ライフサイエンスコーパス: MAPK pathway

1 lammation by cis-regulating MAP3K4 via a p38 MAPK pathway.

2 e intestine to negatively regulate the ERK-5/MAPK pathway.

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

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

5 o family GTPases that also activates the ERK/MAPK pathway.

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

7 malian extracellular signal-regulated kinase MAPK pathway.

8 n relied upon constitutive activation of the MAPK pathway.

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

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

11 motes RAF dimerization and activation of the MAPK pathway.

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

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

14 rowth-factor independent by upregulating the MAPK pathway.

15 RAF kinase equipped for participating in the MAPK pathway.

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

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

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

19 lates the response through a differentiation MAPK pathway.

20 as indicative of increased activation of the MAPK pathway.

21 dependent signaling and the Smad-independent MAPK pathway.

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

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

24 CP1 and the subsequent activation of the SRC/MAPK pathway.

25 also often exhibited upregulation of the RAS/MAPK pathway.

26 ered pathway was Wnt pathway followed by the MAPK pathway.

27 SHP2, that suppresses signaling through the MAPK pathway.

28 iven by sporadic activating mutations in the MAPK pathway.

29 ) and is required for full activation of the MAPK pathway.

30 a post-transcriptional mechanism through the MAPK pathway.

31 teins resided on endosomes and activated the MAPK pathway.

32 resistance, likely due to activation of the MAPK pathway.

33 GM-CSF production from ILC3s through the p38 MAPK pathway.

34 drive proliferation independently of the ERK/MAPK pathway.

35 e signaling from tyrosine kinases to the Ras-MAPK pathway.

36 BRAF-like tumors) and induced the downstream MAPK pathway.

37 activation of both the Lyn/PI3K/Akt and ERK/MAPK pathways.

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

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

40 is involved in regulating multiple conserved MAPK pathways.

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

42 ctions for Rho GTPase adaptors in regulating MAPK pathways.

43 ites with concomitant activation of PI3K and MAPK pathways.

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

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

46 e observed significant activation of AKT and MAPK pathways.

47 BDNF transcripts, mainly through activating MAPK pathways.

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

49 -alpha and IL-10, dependent on NF-kappaB and MAPK pathways.

50 tivate the mitogen-activated protein kinase (MAPK) pathway.

51 nase (ERK)/mitogen activated protein kinase (MAPK) pathway.

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

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

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

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

56 ed p38 mitogen-activated protein kinase (p38-MAPK) pathway.

57 eam of the mitogen-activated protein kinase (MAPK) pathway.

58 n the RAS/mitogen-activating protein kinase (MAPK) pathway.

59 vating the mitogen-activated protein kinase (MAPK) pathway.

60 K-RAS in mitogen-activated protein kinases (MAPK) pathway.

61 downstream mitogen-activated protein kinase (MAPK) pathways.

62 appaB) and mitogen-activated protein kinase (MAPK) pathways.

63 redox-sensitive signaling including Akt and MAPKs pathways.

64 ons in the mitogen-activated protein kinase (MAPK) pathway(1,2).

65 167/442)], followed by genes involved in the MAPK pathway [31.2% (138/442)], PI3K signaling [18.1% (8

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

67 er types prone to the genomic acquisition of MAPK pathway-activating alterations.

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

69 ctivation, squamous cell carcinomas with Ras/MAPK pathway activation also arise, and the molecular ba

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

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

72 n could partially be attributed to increased MAPK pathway activation and thromboxane generation.

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

74 nating the signals between cytokines and the MAPK pathway activation in melanoma cells.

75 Ras/MAPK pathway activation is associated with significantly

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

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

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

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

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

81 ugh accumulation of ARID1A mutations and RAS/MAPK pathway activation.

82 n to provide specificity of signaling during MAPK pathway activation.

83 rimary cilia removal in BCCs potentiated Ras/MAPK pathway activation.

84 ow HH pathway signature showed increased Ras/MAPK pathway activation.

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

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

87 increased mitogen-activated protein kinase (MAPK) pathway activation that could be exploited as a th

88 tment, and mitogen-activated protein kinase (MAPK) pathway activation.

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

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

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

92 and assess the efficacy of inhibition of the MAPK pathway alone and in combination with other gene ta

93 Short-term inhibition of MAPK pathway also induced mechanosignaling associated wi

94 ures in non-responders, and an enrichment of MAPK pathway alterations (PTPN11, BRAF) in responders.

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

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

97 of FGFR1 by hypoxia was mediated through the MAPK pathway and attenuated induction of the proapoptoti

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

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

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

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

102 hosphoproteomic data revealed alterations in MAPK pathway and its downstream targets in SCC-R cells.

103 logical inhibition of PAK6 perturbed the RAS/MAPK pathway and mitochondrial activity, sensitizing the

104 47L, whose expression robustly activated the MAPK pathway and sensitized cells to BRAF and MEK inhibi

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

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

107 ion of the mitogen-activated protein kinase (MAPK) pathway and subsequent cellular proliferation.

108 ar genes were APC (in Wnt pathway), KRAS (in MAPK pathway) and PIK3CA (in PI3K pathway) in the colore

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

110 cluding different oncogenes belonging to the MAPK pathway, and its expression highly correlated with

111 proto-oncogenes ERK2, a component of the ERK/MAPK pathway, and VAV1, a guanine nucleotide exchange fa

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

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

114 Mutations activating the MAPK pathway are found in more than 80% of patients with

115 ntly, genes of the PUFA biosynthesis and p38-MAPK pathway are required for multiple paradigms of DR-m

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

117 Although core regulators of MAPK pathways are well known, new pathway regulators con

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

119 ations in the BRAF gene, a key player in the MAPK pathway, are described in multiple tumor types, inc

120 luding the mitogen-activated protein kinase (MAPK) pathways, are responsible for sensing environmenta

121 a rationale for exploring inhibition of the MAPK pathway as a therapy for iMCD-TAFRO.

122 s highlight the GNAQ/11 -> PLCbeta -> PKC -> MAPK pathway as the central signaling axis to be suppres

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

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

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

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

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

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

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

130 phorylation of proteins in the NF-kappaB and MAPK pathways, both known to regulate cytokine expressio

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

132 Targeting the MAPK pathway by combined inhibition of BRAF and MEK has

133 difies the mitogen-activated protein kinase (MAPK) pathway by downregulating the phosphorylation of M

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

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

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

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

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

139 phosphorylated tyrosine, and phosphorylation MAPK pathway components.

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

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

142 within the mitogen-activated protein kinase (MAPK) pathway controlling cell growth, differentiation,

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

144 MAPK pathway-directed targeted therapy, administered alo

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

146 Here, by measuring activation of the MAPK pathway downstream of GPCR-Galphas-cAMP signaling,

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

148 nderstanding of the mechanisms controlled by MAPK pathway driving melanogenesis will help develop new

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

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

151 nts of the mitogen activated protein kinase (MAPK) pathway enhancing GFP(rare) expression.

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

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

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

155 Thus, our study shows that PUFAs and p38-MAPK pathway function downstream of DR to help communica

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

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

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

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

160 environment exposure, including induction of MAPK pathway genes.

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

162 MAPK pathway genomic alterations at baseline did not aff

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

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

165 appaB) and mitogen activated protein kinase (MAPK) pathways have been implicated in tendon healing.

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

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

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

169 0, RAFi) cause paradoxical activation of the MAPK pathway in BRAF-fusion tumors, inhibition can be ac

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

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

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

173 mor growth in vivo through activation of the MAPK pathway in RAS-mutant transformed cells.

174 receptors Neo1 and Unc5B co-regulate Wnt and MAPK pathways in both mouse and human ESCs.

175 to a novel perturbation dataset on PI3K and MAPK pathways in isogenic models of a colon cancer cell

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

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

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

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

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

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

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

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

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

185 7 phosphorylation downstream of the PI3K and MAPK pathways influences the ubiquitination and stabilit

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

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

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

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

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

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

192 Dual MAPK pathway inhibition with BRAF and MEK inhibitors in

193 t erlotinib-resistant cells are sensitive to MAPK pathway inhibition.

194 lines or patient-derived xenograft models to MAPK pathway inhibition.

195 The administration of a MAPK pathway inhibitor plus GH was the most beneficial t

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

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

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

199 l rationale for exploring the combination of MAPK pathway inhibitors with immunotherapy in NSCLC, ind

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

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

202 on RAS and mitogen-activated protein kinase (MAPK) pathway inputs for the induction of EMTs(12-19).

203 DR represses an evolutionarily conserved p38 MAPK pathway involved in innate immunity, leading to dim

204 The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3

205 of BOP1 and the resulting activation of the MAPK pathway is a clinically relevant mechanism for acqu

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

207 ics analysis revealed that activation of the MAPK pathway is a key upstream event, which can be furth

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

209 data indicates that therapeutic targeting of MAPK pathway is an effective strategy for treating erlot

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

211 The MAPK pathway is often found to be highly activated in TN

212 Stimulation of the ERK/MAPK pathway is required for the exit from pluripotency

213 The MAPK pathway is responsible for cell proliferation and p

214 The mitogen-activated protein kinase (MAPK) pathway is a key cell signaling pathway involved i

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

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

217 ase in the mitogen-activated protein kinase (MAPK) pathway, is mutated in 70% of canine TCCs.

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

219 regulates mitogen-activated protein kinase (MAPK) pathways (mating, filamentous growth or fMAPK, and

220 Identifying new regulators of MAPK pathways may provide new insights into signal integ

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

222 Alterations affecting the MAPK pathway, most commonly KRAS/BRAF, are present in 30

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

224 Groups 2 and 3 gliomas harbor RAS/MAPK pathway mutations and arise in the hemispheres and

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

226 data support the hypothesis that activating MAPK pathway mutations enhance PI resistance by increasi

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

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

229 ntified in these patients confirmed that the MAPK-pathway mutations were activating.

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

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

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

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

234 nts of the mitogen-activated protein kinase (MAPK) pathway (p38 and JNK) in mouse hippocampal culture

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

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

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

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

239 8, and JNK mitogen-activated protein kinase (MAPK) pathways.R-PIA also decreased the expression of ST

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

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

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

243 Inhibitors of the p38alpha/beta and ERK1/2 MAPK pathways reduced the production of IL-5, IL-6, IL-9

244 MAPK pathways regulate different responses yet can share

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

246 additional mitogen-activated protein kinase (MAPK) pathway regulators is invaluable in aiding our und

247 by the p38 mitogen-activated protein kinase (MAPK) pathway responding to oxidative stress.

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

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

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

251 by activating mTOR and STAT1 and inhibiting MAPK pathways, shifting the iTreg polarization in favor

252 Each MAPK pathway showed a unique activation profile, with th

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

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

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

256 which might contribute to longer duration of MAPK pathway signaling in cancer cells.

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

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

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

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

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

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

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

264 nd tumour growth due to adaptive rewiring of MAPK pathway signalling, which restores a CDK-dependent

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

266 ant lineage gatekeeper, preventing HH-to-Ras/MAPK pathway switching.

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

268 We conclude that MAPK pathway targeting therapies mechanically reprogram

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

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

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

272 s well as EGFR-independent activation of the MAPK pathway through alternate RTK (RTK-bypass).

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

274 In contrast, activation of the MAPK pathway through overexpression of a constitutively

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

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

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

278 of MAPK signaling, thus fine tuning the RAS-MAPK pathway to optimize proliferation in cancer.

279 regulates an epidermal p38 stress-responsive MAPK pathway to promote larval development in C. elegans

280 the strong dependence of the oncogene on the MAPK pathway to propagate signaling.

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

282 Targeted inhibition of the ERK-MAPK pathway, upregulated in a majority of human cancers

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

284 By constitutively activating the Ras/MAPK-pathway via Ras(V12)-overexpression in the postmito

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

286 a downstream signaling target of BRAF in the MAPK pathway, was evaluated and demonstrated synergistic

287 Also, the mutation rates for Wnt pathway and MAPK pathway were calculated to be 23% (95% CI, 14-33%)

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

289 To address this question, Cdc42p-dependent MAPK pathways were compared in the filamentous (Sigma127

290 signaling, whereas in B cells, NF-kappaB and MAPK pathways were regulated by both BTK and IRAK4.

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

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

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 ivates the mitogen-activated protein kinase (MAPK) pathways, which are common inducers of inflammator

298 NF-kB and mitogen-activated protein kinase (MAPK) pathways, which coordinate the transcription and s

299 he RAS-mitogen-activated protein kinase (RAS/MAPK) pathway yet show unexplained variability in their

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