ライフサイエンスコーパス: MAPK pathway

1 the well-characterized p38 osmosensing (OS) MAPK pathway.

2 er the normal function and regulation of the MAPK pathway.

3 rowth-factor independent by upregulating the MAPK pathway.

4 RAF kinase equipped for participating in the MAPK pathway.

5 -H1(+) tumor-reactive CD8(+) T cells via p38 MAPK pathway.

6 h, and proliferation by participating in the MAPK pathway.

7 ge of the outputs of the cell wall integrity MAPK pathway.

8 lates the response through a differentiation MAPK pathway.

9 dependent signaling and the Smad-independent MAPK pathway.

10 interest in ERK, a downstream target of the MAPK pathway.

11 ng pleiotropic functions in the insulin/PI3K/MAPK pathway.

12 of multiple inhibitors targeting the RTK/Ras/MAPK pathway.

13 s downstream heterochronic genes and the p38 MAPK pathway.

14 Raf causing a paradoxical hyperactivation of MAPK pathway.

15 nesis by signaling primarily through the Ras-MAPK pathway.

16 aired their intestinal sequestration via p38-MAPK pathway.

17 owed mutations predicted to activate the RAS-MAPK pathway.

18 tathmin conjunctly control activation of the MAPK pathway.

19 t neuromuscular junction in vivo through the MAPK pathway.

20 y regulates multiple pathways, including the MAPK pathway.

21 ight impair the formation of LTM via the p38 MAPK pathway.

22 regression or suppress signaling through the MAPK pathway.

23 nd may support tumor cell growth via the ERK-MAPK pathway.

24 several proteins that were implicated in the MAPK pathway.

25 an ALK-5-dependent manner involving the ERK/MAPK pathway.

26 malian extracellular signal-regulated kinase MAPK pathway.

27 n relied upon constitutive activation of the MAPK pathway.

28 tested had cooperating mutations in the Ras/MAPK pathway.

29 ly validate the activity of compounds on the MAPK pathway.

30 motes RAF dimerization and activation of the MAPK pathway.

31 channel PMCA4b to activate the PI3K/AKT and MAPK pathways.

32 injury by signaling through the PI3K-AKT and MAPK pathways.

33 ircuitry including Shh, Wnt, Hippo, PI3K and MAPK pathways.

34 e observed significant activation of AKT and MAPK pathways.

35 BDNF transcripts, mainly through activating MAPK pathways.

36 expressing cells, activates both the AKT and MAPK pathways.

37 is involved in regulating multiple conserved MAPK pathways.

38 how that it signals through PI3K and the p38 MAPK pathways.

39 idence for a role of the nitric oxide or ERK MAPK pathways.

40 iated neurotrophin signaling via the AKT and MAPK pathways.

41 d dependent on MEK-ERK signaling, one of the MAPK pathways.

42 non-receptor tyrosine kinase), PI3K, ERK, or MAPK pathways.

43 her inhibition or activation of the PI3K and MAPK pathways.

44 f the CEK mitogen activated proteins kinase (MAPK) pathway.

45 ingly, the mitogen-activated protein kinase (MAPK) pathway.

46 of the p38 mitogen-activated protein kinase (MAPK) pathway.

47 by the Ras/mitogen-activated protein kinase (MAPK) pathway.

48 hrough the mitogen-activated protein kinase (MAPK) pathway.

49 of the Ras/mitogen-activated protein kinase (MAPK) pathway.

50 redox-sensitive signaling including Akt and MAPKs pathways.

51 frequency of activating mutations in the RAS-MAPK pathway (11/18; 61%), and these lesions predicted s

52 167/442)], followed by genes involved in the MAPK pathway [31.2% (138/442)], PI3K signaling [18.1% (8

53 Pharmacological inhibition of the MAPK pathway abrogates the stimulus-dependent recruitmen

54 atment resistance as a result of a secondary MAPK pathway-activating mutation during BRAF inhibition

55 te gastric adenocarcinoma subtypes where RAS/MAPK pathway activation and E-cadherin attenuation are c

56 Moreover, in CFC cells, Ras/MAPK pathway activation and morphological abnormalities

57 ly works to limit the NK cell's PI3K/AKT and MAPK pathway activation and the consequent mobilization

58 inate the issues associated with paradoxical MAPK pathway activation and to provide therapeutic benef

59 KIT knockdown also increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant human me

60 hibitor PD0325901 more completely suppressed MAPK pathway activation in mouse and human ATC cell line

61 Ras/MAPK pathway activation is associated with significantly

62 se findings indicate that loss of CL impairs MAPK pathway activation, and decreased activation of the

63 This leads to elevated MAPK pathway activation, as direct Notch-mediated transc

64 of treatment, driven by paradoxical RAS/RAF/MAPK pathway activation.

65 nimals were more invasive and had higher RAS/MAPK pathway activation.

66 nce developed in the absence of constitutive MAPK pathway activation.

67 enotype shared by all the RASopathies is Ras/MAPK pathway activation.

68 on through mitogen-activated protein kinase (MAPK) pathway activation and de-regulated expression of

69 C, p42/p44 mitogen-activated protein kinase (MAPK) pathway activation is essential for HIF-1-mediated

70 gative" PCs are notable for elevated FGF and MAPK pathway activity, which can bypass AR dependence.

71 ributed to an autocrine function that drives MAPK pathway activity.

72 invasion, and tumor growth by downregulating MAPK pathway activity.

73 dose-response behaviors of the NFkappaB and MAPK pathways allow dose-specific gene expression progra

74 rationale for the combined targeting of the MAPK pathway along with inhibitors of RTKs, SRC or STAT3

75 The baseline presence of MAPK pathway alterations was not associated with benefit

76 hrough p38 and c-Jun N-terminal kinase (JNK) MAPK pathways alters gene expression and leads to morpho

77 is a new regulator of the filamentous-growth MAPK pathway and binds to general proteins, like Cdc42p

78 in cell signaling activation through the ERK/MAPK pathway and by reversal of the LD-loaded phenotype

79 xcessive KIT activity hyperactivates the RAS/MAPK pathway and can drive formation of melanomas, most

80 red expression of a number of kinases in the MAPK pathway and diminished expression of several recept

81 hibitors prime wild-type RAF to activate the MAPK pathway and enhance growth' by Hatzivassiliou and c

82 was to evaluate the interaction between the MAPK pathway and estrogen induction of telomerase activi

83 RPV4 interfered with the prolipogenic ERK1/2 MAPK pathway and resulted in the downregulation of nucle

84 47L, whose expression robustly activated the MAPK pathway and sensitized cells to BRAF and MEK inhibi

85 ll number of genes in the Ras processing and MAPK pathways and pinpoint PREX1 as an AML-specific acti

86 noviral over-expression of DUSP1 inactivated MAPK pathways and reduced expression of all 11 inflammat

87 of DUSP2 is not restricted to the classical MAPK pathways and that DUSP2 can also regulate the atypi

88 tivate the mitogen-activated protein kinase (MAPK) pathway and stimulate growth of RAS-mutated cells,

89 binds to IQGAP1, a hub for activation of the MAPK pathway, and impedes IQGAP1-dependent phosphorylati

90 ng pathways, including the PI3K/Akt/mTOR and MAPK pathways, and with other receptors, including estro

91 -activated mitogen-activated protein kinase (MAPK) pathway, and alters sensitivity to oxidative stres

92 Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical respo

93 Cs we experimentally show that NF-kappaB and MAPK pathways are involved in the downregulation of GPR3

94 Mitogen-activated protein kinase (MAPK) pathways are conserved from yeast to man and regul

95 Mitogen-activated protein kinase (MAPK) pathways are involved in several signal transducti

96 MAPK activation in BV2 cells, suggesting the MAPK pathway as the signaling mechanism underlying the e

97 activation of the protein kinase C (PKC) and MAPK pathways as a consequence of GNAQ or GNA11 mutation

98 Using TGF-beta, Notch and MAPK pathways as examples, SMAD2/3, NOTCH1/2/3 and MEK3/

99 entify the mitogen-activated protein kinase (MAPK) pathway as a mediator of prednisolone resistance i

100 rons involved aberrant activation of the p38 MAPK pathway, as also reported for ALS-linked forms of C

101 strates that this is due to the K-Ras/ERK1/2 MAPK pathway, as loss of p53 had little effect on KIF2C

102 Activity of the MAPK pathway, as well as other factors, such as HIF1alph

103 ing, including downstream AKT-mTOR pathways, MAPK pathway, as well as redox enzymes were downregulate

104 analysis revealed dynamic changes within the MAPK pathways, as well as in CREB-associated gene expres

105 SKD showed chronic activation of the p38 MAPK pathway associated with apoptotic cell death.

106 thways for a short time, after which the Ras/MAPK pathway becomes reactivated.

107 amycin and mitogen-activated protein kinase (MAPK) pathways blocks the development of nociceptor sens

108 ing infection of DCs, YopJ potently inhibits MAPK pathways but does not prevent activation of IKK- or

109 on was mediated by activation of the ERK-1/2 MAPK pathway, but not p38 MAPK or PI3K, suggesting a bia

110 Inhibition of the p38 MAPK pathway, but not the Erk pathway, significantly imp

111 GTPase RAS-mitogen-activated protein kinase (MAPK) pathway, but not other known ALK effectors, is req

112 overexpressed PIST reduces activation of the MAPK pathway by beta1-adrenergic receptor (beta1AR) agon

113 provide evidence that stimulation of the Ras/MAPK pathway by EGFR results in FLJ00018 phosphorylation

114 de of the RAS-activated proproliferative RAF/MAPK pathway by tumor suppressor menin.

115 Targeting multiple components of the MAPK pathway can prolong the survival of patients with B

116 rrant signaling through the Raf/MEK/ERK (ERK/MAPK) pathway causes pathology in a family of neurodevel

117 Alternatively activation of the RAS-MAPK pathway circumvents Shh pathway dependency, drives

118 ctivity after constitutive activation of the MAPK pathway, commonly through Ras mutations.

119 s, results in JNK-mediated inhibition of RAS-MAPK pathway components SOS and RAF.

120 ss-tolerance by decreased phosphorylation of MAPK pathway components.

121 could be mapped to genes in the JAK/STAT and MAPK pathways, confirming the ability of this strategy t

122 positive-feedback loop between BASL and the MAPK pathway constitutes a polarity module at the cortex

123 cts to Pten restoration, suggesting that the MAPK pathway contributes to the maintenance of advanced

124 Mitogen-activated protein kinase (MAPK) pathways control many cellular processes, includin

125 Importantly, activation of the MAPK pathway correlated with in vitro stabilities of ter

126 PI3K and MAPK-pathway dependencies were quantified by measuring i

127 either inhibit or paradoxically activate the MAPK pathway, depending whether activation is by BRAF mu

128 as human T-ALL carrying mutations in the RAS/MAPK pathway display a genetic signature indicative of C

129 ivation of this MAPK cascade, and this Sarm1-MAPK pathway disrupts axonal energy homeostasis, leading

130 ion of the mitogen-activated protein kinase (MAPK) pathway driven by mutant BRAF or NRAS is a primary

131 we found that these treatments activated the MAPK pathway due to attenuation of an IKBKE feedback mec

132 Co-occurring mutations in NRAS and other MAPK pathway effectors were enriched in nonresponding pa

133 r tyrosine kinase Src to promote the Ras/Raf/MAPK pathway essential for proliferation, differentiatio

134 ation of FGF receptor-mediated intracellular MAPK pathway, FGF16 regulates the expression of MMP2, MM

135 ide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR) sig

136 ion of the mitogen-activated protein kinase (MAPK) pathway following EGFR blockade.

137 llular signal-regulated kinase kinase-Erk1/2(MAPK) pathway for Cmpd1-induced modulation of Stat3 sign

138 3/MKK6-p38 mitogen-activated protein kinase (MAPK) pathway for controlling the activity of ATF6.

139 , with recurrent mutations in KIT, TSC2, and MAPK pathway genes (BRAF, KRAS, and NRAS) also identifie

140 pairs across multiple cell types, including MAPK pathway genes and apoptotic genes.

141 Mutually exclusive somatic mutations in MAPK pathway genes have been identified in approximately

142 environment exposure, including induction of MAPK pathway genes.

143 tic disorders induced by somatic mutation of MAPK pathway genes.

144 ons of the mitogen-activated protein kinase (MAPK) pathway genes ARAF and ERBB3 were also detected.

145 ression of mitogen-activated protein kinase (MAPK) pathway genes, MAPK signaling, and proliferation.

146 The Ras/MAPK pathway has been well studied in the context of can

147 Drugs that inhibit the MAPK pathway have therapeutic benefit in melanoma, but r

148 (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have led to clinical responses in lung and

149 ions identified have been within the RAF/RAS/MAPK pathway, hence supporting the previously introduced

150 , phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways; human biliverdin reductase (hBVR) is an I

151 MAPK pathway hyperactivation (through Braf(V600E) or Kra

152 s cells of origin for cSCC, and that RAS/RAF/MAPK pathway hyperactivation or Tp53 mutation, coupled w

153 Compound 22 blocks the MAPK pathway, impairs cellular migration under hypoxic c

154 enetic and pharmacological inhibition of Ras-MAPK pathway impeded epidermal hyperplasia in Pten anima

155 e ATP-competitive B-Raf inhibitors block the MAPK pathway in B-Raf mutant cells, they induce conforma

156 0, RAFi) cause paradoxical activation of the MAPK pathway in BRAF-fusion tumors, inhibition can be ac

157 ess mutant BRAF cells without activating the MAPK pathway in cells bearing upstream activation.

158 F in mediating paradoxical activation of the MAPK pathway in cells treated with RAF inhibitors.

159 r data demonstrate a crucial function of the MAPK pathway in controlling the balance between prolifer

160 e findings reveal a critical role of the RAS-MAPK pathway in drug resistance and tumor evolution of S

161 upstream of the high osmolarity glycerol/p38 MAPK pathway in fungi.

162 derscore the potential importance of the ERK/MAPK pathway in human movement disorders.

163 Despite the importance of the RAS-RAF-MAPK pathway in normal physiology and disease of numerou

164 and abrogates paradoxical activation of the MAPK pathway in preclinical models of BRAF-mutated melan

165 activity without agonistically affecting the MAPK pathway in wild-type B-Raf cells.

166 thus affecting phosphoinositide 3-kinase and MAPK pathways in human mast cells (huMCs) from HMC-1, LA

167 ndicated that Mst50 is involved in all three MAPK pathways in M. oryzae although its functions differ

168 mononuclear cells while also activating ERK MAPK pathways in murine bone marrow-derived macrophages.

169 tivity through PLCgamma/calcineurin/NFAT and MAPK pathways in SaOS-2 and MC3T3-E1 osteoblasts.

170 However, the roles of these two MAPK pathways in the control of expression of key genes

171 pheromone-induced and osmotic stress-induced MAPK pathways in yeast and in the mammalian extracellula

172 ion of the mitogen-activated protein kinase (MAPK) pathway in BRAF wild-type cells.

173 downstream mitogen-activated protein kinase (MAPK) pathway in cancer cells.

174 er via the mitogen-activated protein kinase (MAPK) pathway in non-small cell lung cancer (NSCLC).

175 dgehog and mitogen-activated protein kinase (MAPK) pathways in over 80% of ameloblastomas, locally de

176 We studied the implication of the MAPK pathways, in particular, ERK1/2, in the gustatory d

177 Treatment with inhibitors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS) in

178 tenuation of DUSP4 activated the ERK and p38 MAPK pathways, increased stem-like properties, and spawn

179 er, our data indicate that inhibition of the MAPK pathway increases chemosensitivity to glucocorticoi

180 ngs reveal a regulatory role for BRAF in the MAPK pathway independent of its kinase activity but depe

181 blated tumor cell sensitivity, including the MAPK pathway-inducer KSR1.

182 7 phosphorylation downstream of the PI3K and MAPK pathways influences the ubiquitination and stabilit

183 aling revealed that inhibiting the Ras/Raf-1/MAPK pathway inhibited EphB2 expression, and inhibiting

184 n of PKC and MEK inhibition led to sustained MAPK pathway inhibition and tumor regression in vivo.

185 together, our data suggest that although Ras/MAPK pathway inhibition can increase tumor immunogenicit

186 Dissociating MAPK pathway inhibition from paradoxical activation migh

187 shared by all three models, we discover that MAPK pathway inhibition impinges uniquely on this event,

188 inavir suppresses MITF expression induced by MAPK pathway inhibition in melanoma cells and sensitizes

189 cancer to examine the effect of Jak/STAT and MAPK pathway inhibition in vitro.

190 ombiDT therapy failed to achieve significant MAPK pathway inhibition or immune infiltration in most p

191 Dual MAPK pathway inhibition with BRAF and MEK inhibitors in

192 reversed when cells were pretreated with the MAPK pathway inhibitor.

193 t would be amenable to combined therapy with MAPK pathway inhibitors for the treatment of PTEN(LOF)/B

194 , and these data suggest that small-molecule MAPK pathway inhibitors hold clinical promise in the tre

195 mbinations of panPI3K, PI3Kbeta + IGF1R, and MAPK pathway inhibitors in PTEN(LOF)/BRAF(MUT) melanoma

196 The introduction of MAPK pathway inhibitors paved the road for significant a

197 The ability of MAPK pathway inhibitors to suppress MAPK kinase and ERK

198 l-like tumor cells are resistant to PI3K and MAPK pathway inhibitors, suggesting that epigenetic mech

199 tizes BRAF and NRAS mutant melanoma cells to MAPK-pathway inhibitors.

200 ns indicate that the signal intensity of the MAPK pathway is a critical determinant not only in tumou

201 The MAPK pathway is activated in the majority of melanomas a

202 coids and possibly other agents and that the MAPK pathway is an attractive target for prevention and/

203 pathways and suggest that FGF-activated Ras-MAPK pathway is an effective therapeutic target for prev

204 The ERK/MAPK pathway is an important developmental signaling pat

205 The MAPK pathway is known to be downstream from integrins an

206 The MAPK pathway is responsible for cell proliferation and p

207 volving the Ras/PI3K/Akt and the Ras/Raf/ERK MAPK pathways is causally involved in the development of

208 of the Ras-mitogen activated protein kinase (MAPK) pathway is an early event in many different cancer

209 ity in the mitogen-activated protein kinase (MAPK) pathways is controlled by disordered domains of th

210 The mitogen-activated protein kinases (MAPKs) pathway is critical for cellular signaling, and p

211 Further, MKK4, a key component in the Sarm1-MAPK pathway, is antagonized by AKT signaling, which mod

212 mechanisms arising in metastatic melanoma to MAPK pathway kinase inhibitors as a strategy to identify

213 enes encoding proteins with roles in the RAS-MAPK pathway, leading to pathway dysregulation.

214 of oncogenic Ras or direct activation of the MAPK pathway leads to increased mitochondrial fragmentat

215 the filamentous-growth pathway but not other MAPK pathways (mating or high-osmolarity glycerol respon

216 suggest that differential inhibition of the MAPK pathway may be a potential therapeutic strategy to

217 ontrast, insulin's activation of the Grb/Shc/MAPK pathway mediates the expressions of ET-1 and PAI-1

218 However, secondary roles for canonical MAPK pathway members are being discovered.

219 We show that knockdown of the specific MAPK pathway members MEK2 and MEK4 increased sensitivity

220 adults characterized by a high prevalence of MAPK pathway mutations and a near absence of mutations i

221 ata show that, in contrast to adult MDS, Ras/MAPK pathway mutations are common in pediatric MDS (45%

222 of relapse neuroblastomas and show that RAS-MAPK pathway mutations may function as a biomarker for n

223 owever, by using tumor cells with activating MAPK pathway mutations, we have identified a role for HM

224 etreatment mitogen-activated protein kinase (MAPK) pathway mutations or activation.

225 We demonstrate downstream activation of the MAPK pathway necessary for tumor homing.

226 Infection with MsmRv3242c also activated the MAPK pathway, NF-kappaB, and inflammatory cytokines.

227 ere not previously linked to the JAK/STAT or MAPK pathways nor shown to functionally contribute to le

228 Inhibiting either the MAPK pathway or the AKT pathway enhanced the effects of

229 pathological conditions, such as continuous MAPK pathway overactivation due to oncogenic alterations

230 nd increased phosphorylation was observed in MAPK pathways (p38, ERK, JNK) and the NF-kappaB pathway

231 Recent developments show how MAPK pathways perform exquisite spatial and temporal sig

232 Combined inhibition of the MAPK pathway, PI3Kbeta, and PI3Kalpha or insulin-like gr

233 The ERK/MAPK pathway plays a central role in the regulation of c

234 Failure to inhibit the MAPK pathway provides a likely explanation for the limit

235 8, and JNK mitogen-activated protein kinase (MAPK) pathways.R-PIA also decreased the expression of ST

236 Notably, MDSC restoration relied upon MAPK pathway reactivation and downstream production of t

237 kinase (RAF) inhibitor, PLX8394, that evades MAPK pathway reactivation in BRAF-mutant LA models.

238 drives resistance to RAF inhibition through MAPK pathway reactivation" by Johannessen and colleagues

239 ly altered molecular interactions underlying MAPK pathway reactivation.

240 Inhibition of FGFR as well as MAPK pathway reduces the proliferative and invasive beha

241 tor previously shown to be downstream of the MAPK pathway, regulates KLF4 expression and that KLF4 in

242 and in vivo growth and induced expression of MAPK pathway response genes; by contrast the paradox bre

243 In the MAPK pathway responsible for cell growth, ERK2 initiates

244 Germ-line mutations in components of the Ras/MAPK pathway result in developmental disorders called RA

245 Stimulation of the MAPK pathway results in mitogen- and stress-activated pr

246 By tuning the MAPK pathway, S. cerevisiae therefore programs the numbe

247 The p38 MAPK pathway seems to be involved in pathogenesis of chr

248 Furthermore, timed modulation of the FGF-MAPK pathway shows that individual progenitors commit to

249 epresents a novel scaffold for disruption of MAPK pathway signaling and may serve as a useful structu

250 , a novobiocin analogue, was identified as a MAPK pathway signaling disruptor that lacked Hsp90 inhib

251 Ras/MAPK pathway signaling is a major participant in neurode

252 focal adhesion kinase (FAK) sustain AKT and MAPK pathway signaling under continuous EGFR inhibition

253 resistance often result from reactivation of MAPK pathway signaling, thus limiting durable responses

254 V600E) that promotes vemurafenib-insensitive MAPK pathway signaling.

255 decreased mitogen-activated protein kinase (MAPK) pathway signaling and increased phosphoinositol-3-

256 promoting mitogen-activated protein kinase (MAPK) pathway signaling.

257 activated mitogen-activated protein kinase (MAPK) pathway signaling.

258 ndependent mitogen-activated protein kinase (MAPK) pathway signalling.

259 d dramatic defects on both the NF-kappaB and MAPK pathways, suggesting a role in transcriptional prim

260 stant cells retained sensitivity to vertical MAPK pathway suppression when combinations of ERK, BRAF,

261 d to PLGG clinical trials utilizing RAF- and MAPK pathway-targeted therapeutics.

262 ity and identify four genes in the pheromone MAPK pathway that are expressed at significantly higher

263 s (bud-site-selection proteins) regulate the MAPK pathway that controls filamentous growth (fMAPK pat

264 ERK-MAPK pathway that regulates alternative splicing facilit

265 ulates the mitogen-activated protein kinase (MAPK) pathway that controls filamentous growth in Saccha

266 -dependent mitogen-activated protein kinase (MAPK) pathway that controls filamentous growth in yeast.

267 canonical mitogen-activated protein kinase (MAPK) pathway that recruits the MAPKK kinase YODA (YDA)

268 e.g., the mitogen-activated protein kinase (MAPK) pathway, the phosphatidylinositol-3-kinase (PI3K)/

269 cilitates FA disassembly and connects to the MAPK pathway through Grb2 association, but requires diss

270 TGF-beta also activates the Erk MAPK pathway through recruitment and Tyr phosphorylation

271 (MAPK) kinase kinase (MAP3K) which activates MAPK pathways through either kinase-dependent or -indepe

272 ere, we show that the over-activation of the MAPK pathway, through conditional expression of the gain

273 we report that MNV1 infection modulates the MAPK pathway to activate eIF4E phosphorylation.

274 latory mechanism by which stress engages p38 MAPK pathway to destabilize Drosha and inhibit Drosha-me

275 sponse to pheromones, yeast cells activate a MAPK pathway to direct processes important for mating, i

276 NGF signals through the ERK/MAPK pathway to promote expression of Cbfb but not Runx1

277 miRNAs, abrogate NOD2-induced PI3K-PKCdelta-MAPK pathway to suppress beta-catenin-mediated expressio

278 This work links Akt and MAPK pathways to NF-kappaB through Bcl3 and provides mec

279 that relaxin activates the cAMP/PKA and p38 MAPK pathways to phosphorylate CREB, resulting in increa

280 lating the mitogen-activated protein kinase (MAPK) pathway to promote cancer.

281 nase leads to an anomalous regulation of the MAPK pathway, uncontrolled cell proliferation, and initi

282 Reactivation of the MAPK pathway via either a gain in the number of copies o

283 We found that Notch1 regulates Ras/MAPK pathway via HES1-induced repression of the DUSP1 pr

284 n by activating IKKbeta-IkappaBalpha and p38 MAPK pathways via NF-kappaB nuclear translocation-depend

285 Moreover, activation of MAPK pathway was ablated in APRIL-stimulated XID cells.

286 eported that RAF inhibitor activation of the MAPK pathway was dependent on CRAF but not BRAF, and Fig

287 The TGFbetaR1 containing p38-MAPK pathway was significantly associated with oropharyn

288 and intracellular signaling by NF-kappaB and MAPK pathways were comparable in oxLDL-loaded Mvarphis,

289 Both PKC and high osmolarity glycerol (HOG) MAPK pathways were shown previously to be required for m

290 d that the mitogen-activated protein kinase (MAPK) pathways were predominantly affected, with increas

291 conserved mitogen-activated protein kinase (MAPK) pathways when cells are grown in constant conditio

292 e provide evidence that activation of a TrkB-MAPK pathway, when paired with the deactivation of a GR-

293 lling evidence linking FGFR2 with the ERK1/2-MAPK pathway, which converges with the PI3K/Akt/mTOR (me

294 elevated c-Src renews activation of the Ras/MAPK pathway, which enhances cell survival by accelerati

295 itric-oxide synthase, NO production, and p38 MAPK pathway, which in turn was responsible for the incr

296 idative stress-induced activation of the Ras/MAPK pathway, which in turns drives ISC proliferation.

297 l role of CUL7/Fbxw8 ubiquitin ligase in the MAPK pathway, which plays a critical role in cell prolif

298 activator (uPA) drives signaling through the MAPK pathway, which results in suppression of the proapo

299 tight coupling between the host ERK and p38 MAPK pathways, which are generally thought to control di

300 ced DUSP1 is involved in feedback control of MAPK pathways, ZFP36 exerts negative (incoherent) feed-f