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

1 Here, we show that mitogen-activated protein 3 kinase 4 (MEKK4) expression

2 ignaling molecules that include those in the mitogen-activated protein and AKT kinase pathways.

3 Chemical inhibition of IkappaB kinase (IKK), mitogen-activated protein extracellular signal-regulated

4 deficient tumors, we report that the Ras/Raf/mitogen-activated protein, extracellular signal-regulate

5 regulatory effects of BCL6 on both MEK-ERK (mitogen-activated protein/extracellular signal-regulated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 Mitogen-activated protein kinase (MAPK) pathway antagoni

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Mitogen-activated protein kinase (MAPK) scaffold protein

63 Mitogen-activated protein kinase (MAPK) signal transduct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 2 phosphorylation, suggesting an increase in mitogen-activated protein kinase activity.

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

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

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

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

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

118 3 and PLD1, genes downstream of CDC42 in the mitogen-activated protein kinase and mammalian target of

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

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

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

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

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

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

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

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

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

128 Mitogen-activated protein kinase cascades are conserved

129 Mitogen-activated protein kinase cascades are important

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

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

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

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

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

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

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

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

138 p38 mitogen-activated protein kinase inhibition via SB203580

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

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

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

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

143 Mitogen-activated protein kinase interacting protein kin

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

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

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

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

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

149 Mitogen-activated protein kinase kinase (MEK) mutations

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 Mitogen-activated protein kinase kinase/extracellular re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 Mitogen-activated protein kinase phosphatases (MKPs) pla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 2, 4, 12 and 24 h, to analyse activation of mitogen activated protein kinases (MAPKs) and phosphatid

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

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

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

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

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

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

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

259 Mitogen-activated protein kinases (MAPKs) are important

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

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

262 Mitogen-activated protein kinases (MAPKs) form important

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

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

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

266 Mitogen-activated protein kinases (MAPKs) regulate brain

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

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

269 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated protein kinases (MAPKs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 growth rate through their activation of the mitogen-activated protein (MAP) kinase (extracellular si

292 c sterol precursors target a single ERK-like mitogen-activated protein (MAP) kinase (MAK-1)-signaling

293 analyses revealed a drought stress-activated mitogen-activated protein (MAP) kinase cascade consistin

294 ivate their common downstream effectors, the mitogen-activated protein (MAP) kinase Erk and protein k

295 T/phosphatydylinositol-3'-kinase (PI3-K) and mitogen-activated protein (MAP) kinase pathways via TpoR

296 duction of reactive oxygen species (ROS) and mitogen-activated protein (MAP) kinase phosphorylation,

297 Stress-associated p38 and JNK mitogen-activated protein (MAP) kinase signaling cascade

298 Mitogen-activated protein (MAP) kinase substrates are be

299 of TAK1 as well as downstream NF-kappaB and mitogen-activated protein (MAP) kinases.

300 ns and a homozygous nonsense mutation in the mitogen-activated protein triple kinase ZAK.