ライフサイエンスコーパス: MAP kinase pathway

1 ally regulated by STAT complexes and the p38 MAP kinase pathway.

2 ocked the capacity of PEA-15 to activate the MAP kinase pathway.

3 matically reshape output of the yeast mating MAP kinase pathway.

4 he CaSR and signal mediation by the p38alpha MAP kinase pathway.

5 tcome from activation of the multipotent ERK MAP kinase pathway.

6 1 cytokine through the activation of the p38 MAP kinase pathway.

7 s that were over-represented in genes of the MAP kinase pathway.

8 s the nuclear export of Hdm2 and p53 via the MAP kinase pathway.

9 ediated Cdx regulation is independent of the MAP kinase pathway.

10 diabetes, induce chymase via the RAGE-ERK1/2 MAP kinase pathway.

11 nhibit chondrocyte proliferation via the Erk MAP kinase pathway.

12 egments with PD98059, an inhibitor of p42/44 MAP kinase pathway.

13 vation of the EGFR and activation of the ERK/MAP kinase pathway.

14 functions as a molecular scaffold in the Ras/MAP kinase pathway.

15 ent with PD98059, an inhibitor of the p42/44 MAP kinase pathway.

16 t in the presence of an inhibitor of the p38 MAP kinase pathway.

17 n that functions upstream of a conserved p38 MAP kinase pathway.

18 ndidate components of the filamentous growth MAP kinase pathway.

19 -1 in response to signalling through the ERK MAP kinase pathway.

20 d the Pap1p component of the stress response MAP kinase pathway.

21 al-regulated kinase (ERK) kinase [MEK]-->ERK MAP kinase pathway.

22 EGFR, and activation of the MEK1/2-dependent MAP kinase pathway.

23 was mediated via the PI 3-kinase and not the MAP kinase pathway.

24 the neuron survival-related functions of the MAP kinase pathway.

25 activity, and also induced activation of the MAP kinase pathway.

26 er channel activity and route signals to the MAP kinase pathway.

27 f Ser(791), depends on activation of the Erk MAP kinase pathway.

28 tive activation of the MKK3/p38 beta protein MAP kinase pathway.

29 ion as well as acting as an inhibitor of the MAP kinase pathway.

30 may suppress HBV replication through the Ras-MAP kinase pathway.

31 also found to directly stimulate the p42/44-MAP kinase pathway.

32 through ALK in NIH3T3 fibroblasts is via the MAP kinase pathway.

33 with an increased ability to turn on the Ras-MAP kinase pathway.

34 scriptional complexes or function in the PKC-MAP kinase pathway.

35 to tumor cells through the activation of the MAP kinase pathway.

36 r mitogenic effect through activation of the MAP kinase pathway.

37 otubules, and depends on a functioning DLK-1 MAP kinase pathway.

38 protein 2, as well as activation of the Erk MAP kinase pathway.

39 xcitatory input through the protein kinase C/MAP kinase pathway.

40 t BRAF functions distinctly from CRAF in the MAP kinase pathway.

41 of apoptosis involving multiple genes in the MAP kinase pathway.

42 RS2alpha to promote activation of the ERK1/2 MAP kinase pathway.

43 gesting that the activity is mediated by the MAP kinase pathway.

44 independently of bulk activation of the ERK MAP-kinase pathway.

45 ement in both the Ras1-adenylate cyclase and MAP kinase pathways.

46 mple of Nox-specific differential control of MAP kinase pathways.

47 dently, each by a subset of genes in the Wnt/MAP kinase pathways.

48 lk-1 to the ERK and the stress-activated p38 MAP kinase pathways.

49 ling different classes of NMDARs to distinct MAP kinase pathways.

50 togen-activated protein (MAP) kinase and p38 MAP kinase pathways.

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

52 ctivation regulates downstream engagement of MAP kinase pathways.

53 SK1-3) are apical kinases of the p38 and JNK MAP kinase pathways.

54 pe 1 and mediates the IkappaB kinase and p38 MAP kinase pathways.

55 osphatidylinositol 3-kinase (PI3-kinase) and MAP kinase pathways.

56 nt a general mechanism for the regulation of MAP kinase pathways.

57 ogression, and the activation of p38 and ERK MAP kinase pathways.

58 ther G-protein or arrestin-mediated cAMP and MAP kinase pathways.

59 and genetic networks that include the major MAP kinase pathways.

60 hibition of the phosphoinositol 3-kinase and MAP kinase pathways.

61 inflammatory responses through inhibition of MAP kinase pathways.

62 in addition to its known role in regulating MAP kinase pathways.

63 s through its regulation of the mTOR and p38 MAP kinase pathways.

64 activation of the mitogen-activated protein (MAP) kinase pathway.

65 sly described p38 mitogen-activated protein (MAP) kinase pathway.

66 rity growth (HOG) mitogen-activated protein (MAP) kinase pathway.

67 l integrity (CWI) mitogen-activated protein (MAP) kinase pathway.

68 pated role in the mitogen-activated protein (MAP) kinase pathway.

69 hway, but not the mitogen-activated protein (MAP) kinase pathway.

70 d kinase (ERK)1/2 mitogen-activated protein (MAP) kinase pathway.

71 d proinflammatory mitogen-activated protein (MAP) kinase pathways.

72 , an inhibitor of mitogen-activated protein (MAP) kinase pathways.

73 int for different mitogen-activated protein (MAP) kinase pathways.

74 JAK-STAT) and p38 mitogen-activated protein (MAP) kinase pathways.

75 signaling showed a greater dependence on the MAP kinase pathway (2.9-fold increase in ERK 1 and 2 act

76 aces G(s) and induces signalling through the MAP kinase pathway(2).

77 el coupling of 5-HT2 receptors to the ERK1/2/MAP Kinase pathway, a signaling cascade known to regulat

78 ide evidence for a novel function of the p38 MAP kinase pathway, acting as a negative regulator of ar

79 MAP kinase pathway activation alters the expression of m

80 For MAP kinase pathway activation in KRAS-mutant cells, the

81 analog 1-oleyl-2-acetylglycerol rescues the MAP kinase pathway activation in the mutant cells.

82 -95-type molecules, IgCAM internalization by MAP kinase pathway activation, and postsynaptic IgCAM ex

83 spho-ERK and cyclin D1 expression suggesting MAP-kinase pathway activation in both groups of Spitz ne

84 iption factor expression suggesting stronger MAP-kinase pathway activation in this group.

85 -induced calcium flux, activation of the ERK MAP kinase pathway, activation of the NF-kappaB transcri

86 -Jun mRNA and p38 mitogen-activated protein (MAP) kinase pathway activity.

87 duced by pharmacologically inhibiting p42/44 MAP kinase pathway (also by siRNA down-regulating ERK-1/

88 The discovery of BRAF mutations and of other MAP kinase pathway alterations, as well as the co-occurr

89 signaling through TACE activation by the Erk MAP kinase pathway and a strategy for evasion of tumor s

90 ophila, where chemical inhibition of the p38 MAP kinase pathway and autophagy factor depletion failed

91 Dicer is phosphorylated by the ERK-MAP kinase pathway and because this pathway is activated

92 methasone and as a negative regulator of the MAP kinase pathway and downstream release of inflammator

93 We show here that the JNK MAP kinase pathway and one of its most important substra

94 t serine 28 occurs through activation of the MAP kinase pathway and phosphorylated histone H3 is more

95 ho exchange factors to activation of the JNK MAP kinase pathway and that signaling specificity is ach

96 ects include the PI3 kinase/Akt pathway, the MAP kinase pathway and the beta-catenin pathway.

97 ulation activates signaling through both the MAP kinase pathway and the PI-3 kinase pathway in Xenopu

98 ion by PMA required the activation of Erk1/2 MAP kinase pathway and was protein kinase C independent.

99 runculin A treatment also activates the Sty1 MAP kinase pathway and, strikingly, we find that loss of

100 ics screen suggest that intersections of the MAP kinase pathways and autophagy machinery are critical

101 ta) coordinates cAMP-dependent, calcium, and MAP kinase pathways and is important for cellular hypert

102 first splicing factor regulated by multiple MAP kinase pathways and show effects of both SPF45 overe

103 regulates mitogen-activated protein kinase (MAP kinase) pathways and, therefore, hypothesized that t

104 dentified the p38 mitogen-activated protein (MAP) kinase pathway and autophagy machinery as both a li

105 aling through the mitogen-activated protein (MAP) kinase pathway and promote melanoma development.

106 (NF-kappaB), and mitogen-activated protein (MAP) kinase pathways and the inflammasome.

107 itogenic signaling pathways, like the ERK1/2 MAP kinase pathway, and innate immune signaling.

108 tion of ZAP-70 substrates, activation of the MAP kinase pathway, and intracellular Ca(2+) levels.

109 s paralleled by inactivation of mTOR and p38 MAP kinase pathways, and inhibition of mTOR and p38 MAP

110 nase (ERK)/mitogen-activated protein kinase (MAP) kinase pathway, and localises to non-compact myelin

111 MAP kinase pathways are crucial in many aspects of the i

112 The cAMP-PKA and MAP kinase pathways are essential for plant infection in

113 Quorum sensing, the efg1-signaling and cek1 MAP kinase pathways are involved in this process.

114 Collectively, our results demonstrate that MAP kinase pathways are most likely targeted by C. burne

115 Mitogen-activated protein (MAP) kinase pathways are three-kinase modules that media

116 injury resulted in rapid activation of the 3 MAP kinase pathways as well as NF-kappaB.

117 rs engage the Ras/mitogen-activated protein (MAP) kinase pathway as part of their signaling activitie

118 as and downstream mitogen-activated protein (MAP) kinase pathways as essential mediators of FucT-VII

119 y mediated by the mitogen-activated protein (MAP) kinase pathway, as it was accompanied by activation

120 to butyrate causes a rapid activation of the MAP kinase pathway, associated with increased phosphoryl

121 that they target mitogen-activated protein (MAP) kinase pathways at four levels: mitogen receptors,

122 ase complex, a key negative regulator of the MAP kinase pathway, binds to MAP3K2 and this interaction

123 Furthermore, inhibition of the MAP kinase pathway, but not the PI3K/AKT pathway, abroga

124 kinase Ctheta (PKCtheta) turning on the Erk MAP kinase pathway, but the biochemical mechanism respon

125 ith Notch as well as canonical NF-kappaB and MAP kinase pathways, but downregulated expression of Not

126 ls this response is mediated via ERK and p38 MAP kinase pathways, but the identity of the downstream

127 293 cells, VP24 also interferes with the p38 MAP kinase pathway by blocking IFN-beta-stimulated phosp

128 ific depletion of various members of the p38 MAP kinase pathway by the use of RNA interference reveal

129 y response to hypoxia, and inhibition of p38 MAP kinase pathway by variety of approaches abolished hy

130 ssociated with a defect in the activation of MAP kinase pathways by TCR signals.

131 ivator of the p38 mitogen-activated protein (MAP) kinase pathway by a mechanism that requires the MAP

132 ing activation of mitogen-activated protein (MAP) kinase pathways by certain cytokines, excessive act

133 In turn, this MAP kinase pathway can control both neuroendocrine neuro

134 These data indicate that the MAP kinase pathway can target and inhibit post-cytochrom

135 y isoform involved and the cellular context, Map kinase pathways can mediate signals that either prom

136 T cells, is maintained by a block in the Ras/MAP kinase pathway, can be reversed by IL-2 or anti-OX40

137 The polyQ expansion in AR activates three MAP kinase pathways, causing increasing levels of phosph

138 genes within the mitogen-activated protein (MAP) kinase pathway commonly mutated in melanomas on int

139 ocyte growth factor receptor (c-MET) and the MAP kinase pathway component B-Raf, providing a proof of

140 ytokine increased phosphorylation of the p38 MAP kinase pathway components and altered TM cell morpho

141 acts with several mitogen-activated protein (MAP) kinase pathway components, including Raf, MAP/extra

142 report that RPM-1 negatively regulates a p38 MAP kinase pathway composed of the dual leucine zipper-b

143 nt phenotypes are enhanced by mutations in a MAP kinase pathway composed of the MAPKKK DLK-1, the MAP

144 The MAP-kinase pathway, consisting of the kinases RAS, RAF,

145 P kinase, a major mitogen-activated protein (MAP) kinase pathway converting signals of various extrac

146 We propose that the conserved MAP kinase pathway coordinates CO designation with the d

147 We report that activation of the Erk MAP kinase pathway decreases the TGF-beta-induced Smad3

148 n in spinal cord astrocytes, whereas the Ras-MAP kinase pathway does not appear to be involved.

149 h antagonizes the mitogen-activated-protein (MAP) kinase pathway downstream of the FGFR3 receptor and

150 Toll-like receptor activation of the ERK-1/2 MAP kinase pathway during inflammatory responses, but it

151 inase is essential for activation of the Erk MAP kinase pathway during innate immune responses.

152 To study the potential function of the MAP kinase pathway during mitosis, RNAi was used to spec

153 gonizes the activity of the EGF receptor-Ras-MAP kinase pathway during VPC specification.

154 ll wall integrity mitogen-activated protein (MAP) kinase pathway during cell wall stress and unstress

155 tions in multiple mitogen-activated protein (MAP) kinase pathways, each with unique dynamical and dev

156 of this study was to investigate the role of MAP kinase pathways (ERK1/2 and p38 kinase) and the mole

157 The 4 best-characterized MAP kinase pathways, ERK1/2, JNK, p38, and ERK5, have be

158 reas S179D PRL signals primarily through the MAP kinase pathway especially after prolonged exposure.

159 YCF1 or mutations in a component of the Pkc1-MAP kinase pathway exhibit little or minor sensitivity t

160 uction of G1 arrest by activation of the p38 MAP kinase pathway has attracted recent attention with r

161 The p38 mitogen-activated protein kinase (MAP kinase) pathway has been implicated in regulating th

162 rate a critical role for hypoxia-induced p38 MAP kinase pathway in androgen-independent AR activation

163 We examined activation of the MAP kinase pathway in atypical nevi and melanoma cells a

164 The role of the MAP kinase pathway in both sexual and asexual developmen

165 Although the involvement of the p38 MAP kinase pathway in cellular responses to stress has b

166 study was to investigate the role of the p38 MAP kinase pathway in epidermal growth factor (EGF)-indu

167 provide new evidence for the involvement of MAP kinase pathway in focal ischemic brain injury and su

168 hat HF induced a rapid activation of the Ras/MAP kinase pathway in human prostate cancer DU145 cells

169 elective and sustained activation of the Raf/MAP kinase pathway in MCF-10A Delta Raf-ER cells, a spon

170 to improve the efficacy of targeting the ERK/MAP kinase pathway in melanoma.

171 eover, these data identify activation of the MAP kinase pathway in microglia as a cause of neurodegen

172 To evaluate the role of the MEK/ERK MAP kinase pathway in murine collagen-induced arthritis

173 ts indicate that oncogenic activation of the MAP kinase pathway in murine fibroblasts converts p53 in

174 Recurrent mutational activation of the MAP kinase pathway in plasma cell myeloma implicates gro

175 ysis establishing that the known role of the MAP kinase pathway in pseudohyphal growth is linked to M

176 lamine afferent system selectively engages a MAP kinase pathway in rat paraventricular hypothalamic C

177 Thus, despite the central importance of the MAP kinase pathway in some aspects of T cell function, M

178 ingly, MTA was able to strongly activate the MAP kinase pathway in the absence of Src family kinase a

179 s communication, we examined the role of the MAP kinase pathway in the G2/M phase of the cell cycle.

180 Here, the involvement of the JNK-MAP kinase pathway in this process was evaluated.

181 that CBU0388 enhances the activation of this MAP kinase pathway in yeast, while CBU0885 and CBU1676 a

182 that these three effectors modulate the CWI MAP kinase pathway in yeast.

183 sease processes, TGF-beta usurps branches of MAP kinase pathways in conjunction with Smads to induce

184 ta confirm the importance of the p38 and ERK MAP kinase pathways in macrophage activation by bacteria

185 have revealed significant new insights about MAP kinase pathways in the heart.

186 In this review, the involvement of various Map kinase pathways in the pathophysiology of hematologi

187 Distinct MAP kinase pathways in yeast share several signaling com

188 activation of the mitogen-activated protein (MAP) kinase pathway in antigen-stimulated cells.

189 in activating the mitogen-activated protein (MAP) kinase pathway in the ventral tegmental area (VTA),

190 se (PI3K)/Akt and mitogen-activated protein (MAP) kinase pathways in established mouse cells.

191 lar and pheromone mitogen-activated protein (MAP) kinase pathways in the yeast Saccharomyces cerevisi

192 either PD0325901or MEK162, led to sustained MAP-kinase pathway inhibition and showed a strong synerg

193 ogy, who would benefit from treatment with a MAP kinase pathway inhibitor.

194 MAP kinase pathway inhibitors block L1-CAM-mediated neur

195 es both BRM acetylation and BRM silencing as MAP kinase pathway inhibitors both induced BRM as well a

196 rmine the effects of these cytokines and p38 MAP kinase pathway inhibitors on MMP-3 protein levels, p

197 nsitive to p42/44-mitogen-activated protein (MAP) kinase pathway inhibitors.

198 ether, these findings establish that the p38 Map kinase pathway is a common effector for type I IFN a

199 in lactate production which occurs when the MAP kinase pathway is activated, using a non-equilibrium

200 d why this noncanonical configuration of the MAP kinase pathway is adopted by these key immune cells

201 The yeast Hog1 MAP kinase pathway is believed to control the transcript

202 Signaling through RAS/MAP kinase pathway is central to biology.

203 The ability of mRon to activate the MAP kinase pathway is dependent on c-Src activity, and w

204 In Magnaporthe oryzae, the Mst11-Mst7-Pmk1 MAP kinase pathway is essential for appressorium formati

205 We demonstrate that activation of the p38 MAP kinase pathway is necessary for the full transcripti

206 ivates ERK and that activation of the p42/44 MAP kinase pathway is necessary to promote muscle regene

207 xperiments demonstrate that this specialized MAP kinase pathway is required for both mating and cell

208 in gastrula stage embryos indicates that the MAP kinase pathway is required for Cdx gene expression,

209 Signalling via the MAP kinase pathway is significantly impaired in this mut

210 effector-loop mutants that activate the Ras/MAP kinase pathway is sufficient to reduce the androgen

211 Activation of the p38 MAP kinase pathways is crucial for the adaptation of mam

212 Thus, activation of two MAP kinase pathways is required for cytotoxic granule an

213 ow that the DLK-1 mitogen-activated protein (MAP) kinase pathway is essential for regeneration in Cae

214 Activation of the MAP kinase pathways leads to changes in gene expression

215 e metabotropic receptor that, activating the MAP kinase pathway, leads to synaptic and behavioral def

216 (MAK-1)-signaling cascade, whereas a second MAP kinase pathway (MAK-2), which is also involved in ce

217 ctivator of twitchin kinase and that the p38 MAP kinase pathway may be involved in the regulation of

218 This suggests that activation of the MAP kinase pathway may contribute to the okadaic acid-in

219 ons, 5-HT-mediated stimulation of the ERK1/2/MAP Kinase pathway may provide an alternative signaling

220 y suggest that targeting the RAGE or the ERK MAP kinase pathway may provide new therapeutic strategie

221 ns-the HBP1 transcription factor and the p38 MAP kinase pathway-may now participate together in a G1

222 that the primary mechanism by which the p38 Map kinase pathway mediates hematopoietic suppression is

223 The RAS-RAF-MEK-ERK-MAP kinase pathway mediates the cellular response to ext

224 Our results suggest that the stress MAP kinase pathway mobilizes programs to promote complet

225 activation of the mitogen-activated protein (MAP) kinase pathway ("noncanonical" BMP Signaling pathwa

226 tivate the mitogen-activated protein kinase (MAP kinase) pathway occur commonly in cancer.

227 whereas intramyocellular lipogenesis via the MAP kinase pathway of insulin may continue unabated.

228 Downstream effectors of CaMKI include the MAP-kinase pathway of Ras/MEK/ERK and the transcription

229 s can be up-regulated due to activation of a MAP kinase pathway or inactivation of the tumor suppress

230 ign nevi with constitutive activation of the MAP-kinase pathway, p16 functions as an essential mediat

231 work by several groups has established that Map kinase pathways play critical roles in the pathogene

232 s-activated plant mitogen-activated protein (MAP) kinase pathways play roles in growth adaptation to

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

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

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

236 to show that dual inhibition of JAK and the MAP kinase pathway provided enhanced therapeutic efficac

237 The link between GSTs and the MAP kinase pathway provides a rationale as to why in man

238 Both the MAP kinase pathway (Ras/Raf/MEK/ERK) and Ca(2+)-dependen

239 mbrane to the cytoplasm, which inhibited the MAP kinase pathway, reduced activity of the PI3K/Akt pat

240 U0126, which selectively inhibits the p44/42 MAP kinase pathway, reduces AR112-stimulated cell death.

241 gether, our data establish that the p38alpha Map kinase pathway regulates activation of downstream ef

242 These results demonstrate that the MAP kinase pathway regulates L1-CAM-mediated nerve growt

243 energy transfer, we have determined that the MAP kinase pathway regulates the phosphorylation of the

244 so found that the mitogen-activated protein (MAP) kinase pathway regulates both BRM acetylation and B

245 The Ras-mitogen-activated protein (Ras-MAP) kinase pathway regulates various cellular processes

246 Inhibition of the p38 MAP kinase pathway rescues by 80% the initiation of pX-m

247 This dysregulation of the MAP kinase pathway results in increased CTNNB1, increase

248 tor PD98059 but not by inhibitors of the p38 MAP kinase pathway (SB202190) or c-Jun N-terminal protei

249 Multiple MAP kinase pathways share components yet initiate distin

250 Analysis of the MAP kinase pathway showed U-PRL capable of activation of

251 C-2 and SUMO loss following stress-activated MAP kinase pathway signaling.

252 ibitors, only specific inhibitors of the p38 MAP kinase pathway significantly reduced both basal and

253 these clusters are enriched for genes of the MAP kinase pathway, suggesting a possible role for this

254 chimeras were weak activators of the ERK1/2 MAP kinase pathway, suggesting that the suppression of i

255 increases phosphorylation of the downstream MAP kinase pathway targets, MAPK11, MAP3K and MAPK1.

256 nlB leads to a greater activation of the Ras-MAP kinase pathway than does HGF.

257 gainst components of the tyrosine kinase-Ras-Map kinase pathway that have been activated by mutation.

258 olarity of the embryo and is controlled by a MAP kinase pathway that includes the MAPKKK YODA (YDA).

259 iquitin ligase, RPM-1 negatively regulates a MAP kinase pathway that includes: dlk-1, mkk-4, and the

260 nase exhibits constitutive activation of the MAP kinase pathway that is independent of the two dockin

261 EGFR transactivation triggers a NT-mediated MAP kinase pathway that leads to IL-8 gene expression in

262 ion of FAP1, a critical regulator of Src and MAP kinase pathway that play an important role in the pr

263 pled receptor that initiates signaling via a MAP kinase pathway that prepares haploid cells for matin

264 ters of target genes of the EGF receptor-Ras-MAP kinase pathway that promote vulval fates.

265 reatment caused activation of a Ras-mediated MAP kinase pathway that significantly contributes to NT-

266 atory role in the mitogen-activated protein (MAP) kinase pathway that participates in cellular surviv

267 regulation of the mitogen-activated protein (MAP) kinase pathway, the precise mechanisms are unknown.

268 ulator of the Ras/mitogen-activated protein (MAP) kinase pathway, the role of KSR in Cot-mediated MAP

269 vating mutations in the beta-catenin and the MAP-kinase pathways; this characteristic can help in the

270 upled mechanism while stimulating the p42/44-MAP kinase pathway through an alternative G-protein-inde

271 Similarly, a second MAP kinase pathway through ERK was previously shown to b

272 l three kinases are able to activate the p38 MAP kinase pathway through the specific activation of th

273 11 and Ste50, components shared by all three MAP kinase pathways, through their interaction with the

274 pathway with those of the pheromone response MAP kinase pathway to generate the final transcriptional

275 evated glucose in diabetes activates the p38 MAP kinase pathway to increase inflammatory IL-8 gene in

276 onstrates that AGEs activate the RAGE-ERK1/2 MAP kinase pathway to mediate the early TEMT process.

277 of rotenone on DA neurons by activating the MAP kinase pathway to stabilize microtubules.

278 p38 and Jun N-terminal protein kinase (JNK) MAP kinase pathways to influence pro- and anti-inflammat

279 to stimulate the mitogen-activated protein (MAP) kinase pathway to near wild-type levels but failure

280 ary cells, inhibitors of the MEK/ERK and p38 MAP kinase pathways uncovered distinct signaling pathway

281 gether, these results place WNK1 in the ERK5 MAP kinase pathway upstream of MEKK2/3.

282 inase (PI3-K) and mitogen-activated protein (MAP) kinase pathways via TpoR, and autonomous growth in

283 The MAP kinase pathway was activated in the ITC-NAC-treated

284 T pathway was activated in one subtype while MAP kinase pathway was activated in the other.

285 Activation of the Plk1 and MAP kinase pathways was initially evaluated in FT210 cel

286 activation of p38 mitogen-activated protein (MAP) kinase pathway was an early response to hypoxia, an

287 activator of the mitogen-activated protein (MAP) kinase pathways, was used to isolate an enhancer el

288 Inhibitors of the PLC and the Ras/MAP kinase pathway were both able to inhibit the EGF-sti

289 The Smad1/5 and map kinase pathways were activated by BMP4 and VEGF, res

290 HC, and GATA4; and activation of the Akt and MAP kinase pathways were observed at 6 weeks post-induct

291 d normal activation of the Akt, ERK, and p38 MAP kinase pathways when stimulated by the GPCR ligand a

292 A novel inhibitor of the MAP kinase pathway, which is active in plasma, PD184161,

293 -cadherin), directly through the MEK1-ERK1/2 MAP kinase pathway, which is TGF-beta independent.

294 n to be hyperactive in PCa including the RAS/MAP kinase pathway, which phosphorylates Runx2 on multip

295 ommitment to cell growth activates the Slt2p MAP kinase pathway, which phosphorylates the transcripti

296 inases to the Ras/mitogen-activated protein (MAP) kinase pathway, which is implicated in oncogenic ou

297 ique kinase set, we could create a synthetic MAP kinase pathway with non-natural input-output propert

298 Blockade of the JNK MAP kinase pathway with the JNK inhibitor SP600125 abrog

299 xtracellular signal-regulated kinase and p38 MAP kinase pathways with the chemical inhibitors PD98059

300 vation of the Erk mitogen-activated protein (MAP) kinase pathway without the need of new protein synt