

46 high levels of reactive oxygen species in a p38 mitogen-activated protein kinase and phosphatidylino

47 chondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apopt

48 3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory

49 n of TNFAIP3/A20 promotes kinase activity of p38 mitogen-activated protein kinase and protein kinase

50 , CCK(A), and is attenuated by inhibitors of p38 mitogen-activated protein kinase and Tec tyrosine ki

51 Acsl4a promotes the inhibition of p38 mitogen-activated protein kinase and the Akt-mediate

52 1b-dependent changes require the activity of p38 mitogen-activated protein kinase and the cAMP-respon

53 ch is catalyzed by the cooperative action of p38 mitogen-activated protein kinases and Akt kinases.

54 including ligands of the EGFR, involves Src, p38 mitogen-activated protein-kinase and PI3K, but does

55 s: inhibitors of glycogen synthase kinase-3, p38 mitogen-activated protein kinase, and Ca(2+)/calmodu

56 Na(+) and K(+) gradients, phosphorylation of p38 mitogen-activated protein kinase, and cell death, wi

57 oxidative stress in the heart, activation of p38 mitogen-activated protein kinase, and contractile dy

58 ase of phosphorylated heat shock protein 27, p38 mitogen-activated protein kinase, and glycogen synth

59 ess apoptosis; and (3) diminished NF-kappaB, p38 mitogen-activated protein kinase, and JNK2 activatio

60 st activation of nuclear factor (NF)-kappaB, p38 mitogen-activated protein kinase, and JNK2 and upreg

61 lammatory signaling pathways cyclooxygenase, p38 mitogen-activated protein kinase, and nuclear factor

62 transducer and activator of transcription 5, p38 mitogen-activated protein kinase, and nuclear factor

63 subunit p47(phox), phosphorylated and total p38 mitogen-activated protein kinase, and suppressor of

64 ss kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases, and inhibition of

65 and ghrelin receptor, induction of cAMP and p38-mitogen-activated protein kinase, and inhibition of

66 diverts the PI3K-Akt survival signal to the p38-mitogen-activated protein kinase apoptosis pathway.

67 athways identified Jun N-terminal kinase and p38 mitogen-activated protein kinase as antagonistic eff

68 dent activation of nuclear factor kappaB and p38 mitogen-activated protein kinase, as well as intrace

69 e-1, vascular endothelial growth factor, and p38 mitogen-activated protein kinase-beta, as well as de

70 kade of transforming growth factor beta1 and p38 mitogen-activated protein kinase blockade.

71 xtracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase but not of Jun NH(2

72 or both nuclear factor-kappaB activation and p38-mitogen-activated protein kinase, but not for protei

73 Loss of PTPN22 increased levels of p38-mitogen-activated protein kinase, but reduced phosph

74 cted M1-D macrophages revealed activation of p38 mitogen-activated protein kinase by 2 to 3 h postinf

75 Another proposed SERT kinase, the p38 mitogen-activated protein kinase, could not substitu

76 tudies suggest that PV pathogenesis involves p38 mitogen-activated protein kinase-dependent and -inde

77 and 5a1 in cultured aortic fibroblasts in a p38 mitogen-activated protein kinase-dependent fashion,

78 ore robustly than either cue alone through a p38 mitogen-activated protein kinase-dependent mechanism

79 that hypoxia (1% oxygen) induced Cezanne via p38 mitogen-activated protein kinase-dependent transcrip

80 tracellular signal-regulated kinase 1/2, and p38 mitogen-activated protein kinase did not affect nucl

81 igates the role of the protein kinase MK2, a p38 mitogen-activated protein kinase downstream target,

82 serine kinases Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase, enhances the serin

83 en Notch1 intracellular domain, CD133, and p-p38 mitogen-activated protein kinase expression and mali

84 ERK1/2 mitogen-activated protein kinase and p38 mitogen-activated protein kinase expression while se

85 ur intervals from day 0 to day 4, as well as p38-mitogen activated protein kinase expression.

86 ike receptor 4 (TLR4) promotes activation of p38 mitogen-activated protein kinase, extracellular sign

87 Moreover, increased phosphorylation of p38 mitogen-activated protein kinase, Extracellular sign

88 ury in lung contusion demonstrated increased p38 mitogen-activated protein kinases, extracellular sig

89 (p38 mitogen-activated protein kinase alpha, p38 mitogen-activated protein kinase gamma, and c-Jun N-

90 regulates SKN-1 target genes downstream from p38 mitogen-activated protein kinase, glycogen synthase

91 on-associated proteins: PKCdelta, ERK1/2 and p38 mitogen-activated protein kinase in HEK 293T.

92 leading to ROS-dependent hyperactivation of p38 mitogen-activated protein kinase in the presence of

93 To investigate p38 mitogen-activated protein kinase in vivo, we profile

94 f extracellular signal-regulated kinases and p38 mitogen-activated protein kinases in primary human k

95 uced activation of stress-activated p38MAPK (p38 mitogen-activated protein kinase) in microglia and i

96 ve protein kinases (Janus kinase 2, Akt, and p38 mitogen-activated protein kinase) in VSMCs.

97 and cell death in a high osmolarity glycerol-p38 mitogen-activated protein kinase-independent manner,

98 p38 mitogen-activated protein kinase inhibition via SB20

99 of pretreatment with an oral small-molecule p38 mitogen-activated protein kinase inhibitor (Losmapim

100 The novel p38 mitogen-activated protein kinase inhibitor dilmapimo

101 1) but not to TNFR2 and was abolished by the p38 mitogen-activated protein kinase inhibitor SB202190

102 r signal-regulated receptor kinase (ERK) and p38 mitogen-activated protein kinase inhibitors (U0126 a

103 ental stages, glycogen synthase kinase-3 and p38 mitogen-activated protein kinase inhibitors substant

104 The p38 mitogen-activated protein kinase is a key player in

105 p38 mitogen-activated protein kinase is central to the r

106 The p38 mitogen-activated protein kinase isoforms are import

107 xtracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase leading to DR4 and

108 TNF-alpha-induced phosphorylated p38 mitogen-activated protein kinase levels were increas

109 itive; this might be secondary to heightened p38 mitogen-activated protein kinase levels.

110 These are phosphorylated p38 mitogen-activated protein kinase (MAPK) (p38-P), a k

111 Specifically, PTP1B counteracts p38 mitogen-activated protein kinase (MAPK) activation b

112 T cells possess a unique mechanism of p38 mitogen-activated protein kinase (MAPK) activation d

113 Downstream, an Abeta-mediated rise in p38 mitogen-activated protein kinase (MAPK) activation w

114 corticosteroid-regulated genes and cellular p38 mitogen-activated protein kinase (MAPK) activation.

115 racellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) activities.

116 erve injury, here we show that inhibition of p38 mitogen-activated protein kinase (MAPK) activity in

117 Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactiv

118 the differentiation-associated activation of p38 mitogen-activated protein kinase (MAPK) and Akt kina

119 nduced host immune suppression by activating p38 mitogen-activated protein kinase (MAPK) and AKT sign

120 and nitric oxide, causing the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-

121 Activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun NH

122 The p38 mitogen-activated protein kinase (MAPK) and c-Jun NH

123 Selective inhibitors of p38 mitogen-activated protein kinase (MAPK) and extracel

124 igus IgGs to induce blistering and that both p38 mitogen-activated protein kinase (MAPK) and heat sho

125 phosphorylation of stress related molecules p38 mitogen-activated protein kinase (MAPK) and Hsp27 an

126 A. actinomycetemcomitans activates the p38 mitogen-activated protein kinase (MAPK) and MAPK-act

127 deed, knockdown of AUF1 impairs LPS-mediated p38 mitogen-activated protein kinase (MAPK) and NF-kappa

128 ificantly reduced by chemical inhibitors for p38 mitogen-activated protein kinase (MAPK) and NF-kappa

129 ntents, expression, and activation status of p38 mitogen-activated protein kinase (MAPK) and PPARgamm

130 measured as the production of phosphorylated p38 mitogen-activated protein kinase (MAPK) and proinfla

131 decanoylphorbol-13-acetate), suggesting that p38 mitogen-activated protein kinase (MAPK) and protein

132 indicate that SNARE-1 rapidly phosphorylates p38 mitogen-activated protein kinase (MAPK) and Ser(650)

133 CD4(+) T cells increased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and signal t

134 The roles of EGFR ligands, p38 mitogen-activated protein kinase (MAPK) and tumour n

135 Investigators have described p38 mitogen-activated protein kinase (MAPK) as a key reg

136 was performed for p53, p21, and phospho (p)-p38 mitogen-activated protein kinase (MAPK) as markers o

137 Furthermore, inhibition of p38 mitogen-activated protein kinase (MAPK) blocked phos

138 Furthermore, we identify the p38 mitogen-activated protein kinase (MAPK) cascade as a

139 In Caenorhabditis elegans, a p38 mitogen-activated protein kinase (MAPK) cascade prom

140 on of nuclear factor-kappa B (NF-kappaB) and p38 mitogen-activated protein kinase (MAPK) correlated w

141 The protein p38 mitogen-activated protein kinase (MAPK) delta isofor

142 channel activity was accompanied by phospho-p38 mitogen-activated protein kinase (MAPK) expression.

143 p38 mitogen-activated protein kinase (MAPK) has emerged

144 n the current study we investigated the role p38 mitogen-activated protein kinase (MAPK) in astroglio

145 C-A KO mice with enhanced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in podocytes

146 We previously reported activation of p38 mitogen-activated protein kinase (MAPK) in response

147 lly, loss of BMPR2 induced prolonged phospho-p38 mitogen-activated protein kinase (MAPK) in response

148 In this study, we investigated a role of p38 mitogen-activated protein kinase (MAPK) in this proc

149 onversely, levels of PTEN and phosphorylated p38 mitogen-activated protein kinase (MAPK) increased ma

150 A p38 mitogen-activated protein kinase (MAPK) inhibitor, S

151 The anti-inflammatory potential of p38 mitogen-activated protein kinase (MAPK) inhibitors w

152 toplasm, which promotes the translocation of p38 mitogen-activated protein kinase (MAPK) into mitocho

153 p38 mitogen-activated protein kinase (MAPK) is known to

154 lation of Ctgf expression is associated with p38 mitogen-activated protein kinase (MAPK) overactivati

155 that IFN-gamma activates the ASK1-MKK3/MKK6-p38 mitogen-activated protein kinase (MAPK) pathway for

156 The p38 mitogen-activated protein kinase (MAPK) pathway has

157 ished a principal role for a conserved PMK-1 p38 mitogen-activated protein kinase (MAPK) pathway in m

158 The p38 mitogen-activated protein kinase (MAPK) pathway is r

159 AC, in addition to calcineurin, inhibits the p38 mitogen-activated protein kinase (MAPK) pathway, whi

160 ression of the hypoxia-induced mitochondrial p38 mitogen-activated protein kinase (MAPK) pathway.

161 ogramming is linked to the activation of the p38 mitogen-activated protein kinase (MAPK) pathway.

162 STZ induced p38 mitogen-activated protein kinase (MAPK) phosphorylat

163 d a novel function of PXR, that of eliciting p38 mitogen-activated protein kinase (MAPK) phosphorylat

164 The p38 mitogen-activated protein kinase (MAPK) plays an imp

165 ctor (TRAF) homologs trf-1 and trf-2 and the p38 mitogen-activated protein kinase (MAPK) pmk-1 acted

166 iotensin II induced TRPC6 expression through p38 mitogen-activated protein kinase (MAPK) serum respon

167 The p38 mitogen-activated protein kinase (MAPK) signaling pa

168 ction through the Toll-like receptor (TLR) 2/p38 mitogen-activated protein kinase (MAPK) signaling pa

169 oters that are functionally part of IL-1 and p38 mitogen-activated protein kinase (MAPK) signaling pa

170 tion and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pa

171 ed stress-responsive kinases, members of the p38 mitogen-activated protein kinase (MAPK) signaling pa

172 p38 mitogen-activated protein kinase (MAPK) signaling pr

173 p38 mitogen-activated protein kinase (MAPK) signaling se

174 sforming growth factor beta1 (TGF-beta1) and p38 mitogen-activated protein kinase (MAPK) signaling, w

175 PEST domain also controls the activation of p38 mitogen-activated protein kinase (MAPK) through phos

176 rt with a C-terminal serine (S800) target of p38 mitogen-activated protein kinase (MAPK) to regulate

177 Involvement of p38 mitogen-activated protein kinase (MAPK) was assessed

178 gene knockout approach, the alpha isoform of p38 mitogen-activated protein kinase (MAPK) was selectiv

179 nhibition was dependent on the activation of p38 mitogen-activated protein kinase (MAPK) within these

180 nt mediator of vasoregulation) and activates p38 mitogen-activated protein kinase (MAPK), a mediator

181 -regulated kinase (ERK) and STAT1 but not of p38 mitogen-activated protein kinase (MAPK), Akt, or c-J

182 NF-alpha overproduction phenotype depends on p38 mitogen-activated protein kinase (MAPK), an enzyme a

183 d chemokines via nuclear factor (NF)-kappaB, p38 mitogen-activated protein kinase (MAPK), and activat

184 vation of nuclear factor-kappaB (NF-kappaB), p38 mitogen-activated protein kinase (MAPK), and extrace

185 IL-1beta upregulated p38 mitogen-activated protein kinase (MAPK), and inhibit

186 In this study, we show that cPLA2, p38 mitogen-activated protein kinase (MAPK), and Janus k

187 including nuclear factor kappaB (NF-kappaB), p38 mitogen-activated protein kinase (MAPK), and Jun N-t

188 intracellular Ca(2+) levels via calcineurin, p38 mitogen-activated protein kinase (MAPK), and nitric

189 ddition, STEP61 negatively regulates Fyn and p38 mitogen-activated protein kinase (MAPK), and these p

190 n enhancer of activated B cells (NF-kappaB), p38 mitogen-activated protein kinase (MAPK), cyclin D1,

191 rdin-related transcription factor (MRTF) and p38 mitogen-activated protein kinase (MAPK), down-regula

192 ein kinase kinase (MKK)3/MKK6, activation of p38 mitogen-activated protein kinase (MAPK), epidermal g

193 cies (ROS), which act through > or =1 of the p38 mitogen-activated protein kinase (MAPK), extracellul

194 iptional factor 1 (Foxo1), and activation of p38 mitogen-activated protein kinase (MAPK), indicating

195 IkappaB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK), induced by

196 Transcription factors NF-kappaB p65, p38 mitogen-activated protein kinase (MAPK), Jun N-termi

197 athways, including focal adhesion kinase and p38 mitogen-activated protein kinase (MAPK), resulting i

198 Here, we show that p38 mitogen-activated protein kinase (MAPK), which contr

199 p38 mitogen-activated protein kinase (MAPK), which is co

200 , tristetraprolin (TTP), is repressed by the p38 mitogen-activated protein kinase (MAPK)-activated ki

201 a variety of stress-activating stimuli in a p38 mitogen-activated protein kinase (MAPK)-dependent ma

202 lin E (IgE) in a protein kinase A (PKA)- and p38 mitogen-activated protein kinase (MAPK)-dependent ma

203 Although the p38 mitogen-activated protein kinase (MAPK)-dependent pa

204 is mediated by protein kinase G1 (PKGI)- and p38 mitogen-activated protein kinase (MAPK)-linked pathw

205 small GTPases, p21-activated kinase, and the p38 mitogen-activated protein kinase (MAPK)-MAPK-activat

206 p38 Mitogen-activated protein kinase (MAPK)-stimulated i

207 f WASP, but increased activation of PAK1 and p38 mitogen-activated protein kinase (MAPK).

208 d adult cardiomyocytes through activation of p38 mitogen-activated protein kinase (MAPK).

209 ed c-Jun NH(2)-terminal kinase (JNK) 1/2 and p38 mitogen-activated protein kinase (MAPK).

210 in the cornea by blocking phosphorylation of p38 mitogen-activated protein kinase (MAPK).

211 zing HIF-1alpha mRNA upon phosphorylation by p38 mitogen-activated protein kinase (MAPK)/MAPK-activat

212 DNA damage response pathway mediated by the p38 mitogen-activated protein kinase (MAPK)/MAPK-activat

213 e main negative regulator of HSF1; activates p38 mitogen-activated protein kinase (MAPK); and increas

214 tion of ROCK did not block the activation of p38 mitogen-activated protein kinase (MAPK); instead, Rh

215 eam signaling effectors [cAMP, Rac1-GTP, and p38 mitogen-activated protein kinase (MAPK)] as key mech

216 lls resulting from TPA induces activation of p38 mitogen-activated protein kinase (MAPK/p38).

217 st and cellular senescence via activation of p38-mitogen-activated protein kinase (MAPK) and inductio

218 cyclooxygenase-2 (COX-2) expression through p38-mitogen-activated protein kinase (MAPK)-dependent ac

219 ut NF-kappaB siRNA or treated with SB202190 (p38 [mitogen activated protein kinase] MAPK inhibitor) b

220 f macrophage Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs) via reduce

221 nase 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated protein kinases (MAPKs).

222 helial proapoptotic pathways, in particular, p38-mitogen-activated protein kinase-mediated activation

223 ononuclear cells of sepsis patients, whereas p38 mitogen activated protein kinase messenger RNA was u

224 Inhibition of p38 mitogen-activated protein kinase not only reversed i

225 Lamin B1 loss did not depend on the p38 mitogen-activated protein kinase, nuclear factor-kap

226 LPS-induced phosphorylated p38 mitogen-activated protein kinase (p-p38) in monocyte

227 Some changes correlate with activation of p38 mitogen activated protein kinase (p38 MAPK).

228 IL-1beta acts in a p38 mitogen-activated protein kinase (p38 MAP kinase)-de

229 nd is upregulated with aging, which enhances p38 mitogen-activated protein kinase (p38 MAPK) activati

230 racellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) activiti

231 isms for this were related to stimulation of p38 mitogen-activated protein kinase (p38 MAPK) and acti

232 Here we show that p38 mitogen-activated protein kinase (p38 MAPK) phosphor

233 The noradrenergic and p38 mitogen-activated protein kinase (p38 MAPK) systems

234 ation of glucose levels induced PKCdelta and p38 mitogen-activated protein kinase (p38 MAPK) to incre

235 f PKB in relation to mitoK(ATP) channels and p38 mitogen-activated protein kinase (p38 MAPK), and whe

236 Importantly, we show that the p38 mitogen-activated protein kinase (p38 MAPK), cAMP-re

237 LPS induced phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), in part

238 racellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK), two MAP

239 charides induce oxidative stress mediated by p38 mitogen-activated protein kinase (p38 MAPK).

240 phosphatase calcineurin (CaN) or the kinase p38 mitogen-activated protein kinase (p38 MAPK).

241 enase-2, serum C-terminal telopeptide (CTX), p38 mitogen-activated protein kinase (p38), and receptor

242 ation of nuclear factor kappa B (NF-kB/p65), p38 mitogen-activated protein kinase (p38), ERK, and JNK

243 n; inhibitors of phosphodiesterase-4 (PDE4), p38 mitogen-activated protein kinase (p38), Janus kinase

244 es and that EGFR activation is downstream of p38 mitogen-activated protein kinase (p38).

245 llular signal-regulated kinases (Erk1/2) and p38 mitogen-activated protein kinases (p38 MAPK).

246 nd activator of transcription 1 (STAT1)-NOS2-p38 mitogen activated protein kinase (p38MAPK)-activatin

247 ugh in vitro data indicate that ILK controls p38 mitogen-activated protein kinase (p38MAPK) activity,

248 n activates AMP-activated protein kinase and p38 mitogen-activated protein kinase (p38MAPK) signaling

249 n pathways involving protein kinase C (PKC), p38 mitogen-activated protein kinase (p38MAPK), extracel

250 veal a unique cellular pathway involving the p38 mitogen-activated protein kinase (p38MAPK)-mediated

251 gainst Gram-positive bacteria, including the p38 mitogen-activated protein kinase pathway (via TIR-1

252 ysis, VLY activates the conserved epithelial p38 mitogen-activated protein kinase pathway and induces

253 macrophages depressed HMGB1 activity via the p38 mitogen-activated protein kinase pathway and led to

254 Inhibition of the p38 mitogen-activated protein kinase pathway blocked the

255 ngiotensin II-induced phosphorylation of the p38 mitogen-activated protein kinase pathway but not of

256 tly been attributed to the activation of the p38 mitogen-activated protein kinase pathway following a

257 pparent macrophage-specific inhibitor of the p38 mitogen-activated protein kinase pathway in an isoge

258 findings demonstrate an integral role of the p38 mitogen-activated protein kinase pathway in interleu

259 Dysregulation of the p38 mitogen-activated protein kinase pathway in meningoc

260 naling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly

261 We also found out that p38 mitogen-activated protein kinase pathway may be impl

262 Transcripts for genes mapping to the p38 mitogen-activated protein kinase pathway showed sign

263 was restored by addition of TGF-beta via the p38 mitogen-activated protein kinase pathway.

264 on of antimicrobial peptides via a conserved p38 mitogen-activated protein kinase pathway.

265 kinases, phosphatidylinositol-3-kinase, and p38 mitogen-activated protein kinase pathways to upregul

266 l and posttranscriptional levels by PI3K and p38 mitogen-activated protein kinase pathways, respectiv

267 Only p38 mitogen-activated protein kinase phosphorylation was

268 atocyte transactivation, fibrosis, increased p38 mitogen-activated protein kinase phosphorylation, el

269 MP-3, and MMP-9, whereas IFN-gamma inhibited p38 mitogen-activated protein kinase phosphorylation.

270 r factor kappa B p65, protein kinase B1, and p38 mitogen-activated protein kinase phosphorylation.

271 ated with significant reduction of p38-MAPK (p38-mitogen-activated protein kinase) phosphorylation.

272 in the skin in the same subjects related to p38 mitogen-activated protein kinase-related proinflamma

273 oblast transdifferentiation by activation of p38 mitogen-activated protein kinases resulting in upreg

274 atment leads to CXCR4-mediated activation of p38 mitogen-activated protein kinase, resulting in phosp

275 iomyocytes transduced with dominant-negative p38 mitogen-activated protein kinase showed no interleuk

276 hypoxia increased the activation of JNK and p38 mitogen-activated protein kinase signaling in palmit

277 Immunoblotting revealed that p38 mitogen-activated protein kinase signaling mediated

278 ating the nuclear factor-E2-related factor 2/p38 mitogen-activated protein kinase signaling pathway a

279 However, how the p38 mitogen-activated protein kinase signaling pathway i

280 control the unfolded protein response and a p38 mitogen-activated protein kinase signaling pathway r

281 ervous system activates a microbicidal PMK-1/p38 mitogen-activated protein kinase signaling pathway t

282 suppresses Abeta-mediated activation of the p38 mitogen-activated protein kinase signaling pathway,

283 xtracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase signaling pathways

284 xtracellular signal-regulated kinase-1/2, or p38 mitogen-activated protein kinase signaling to drive

285 ylated p38 (P-p38, a marker of activation of p38 mitogen-activated protein kinase signaling).

286 273 and these antiapoptotic effects involved p38 mitogen-activated protein kinase signaling.

287 esponses through multiple pathways including p38 mitogen-activated protein kinase signaling.

288 locking transforming growth factor beta1 and p38 mitogen-activated protein kinase signaling.

289 d this was accompanied by similar changes in p38-mitogen activated protein kinase signaling.

290 vators of neuropathic and inflammatory pain (p38 mitogen-activated protein kinase, STAT3, and mitogen

291 ed by altering phosphorylation of Smads 2/3, p38 mitogen-activated protein kinase, stress-activated p

292 We show that Smad7 and p38 mitogen-activated protein kinase together regulate t

293 g growth factor-beta, nuclear factor-kappaB, p38 mitogen-activated protein kinase, toll-like receptor

294 Furthermore, p38 mitogen-activated protein kinase was found to be a n

295 racellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase were markedly activ

296 xtracellular signal-related kinase (ERK) and P38 mitogen-activated protein kinases were localized in

297 oxidative stress-mediated activation of the p38 mitogen activated protein kinase, which, in turn, in

298 orylation of TGF-beta-activated kinase 1 and p38 mitogen-activated protein kinase, which amplifies th

299 duced migration revealed that Pyk2 activates p38 mitogen-activated protein kinase, which in turn acti

300 due to its site-specific phosphorylation by p38 mitogen-activated protein kinase, which is involved