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

1 efective in activating PAK3 as well as MAPK (mitogen-activated protein kinase).

2 thelial growth factor receptor 2, and p42/44 mitogen-activated protein kinase.

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

4 llagen associated with the activation of p38 mitogen-activated protein kinase.

5 ic phosphorylation and activation of the p38 mitogen-activated protein kinase.

6 it also inhibited the phosphorylation of p38 mitogen-activated protein kinase.

7 anges involving actin polymerization and p38 mitogen-activated protein kinase.

8 receptor also known as TrkA that upregulates mitogen-activated protein kinase.

9 minal kinase, but not by an inhibitor of p38 mitogen-activated protein kinase.

10 hin neurons, including ubiquitin ligases and mitogen activated protein kinases.

11 lmodulin-dependent protein kinase II, Akt or mitogen-activated protein kinases.

12 s, hyperglycemia stimulated proliferation by mitogen-activated protein kinase 1 (MAPK1)- and MAPK3-de

13 We previously demonstrated that the mitogen-activated protein kinase 1/2 inhibitor trametini

14 udy, we show that TGF-beta induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]), which in

15 Here, we report that mitogen-activated protein kinase 3 (MPK3) and MPK6 inter

16 d 8 [CXCL8]), and response to stress (CXCL8, mitogen-activated protein kinase 3, BCL2-associated X pr

17 n-activated Protein Kinase Kinase 4 (GhMKK4)-Mitogen-activated Protein Kinase 6 (GhMPK6) that directl

18 Previously, we demonstrated that Arabidopsis mitogen-activated protein kinase 6 (MPK6) and MPK3 play

19 G sites that was annotated to 9 genes [e.g., mitogen-activated protein kinase 7 (MAPK7), melanin conc

20 ease passive loading of an anti-inflammatory mitogen-activated protein kinase-activated protein kinas

21 g22, PLC2-silenced plants maintain wild-type mitogen-activated protein kinase activation and PHI1, WR

22 mation mainly by inhibition of NF-kappaB and mitogen-activated protein kinase activation but does not

23 Mechanistically, Notch1 upregulates mitogen-activated protein kinase activation through CD13

24 IKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase activation upon MAMP tr

25 GF-beta1 was dependent on both SMAD3 and p38 mitogen-activated protein kinase activation.

26 nce receptor, nprc, was increased as was p38 mitogen-activated protein kinase activation.

27 ammatory response accompanied with increased mitogen-activated protein kinases activation and elevate

28 modules associated with lipid metabolism and mitogen-activated protein kinase activity upregulated in

29 2 phosphorylation, suggesting an increase in mitogen-activated protein kinase activity.

30 ORC and late endosomal/lysosomal adaptor and mitogen activated protein kinase and mechanistic target

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

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

33 ntracellular domain-dependent CD133-mediated mitogen-activated protein kinase and activator protein-1

34 an increase in downstream signaling via the mitogen-activated protein kinase and AKT pathway.

35 n of the receptor, downstream stimulation of mitogen-activated protein kinase and Akt, and promotion

36 nterstitial fibrosis, and phosphorylated p38 mitogen-activated protein kinase and decreases in left v

37 overexpression decreases phosphorylated p38 mitogen-activated protein kinase and elevates tetrahydro

38 ts transforming growth factor beta-activated mitogen-activated protein kinase and hedgehog signaling.

39 3 and PLD1, genes downstream of CDC42 in the mitogen-activated protein kinase and mammalian target of

40 scovery of recurrent mutations affecting the mitogen-activated protein kinase and mTOR-AKT pathways i

41 Thus, MyD88 and downstream mitogen-activated protein kinase and NF-kappaB pathways

42 CXCL2/MIF-stimulated activation of the mitogen-activated protein kinase and nuclear factor kapp

43 mation feeds into various pathways (e.g. the mitogen-activated protein kinase and OXI1 signaling path

44 h levels of reactive oxygen species in a p38 mitogen-activated protein kinase and phosphatidylinosito

45 ionable mutations, most in components of the mitogen-activated protein kinase and phosphoinositol kin

46 extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase and protein kinase B (P

47 TNFAIP3/A20 promotes kinase activity of p38 mitogen-activated protein kinase and protein kinase C, w

48 via the gp130 signaling receptor, activating mitogen-activated protein kinase and signal transducer a

49 content and increases in phosphorylated p-38 mitogen-activated protein kinase and superoxide producti

50 , oxidative stress, early phosphorylation of mitogen-activated protein kinases and Akt, and upregulat

51 induced Nox2 maturation, O2 (.-) production, mitogen-activated protein kinases and nuclear factor kap

52 sin II-induced redox-sensitive activation of mitogen-activated protein kinases and phosphoinositide 3

53 ct-induced phosphorylation of p38 and ERK1/2 mitogen-activated protein kinases and secretion of cytok

54 RES activity was dependent on upstream MAPK (mitogen-activated protein kinase) and MNK1 (MAPK-interac

55 ) and K(+) gradients, phosphorylation of p38 mitogen-activated protein kinase, and cell death, withou

56 of phosphorylated heat shock protein 27, p38 mitogen-activated protein kinase, and glycogen synthase

57 r nuclear factor kappa-light-chain-enhancer, mitogen-activated protein kinase, and transforming growt

58 ied out to characterize the effect of P3G on mitogen-activated protein kinases, and on nuclear transc

59 pathways, phosphatidylinositol-3-kinase and mitogen-activated protein kinase, but express higher lev

60 Mitogen-activated protein kinase cascades are conserved

61 Mitogen-activated protein kinase cascades are important

62 in the calcium-dependent protein kinase and mitogen-activated protein kinase cascades, as well as pr

63 of the extracellular signal-regulated kinase mitogen-activated protein kinase-dependent pathway and 2

64 es the role of the protein kinase MK2, a p38 mitogen-activated protein kinase downstream target, in t

65 ial damage, epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signalling

66 ditionally, pretreatments with inhibitors of mitogen-activated protein kinase enzymes or endocytosis

67 turn, amplifies TRPV3 via activation of the mitogen-activated protein kinase ERK in a positive feedb

68 n in keratinocytes evokes phosphorylation of mitogen-activated protein kinase, ERK, for histaminergic

69 otch1 intracellular domain, CD133, and p-p38 mitogen-activated protein kinase expression and malignan

70 receptor 4 (TLR4) promotes activation of p38 mitogen-activated protein kinase, extracellular signal-r

71 in lung contusion demonstrated increased p38 mitogen-activated protein kinases, extracellular signal-

72 ctivation of various signaling pathways like mitogen-activated protein kinase-extracellular signal-re

73 ed changes in learning-related expression of mitogen-activated protein kinase/extracellular signal-re

74 The mitogen-activated protein kinase/extracellular signal-re

75 ated BTK, phosphoinositide 3-kinase/AKT, and mitogen-activated protein kinase/extracellular signal-re

76 Trametinib inhibition of mitogen-activated protein kinase/extracellular signal-re

77 These data reveal that the mitogen-activated protein kinase/extracellular signal-re

78 with the BRAF inhibitor vemurafenib and the mitogen-activated protein kinase/extracellular signal-re

79 mained intact following CD63 knockout, while mitogen-activated protein kinase/extracellular signal-re

80 n metastatic melanoma with combined BRAF and mitogen-activated protein kinase/extracellular signal-re

81 n N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and controls var

82 of CDKN2C and TP53, and mutations affecting mitogen-activated protein kinase genes.

83 of heparin and potent anti-neointimal drug (Mitogen Activated Protein Kinase II inhibitory peptide;

84 ssociated proteins: PKCdelta, ERK1/2 and p38 mitogen-activated protein kinase in HEK 293T.

85 tracellular signal-regulated kinases and p38 mitogen-activated protein kinases in primary human kerat

86 Surprisingly, S382 can be phosphorylated by mitogen-activated protein kinases in vitro.

87 p38 mitogen-activated protein kinase inhibition via SB203580

88 pretreatment with an oral small-molecule p38 mitogen-activated protein kinase inhibitor (Losmapimod;

89 Finally, it reveals that mitogen-activated protein kinase interacting kinase-1 ha

90 The maintenance of new spines driven by mitogen-activated protein kinase interacting kinase-1 wa

91 tion-independent protein synthesis driven by mitogen-activated protein kinase interacting kinase-1, d

92 Mitogen-activated protein kinase interacting protein kin

93 isphosphate 3-kinase, Akt, or p38 downstream mitogen-activated protein kinase interacting serine/thre

94 by treatment with CGP57380 (an inhibitor of mitogen-activated protein kinase-interacting serine-thre

95 Thus, this selective suppression of specific mitogen-activated protein kinases is independent of the

96 ylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively

97 athways, including Toll-like receptor (TLR), mitogen-activated protein kinase, Jak-STAT, and the nucl

98 ted and ddPCR confirmed somatic mutations in mitogen activated protein kinase kinase 1 (MAP2K1), the

99 To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor

100 h paradoxical MAPK activation; addition of a mitogen-activated protein kinase kinase (MEK) inhibitor

101 e received intraperitoneal injections of the Mitogen-activated protein kinase kinase (MEK) inhibitor,

102 rous retinal disturbances in patients taking mitogen-activated protein kinase kinase (MEK) inhibitors

103 Mitogen-activated protein kinase kinase (MEK) mutations

104 TSLP induced mitogen-activated protein kinase kinase (MEK), c-Fos, in

105 by cytokines and suppressed by inhibition of mitogen-activated protein kinase kinase 1/2, whereas STE

106 Mitogen-activated protein kinase kinase 2 (MEK2) is a ki

107 idated six candidate proteins, including the mitogen-activated protein kinase kinase 2 (MEK2), that i

108 Mitogen-activated protein kinase kinase 3 (MKK3) is a du

109 (MAP) kinase cascade consisting of GhMAP3K15-Mitogen-activated Protein Kinase Kinase 4 (GhMKK4)-Mitog

110 cific transgenic overexpression of activated mitogen-activated protein kinase kinase 6, a direct indu

111 mice with fibroblast-specific activation of mitogen-activated protein kinase kinase 6-p38 developed

112 A specific upstream activator of JNKs is the mitogen-activated protein kinase kinase 7 (MKK7).

113 Focusing on mitogen-activated protein kinase kinase and Bcl-XL targe

114 olished with omega-conotoxin, cilnidipine or mitogen-activated protein kinase kinase inhibitor.

115 ASK1, also known as MAP3K5), a member of the mitogen-activated protein kinase kinase kinase (MAP3K) f

116 nd repressing the downstream gene encoding a mitogen-activated protein kinase kinase kinase (MAPKKK)

117 appaB pathway, including the upstream kinase mitogen-activated protein kinase kinase kinase 14 (MAP3K

118 that Wallenda (Wnd), a protein kinase of the mitogen-activated protein kinase kinase kinase family, b

119 e suggested a role for endothelial cell (EC) mitogen-activated protein kinase kinase kinase kinase 4

120 Previous studies revealed a paradox whereby mitogen-activated protein kinase kinase kinase kinase 4

121 ibers, including, most prominently, MEKK4, a mitogen-activated protein kinase kinase kinase that was

122 Wnt signals, a temporal control pathway, and mitogen-activated protein kinase kinase signaling contro

123 lockade of this rebound activation with MEK (mitogen-activated protein kinase kinase) inhibition enha

124 phorylation and activation of KSR-bound MEK (mitogen-activated protein kinase kinase).

125 particular, we report synergistic effects of mitogen-activated protein kinase kinase, ribosomal S6 ki

126 NF-kappaB-inducing kinase (NIK) and mitogen-activated protein kinase kinase-1 (MEKK-1) were

127 Mitogen-activated protein kinase kinase/extracellular re

128 ghly specific protease, exclusively cleaving mitogen-activated protein kinase kinases (MKKs) and rode

129 ough in situ kinome profiling identified the mitogen-activated protein kinase MAP3K7 (TAK1) as a targ

130 e exchange factor, and the activation of the mitogen activated protein kinase (MAPK) cascade.

131 We apply the method to the mitogen activated protein kinase (MAPK) p38gamma.

132 Deregulation of the Ras-mitogen activated protein kinase (MAPK) pathway is an ea

133 of signalling via regulating the activity of mitogen activated protein kinases (MAPK), the PI3-kinase

134 temperature-dependent activation of the CEK mitogen activated proteins kinase (MAPK) pathway.

135 Pathogen-responsive mitogen-activated protein kinase (MAPK or MPK) cascades

136 ls converging at the MOR promoter, involving mitogen-activated protein kinase (MAPK) activation and m

137 ly led to decrease in negative regulators of mitogen-activated protein kinase (MAPK) activation, incl

138 ed phosphorylation of BRAF-S729 and retained mitogen-activated protein kinase (MAPK) activation.

139 ene required p38 and c-Jun N-terminal kinase mitogen-activated protein kinase (MAPK) activity, which

140 nd cellular senescence via activation of p38-mitogen-activated protein kinase (MAPK) and induction of

141 A. actinomycetemcomitans activates the p38 mitogen-activated protein kinase (MAPK) and MAPK-activat

142 innate immune response, we observed that the mitogen-activated protein kinase (MAPK) and nuclear tran

143 gnal through multiple effectors, such as the mitogen-activated protein kinase (MAPK) and PI3K pathway

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

145 e to mating pheromone activates a prototypic mitogen-activated protein kinase (MAPK) cascade and trig

146 Activating mutations in the mitogen-activated protein kinase (MAPK) cascade, also kn

147 phosphorylation, including the activation of mitogen-activated protein kinase (MAPK) cascades.

148 ERK3 is an atypical mitogen-activated protein kinase (MAPK) containing an S-

149 f nuclear factor-kappa B (NF-kappaB) and p38 mitogen-activated protein kinase (MAPK) correlated with

150 The protein p38 mitogen-activated protein kinase (MAPK) delta isoform (p

151 (ERK1), a member of the extensively studied mitogen-activated protein kinase (MAPK) family, serves a

152 KO mice with enhanced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in podocytes.

153 Smk1 is a meiosis-specific mitogen-activated protein kinase (MAPK) in Saccharomyces

154 sed sensitivity to nuclear factor-kappaB and mitogen-activated protein kinase (MAPK) inhibition, a re

155 The anti-inflammatory potential of p38 mitogen-activated protein kinase (MAPK) inhibitors was c

156 Targeted inhibition of mitogen-activated protein kinase (MAPK) kinase (MEK) can

157 The use of mitogen-activated protein kinase (MAPK) kinase (MEK) inh

158 MLK3 is a mitogen-activated protein kinase (MAPK) kinase kinase (M

159 e paralysis by cleaving and inactivating the mitogen-activated protein kinase (MAPK) kinases (MEKs).

160 IFN-gamma receptor (IFNGR) signaling led to mitogen-activated protein kinase (MAPK) p38 phosphorylat

161 In VSMC, p42/p44 mitogen-activated protein kinase (MAPK) pathway activati

162 nd defects in chromosome segregation through mitogen-activated protein kinase (MAPK) pathway activati

163 Mitogen-activated protein kinase (MAPK) pathway antagoni

164 In melanoma, activation of the mitogen-activated protein kinase (MAPK) pathway driven b

165 chymal transition and by reactivation of the mitogen-activated protein kinase (MAPK) pathway followin

166 sites, SIRT6 downregulates the expression of mitogen-activated protein kinase (MAPK) pathway genes, M

167 arget the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have led

168 ditions due to paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF

169 "paradoxical" upregulation of the downstream mitogen-activated protein kinase (MAPK) pathway in cance

170 mutations act as an oncogenic driver via the mitogen-activated protein kinase (MAPK) pathway in non-s

171 decrease; P = .02) but not with pretreatment mitogen-activated protein kinase (MAPK) pathway mutation

172 kinase BRAF drives tumor growth by promoting mitogen-activated protein kinase (MAPK) pathway signalin

173 Signaling analysis indicated decreased mitogen-activated protein kinase (MAPK) pathway signalin

174 ic cells (DCs) with constitutively activated mitogen-activated protein kinase (MAPK) pathway signalin

175 regulate host protein synthesis through the mitogen-activated protein kinase (MAPK) pathway.

176 t encode components or regulators of the Ras/mitogen-activated protein kinase (MAPK) pathway.

177 ignaling through PI3K and, surprisingly, the mitogen-activated protein kinase (MAPK) pathway.

178 Mitogen-activated protein kinase (MAPK) pathways are con

179 through mechanistic target of rapamycin and mitogen-activated protein kinase (MAPK) pathways blocks

180 daily rhythms in the activation of conserved mitogen-activated protein kinase (MAPK) pathways when ce

181 vity by suppressing the ERK1/2, p38, and JNK mitogen-activated protein kinase (MAPK) pathways.R-PIA a

182 Although the mitogen-activated protein kinase (MAPK) phosphatase, DUS

183 Mitogen-activated protein kinase (MAPK) scaffold protein

184 Mitogen-activated protein kinase (MAPK) signal transduct

185 hatase 6 (DUSP6), leading to reactivation of mitogen-activated protein kinase (MAPK) signaling (via t

186 t phosphoinositide 3-kinase (PI3K)-dependent mitogen-activated protein kinase (MAPK) signaling and in

187 Three-kinase mitogen-activated protein kinase (MAPK) signaling cascad

188 ng in NRAS(G12V) mutant cells and pronounced mitogen-activated protein kinase (MAPK) signaling in NRA

189 We show that mitogen-activated protein kinase (MAPK) signaling is lin

190 tions promote constitutive activation of the mitogen-activated protein kinase (MAPK) signaling pathwa

191 and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pathwa

192 AF gene fusions that aberrantly activate the mitogen-activated protein kinase (MAPK) signaling pathwa

193 ming growth factor beta1 (TGF-beta1) and p38 mitogen-activated protein kinase (MAPK) signaling, which

194 lin D1 expression and profound inhibition of mitogen-activated protein kinase (MAPK) signaling.

195 downstream of its receptor via activation of mitogen-activated protein kinase (MAPK) signaling.

196 mas, which are characterized by elevated RAS-mitogen-activated protein kinase (MAPK) signaling.

197 s of congenital myopathies and implicate the mitogen-activated protein kinase (MAPK) signalling as a

198 acellular Ca(2+) levels via calcineurin, p38 mitogen-activated protein kinase (MAPK), and nitric oxid

199 w that ETO perpetuates DNA damage, activates mitogen-activated protein kinase (MAPK), and triggers mo

200 -related transcription factor (MRTF) and p38 mitogen-activated protein kinase (MAPK), down-regulating

201 its rapid basal turnover in neurons and that mitogen-activated protein kinase (MAPK)-dependent phosph

202 or cell proliferation through the downstream mitogen-activated protein kinase (MAPK)-extracellular si

203 l GTPases, p21-activated kinase, and the p38 mitogen-activated protein kinase (MAPK)-MAPK-activated p

204 regulates myelination by promoting p38gamma mitogen-activated protein kinase (MAPK)-mediated phospho

205 Notably, mitogen-activated protein kinase (MAPK)-targeted therapy

206 have progressed with acquired resistance to mitogen-activated protein kinase (MAPK)-targeted therapy

207 he cornea by blocking phosphorylation of p38 mitogen-activated protein kinase (MAPK).

208 Inhibition of MEK (mitogen-activated protein kinase (MAPK)/ERK kinase) afte

209 f FLT3-ITD, which preceded the inhibition of mitogen-activated protein kinase (MAPK)/extracellular si

210 in negative regulator of HSF1; activates p38 mitogen-activated protein kinase (MAPK); and increases S

211 Mitogen-activated protein kinase (MAPK; 37%), cell cycle

212 Mitogen-activated protein kinases (MAPK) promote MAPK-ac

213 d kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were assessed

214 Recently, an interaction between mitogen-activated protein kinase (MAPK1) and vinculin wa

215 2, 4, 12 and 24 h, to analyse activation of mitogen activated protein kinases (MAPKs) and phosphatid

216 show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (MAPKs) is necessary f

217 nate response was dependent on activation of mitogen activated protein kinases (MAPKs) via stimulatin

218 KIM-PTPs bind and dephosphorylate mitogen-activated protein kinases (MAPKs) and thereby cr

219 Mitogen-activated protein kinases (MAPKs) are important

220 The molecular actions of mitogen-activated protein kinases (MAPKs) are ultimately

221 Although mitogen-activated protein kinases (MAPKs) are usually ac

222 Mitogen-activated protein kinases (MAPKs) form important

223 Cellular mitogen-activated protein kinases (MAPKs) have been show

224 It also modulated the phosphorylation of mitogen-activated protein kinases (MAPKs) in a time- dep

225 Mitogen-activated protein kinases (MAPKs) including Erk,

226 Mitogen-activated protein kinases (MAPKs) regulate brain

227 ted in increased and sustained activation of mitogen-activated protein kinases (MAPKs), morphological

228 HopAI1 targets and suppresses mitogen-activated protein kinases (MAPKs).

229 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated protein kinases (MAPKs).

230 Moreover, GOS stimulates mitogen-activated protein kinases (MAPKs); notably, c-Ju

231 unomodulatory activity of cNK-2 involves the mitogen-activated protein kinases-mediated signalling pa

232 Here, we report that p38gamma mitogen-activated protein kinase mediates inflammatory s

233 K, mechanistic target of rapamycin (mTOR) or mitogen-activated protein kinase (MEK), could effectivel

234 am effector is RAF, leading to activation of mitogen-activated protein kinase (MEK)-extracellular sig

235 uclear cells of sepsis patients, whereas p38 mitogen activated protein kinase messenger RNA was up-re

236 Mitogen-activated protein kinase (MPK) cascades are cons

237 signaling components, including elements of mitogen-activated protein kinase (MPK) cascades.

238 ene editing in the family of closely related mitogen-activated protein kinase (MPK) genes in Oryza sa

239 y PIP5K6 as a target of the pollen-expressed mitogen-activated protein kinase MPK6 and characterize t

240 We show that the mitogen-activated protein kinases (MPKs) MPK4 and MPK12

241 sponses were influenced by the MpkC and SakA mitogen-activated protein kinases of the high-osmolarity

242 eceptor antagonist, and inhibitors of either mitogen-activated protein kinases or phosphoinositide 3-

243 This effect was mediated by mitogen-activated protein kinase p38 phosphorylation and

244 icity phosphatase 1, impairs the activity of mitogen-activated protein kinase p38, increases the acti

245 , which dephosphorylates and inactivates the mitogen-activated protein kinases p38 and Jun N-terminal

246 s upregulated with aging, which enhances p38 mitogen-activated protein kinase (p38 MAPK) activation a

247 for this were related to stimulation of p38 mitogen-activated protein kinase (p38 MAPK) and activati

248 The mitogen-activated protein kinase p38alpha (Mapk14 gene)

249 Here, we described the mitogen-activated protein kinase p38gamma as a cellular

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

251 to 50-fold higher potency in activating the mitogen-activated protein kinase pathway compared with S

252 idence that these mutations activate the RAS/mitogen-activated protein kinase pathway in melanoma and

253 breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-mutant c

254 vance, pretreatment of melanoma cells with a mitogen-activated protein kinase pathway inhibitor, whic

255 st, G1-arrested cells were more sensitive to mitogen-activated protein kinase pathway inhibitor-induc

256 d G2 arrest, did not result in resistance to mitogen-activated protein kinase pathway inhibitors.

257 ng through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-

258 We also found out that p38 mitogen-activated protein kinase pathway may be implicat

259 ted the overexpression of a regulator of the mitogen-activated protein kinase pathway, mitogen-activa

260 Strained cells activated the mitogen-activated protein kinase pathway, whereas specif

261 es have shown the frequent alteration of the mitogen-activated protein kinase pathway.

262 phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-activated protein kinase) pathway coactivation i

263 Blockade or genetic ablation of Notch1 and mitogen-activated protein kinase pathways abolishes mela

264 ination of mutations of the beta-catenin and mitogen-activated protein kinase pathways as characteris

265 In neutrophils of sepsis patients, mitogen activated protein kinase phosphatase-1 messenger

266 sis factor-alpha-induced protein 3 (A20) and mitogen activated protein kinase phosphatase-1 were dete

267 , inactivation and subsequent degradation of mitogen-activated protein kinase phosphatase 1 (MKP-1) i

268 lular signal-regulated kinase 1/2, increased mitogen-activated protein kinase phosphatase 1 expressio

269 ious studies identified a potential role for mitogen-activated protein kinase phosphatase-1 (MKP-1) i

270 he mitogen-activated protein kinase pathway, mitogen-activated protein kinase phosphatase-1 (MKP-1).

271 Mitogen-activated protein kinase phosphatases (MKPs) pla

272 roteins that contribute to this process, the mitogen-activated protein kinase phosphatases (MKPs), di

273 is regulated independently of DNA binding by mitogen-activated protein kinase phosphorylation of the

274 on into early endosomes, and reduces delayed mitogen-activated protein kinase phosphorylation require

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

276 the skin in the same subjects related to p38 mitogen-activated protein kinase-related proinflammatory

277 ation and signaling, stimulating calcium and mitogen-activated protein kinase responses along with tr

278 st transdifferentiation by activation of p38 mitogen-activated protein kinases resulting in upregulat

279 diminished GTP loading of Ras, and inhibited mitogen-activated protein kinase signaling and growth of

280 elanoma cells evolve a 'just right' level of mitogen-activated protein kinase signaling and the addit

281 Whereas suppressing or enhancing Ras/mitogen-activated protein kinase signaling changed how s

282 e renin-angiotensin system in the kidney and mitogen-activated protein kinase signaling in the heart.

283 es, harbor germline mutations in various RAS/mitogen-activated protein kinase signaling pathway genes

284 us system activates a microbicidal PMK-1/p38 mitogen-activated protein kinase signaling pathway that

285 found that ERK1, a downstream kinase in the mitogen-activated protein kinase signaling pathway, phos

286 ed with wild-type mice, along with decreased mitogen-activated protein kinase signaling, tumor angiog

287 crease in NE expression, and upregulation of mitogen-activated protein kinase signaling.

288 GF-induced phosphatidylinositol-3-kinase and mitogen-activated protein kinase signaling.

289 nsducer and activator of transcription 3 and mitogen-activated protein kinase signalling in an inocul

290 The RAS/MAPK (mitogen-activated protein kinase) signalling pathway is

291 In response to environmental cues, the mitogen-activated protein kinase Sty1-driven signaling c

292 rhabditis elegans, we implicate the atypical mitogen activated protein kinase, SWIP-13, in DAT regula

293 observed upon treatment with an inhibitor to mitogen-activated protein kinase that prevents phosphory

294 tivity and hyperactivation of its downstream mitogen-activated protein kinases that are centrally imp

295 ivates nuclear factor-kappaB (NF-kappaB) and mitogen activated protein kinases, thus upregulating dow

296 cantly disrupted 7 signaling pathways (i.e., mitogen-activated protein kinases, tight junctions, foca

297 For example, Toll-like receptors activate mitogen-activated protein kinase/transcription factor pa

298 phospholipase A2(cPLA2alpha) by calcium- and mitogen-activated protein kinases triggers the rapid pro

299 s lost by suppressing the activity of Ras or mitogen-activated protein kinase, whereas the overexpres

300 diverse modes of injury converge on p38alpha mitogen-activated protein kinase within the fibroblast t