ライフサイエンスコーパス: ERK pathway

1 largely abolished by inhibition of RAC1/MEK/ERK pathway.

2 , and this effect requires activation of the Erk pathway.

3 and JNK signaling pathways while inhibiting Erk pathway.

4 ter is a key substrate downstream of the RAS-ERK pathway.

5 is, possibly via reduced activation of the p-ERK pathway.

6 fficiency of signal transduction through the ERK pathway.

7 ity, at least in part, via activation of the ERK pathway.

8 -2 (SPRY2), a negative regulator of the MAPK/ERK pathway.

9 sion by Neu3 sialidase further activates the ERK pathway.

10 rol of T cell polyfunctionality was the MAPK/ERK pathway.

11 Y4 that provide negative feedback to the RAS/ERK pathway.

12 tream effector in the HER2-activated RAF-MEK-ERK pathway.

13 GEF-H1 activation, indicating a role for the ERK pathway.

14 eactivation of the proliferative RAS/RAF/MEK/ERK pathway.

15 he C terminus of both MKP-1 and MKP-2 by the ERK pathway.

16 ciated athanogene, BAG1, an activator of the ERK pathway.

17 In addition, ERbeta5 inhibited the MAPK/ERK pathway.

18 lation of erythropoiesis through the Raf/MEK/ERK pathway.

19 n of Egr-1 and Fosl-1 was induced by the MEK-ERK pathway.

20 stimulation predominantly activates the MEK/ERK pathway.

21 regulates cell signaling through the RAF/MEK/ERK pathway.

22 GRP, activate Ras and the downstream RAF-MEK-ERK pathway.

23 to gene families that converge into the MEK-ERK pathway.

24 hibiting the AngII-AT1-triggered MAPK kinase/ERK pathway.

25 inase-17), leading to activation of the EGFR/ERK pathway.

26 ha-induced apoptosis mainly through the MAPK/ERK pathway.

27 e ligands was inhibited by blocking EGFR and ERK pathway.

28 e of activating mutations in the RAS/RAF/MEK/ERK pathway.

29 of cAMP, in turn, potently activates the PKA/ERK pathway.

30 f ZAP-70, and GAP inhibition of the p21(ras)-ERK pathway.

31 K-Akt pathway, IQGAP1 also scaffolds the Ras-ERK pathway.

32 n of EGFR ligands and activation of EGFR/MEK/ERK pathway.

33 g activation of the PI3K-Akt but not the Ras-ERK pathway.

34 e perineuronal network, and a beta1-integrin/ERK pathway.

35 OX2 promoted cell migration via the EGFR/MEK/ERK pathway.

36 lore its possible mechanism on regulation of ERK pathway.

37 hypertrophy by inhibiting the expression of ERK pathway.

38 ator of transcription 5 (STAT5), and the Mek-Erk pathway.

39 bored lesions in elements of the RAS-RAF-MEK-ERK pathway.

40 af and reduces signaling through the Raf/MEK/ERK pathway.

41 ceptor (VEGFR) signaling through the Ras/MEK/ERK pathway.

42 ly through regulating activation of the EGFR-ERK pathway.

43 e kinase to signal through intracellular Akt/Erk pathways.

44 the JAK/PI3K/AKT (protein kinase B) and MAPK/ERK pathways.

45 ) and mitogen-activated protein kinase (MEK)/ERK pathways.

46 eptor and reduced activation of Src and MAPK/ERK pathways.

47 mediates K25 activation of PI3K/Akt and MEK/ERK pathways.

48 the PI3 kinase/AKT and the Rat sarcoma (RAS)/ERK pathways.

49 s through the activation of PI3K/Akt and MEK/ERK pathways.

50 ptor or STAT3 but not by the PI3K/AKT or MEK/ERK pathways.

51 in addition to activation of pathogenic MEK-ERK pathways.

52 ibition down-regulates both the AKT and Rac1/ERK pathways.

53 and blocks the activation of HER2, AKT, and ERK pathways.

54 liferation (P < 0.001) by modulating AKT and ERK pathways.

55 ly through modulation of the eIF4E, EZH2 and ERK pathways.

56 eading to activation of the PKB/Akt and MAPK/ERK pathways.

57 e MEK/extracellular signal-regulated kinase (ERK) pathway.

58 f the extracellular signal-regulated kinase (ERK) pathway.

59 arrowextracellular signal-regulated kinase (ERK) pathways.

60 s-extracellular signal-regulated kinase (Ras-ERK) pathway, a signal transduction cascade implicated i

61 ndicating the importance of fully evaluating ERK pathway abnormalities in selecting LCH patients for

62 Interestingly, inhibition of the MEK/ERK pathway abolished Pla-induced CCL2 upregulation and

63 reated with decitabine, finding that RAS/MEK/ERK pathway activation and DNMT1 expression correlated w

64 phosphatase) complex plays a key role in RAF-ERK pathway activation by dephosphorylating a critical i

65 ERK pathway activation in cells expressing wild-type BRA

66 tations were associated with downstream MAPK/ERK pathway activation in preneoplastic pancreatic epith

67 Furthermore, MAP3K19 sustained ERK pathway activation in the presence of inhibitors tar

68 ation, when perturbing the spatial extent of Erk pathway activation leads to dramatic disruptions of

69 hylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer s

70 over SHOC2-independent mechanisms of RAF and ERK pathway activation that rely on N-region phosphoryla

71 However, unlike (V600E)Braf, Mek/Erk pathway activation was mediated by both Craf and Bra

72 ed expression of activation genes depends on ERK pathway activation, suggesting that an ERK-AP-1 axis

73 alleles in heterologous cells increased RAS-ERK pathway activation, supporting a causative role in N

74 To identify other genetic causes of ERK pathway activation, we performed whole exome sequenc

75 nsistently, ETS1 was required for robust RAS/ERK pathway activation.

76 g GM130 also results in RasGRF-dependent Ras-ERK pathway activation.

77 itive RAF inhibitors induced paradoxical Mek/Erk pathway activation.

78 This process requires TrkB-dependent ERK pathway activation.

79 uated S aureus-triggered NF-kappaB, p38, and ERK pathways activation and cells treated with these pat

80 eased extracellular signal-regulated kinase (ERK) pathway activation, increased Indian hedgehog (Ihh)

81 l responses to heparin, including effects on ERK pathway activity and BrdU incorporation.

82 ific ablation of EpCAM resulted in increased ERK pathway activity and SNAI2 expression, migration and

83 ed expression of EpCAM resulted in decreased ERK pathway activity and SNAI2 expression, migration and

84 iRs are important for the maintenance of RAS-ERK pathway activity in TNBC cells.

85 genetic or pharmacologic manipulation of the ERK pathway affects viral infection of mosquito cells.

86 ivation negatively regulates the Ras/Raf/MEK/ERK pathway and activates GSK3 to modulate Mcl-1 phospho

87 macrophages (RAW 264.7) dependent on the MEK/ERK pathway and by requiring its proteolytic activity an

88 is found in 50% of melanomas and drives MEK/ERK pathway and cancer progression.

89 on, leading to inhibition of the RAS-RAF-MEK-ERK pathway and cell proliferation.

90 be the differential contributions of the Ras/Erk pathway and concurrent signals, leading to a more qu

91 ation of information loss, we focused on the ERK pathway and developed a stochastic activation model

92 um influx has been shown to regulate the RAS-ERK pathway and downstream events that result in AMPA re

93 d therapies against the oncogenic BRAF->MEK->ERK pathway and immune checkpoint inhibitors for the tre

94 homolog 1 (Raf-1) is a key activator of the ERK pathway and is a target for cross-regulation of this

95 suppressor that inhibits the RAS->RAF->MEK->ERK pathway and is one of the most frequently inactivate

96 ation of Mnk kinases is regulated by the Mek/Erk pathway and is required for the generation of IFN-in

97 roach for simultaneously controlling the Ras/Erk pathway and monitoring a target gene's transcription

98 endothelial cells, can activate the AKT and ERK pathway and promotes angiogenesis in a tumor microen

99 lly affects the cAMP signal to the B-Raf/MEK/ERK pathway and regulates AVP-induced proliferation of A

100 ac activation is upstream from the TACE/EGFR/ERK pathway and regulates T678 phosphorylation.

101 on of gene expression in KCs and HSCs by the ERK pathway and that suppression of its catalytic activi

102 A better understanding of the BRAF/MEK/ERK pathway and the B-cell signaling pathway has allowed

103 at EGFR signals through both the Ras-Raf-MEK-Erk pathway and through the LKB1-AMPK pathway to suppres

104 a genome-wide CRISPR screen, we identify the ERK pathway and USP5 as positive regulators of the m(6)A

105 tibodies confirmed activation of FAK/Src and ERK pathways and caldesmon phosphorylation.

106 at the intersection of the PI3K/Akt and MAPK/ERK pathways and dephosphorylates and inactivates pyruva

107 ated through activation of canonical Wnt and ERK pathways and inhibition of Notch pathway.

108 sed hyperactivation of the PI3K/Akt and MAPK/ERK pathways and promoted metabolic adaptation.

109 uding extracellular signal-regulated kinase (ERK) pathway and NFsmall ka, CyrillicB pathway.

110 d the extracellular signal-regulated kinase (ERK) pathway and promoted Sp1 to suppress EphA4 promoter

111 n the established roles of PI3K, the Ras/Mek/Erk pathway, and Myc in the adenovirus life cycle, our f

112 signaling leads to downregulation of the RAS-ERK pathway, and oogenesis is stalled.

113 s in these kinases are activating toward the ERK pathway, and targeted depletion of the mutated kinas

114 onse to direct activation by the Ras-Raf-MEK-ERK pathway, and this modification stimulates Trim7 E3 u

115 are primarily signaling through the BCR-ABL-ERK pathway, and we show that imatinib treatment not onl

116 on of PI3K/Akt and inhibition of MAPK kinase/ERK pathways, and Ang(1-7)-Mas antagonizes the antiadipo

117 s studies have shown that CaMKII and the RAS-ERK pathway are critical for several forms of synaptic p

118 Signals conveyed through the RAS-ERK pathway are essential for the determination of cell

119 utations in upstream elements regulating the ERK pathway are genetically linked to autism and other d

120 rs, suggesting both the SIRT1/FoxO3a and MEK/ERK pathway are involved in MnSOD regulation by AC5.

121 fied that both the PI3K/protein kinase B and ERK pathways are activated downstream of IGF1 and intera

122 Consequently, p-mTOR, p-Akt and p-ERK pathways are highly upregulated in the brain tumors,

123 We propose that distinct p38/ERK pathways are related to E-cadherin levels and functi

124 , and extracellular signal-regulated kinase (ERK) pathways are enriched in Tmprss6-/- vs WT MEPs.

125 his effect is likely mediated by the Raf/MEK/ERK pathway as constitutively active B-Raf or MEK1 are a

126 ctivation of MAPK kinases, including the MEK/ERK pathway as well as several transcription factors inc

127 h as CD44, CD133 and CD29, by inhibiting the ERK pathway, as the ERK1/2 inhibitor U0126 abolishes the

128 lls, Id1 expression is regulated by the MAPK/ERK pathway at the transcriptional level.

129 ytes through activation of the PI3K/AKT1 and ERK pathways at similar concentrations of IL-7 detected

130 ot initiate early activation of IKKbeta-Tpl2-ERK pathway but instead induce delayed, NADPH-oxidase-de

131 is unaffected by inhibition of the endosomal ERK pathway but is suppressed by ECE-1 inhibition or bet

132 anied by significant blockade of the Raf/Mek/Erk pathway, but rather by reductions in Akt and beta-ca

133 ls not only inhibited activation of the EGFR-ERK pathway by blocking EGF-mediated EGFR dimerization a

134 at paradoxical activation of the RAF-RAS-MEK-ERK pathway by BRAF inhibitors when applied to BRAF(WT)

135 m involves reactivation of the MAPK (RAF/MEK/ERK) pathway by a variety of mechanisms.

136 Thus, feedback interactions within the ERK pathway can regulate cell proliferation and transfor

137 In contrast, a MEK1/2 inhibitor (ERK pathway) completely abolished arginase II expression

138 f epidermal growth factor receptor, EGFR and ERK pathway components at EGF-responsive genes was highl

139 and protein kinase inhibitors targeting the ERK pathway confirmed the prediction.

140 According to our previous study, the RTK/ERK pathway containing nearly 40 genes was associated wi

141 nt, bone morphogenetic protein (BMP), or Ras/ERK pathways, converging on shared nuclear targets that

142 f/MEK/extracellular signal-regulated kinase (ERK) pathway cooperate to restrict eEF2K activity.

143 The ERK pathway defect is due to impaired phosphorylation of

144 S-mutant melanoma, may be effective in other ERK pathway-dependent settings.

145 teractions between NANOG, GATA6, and the FGF/ERK pathway determine ICM cell fate.

146 a context-dependent contribution of SHOC2 to ERK pathway dynamics that is preferentially engaged by K

147 tely 2-fold through both the Smad2/3 and the ERK pathways elicited by TGF-beta1.

148 tosis but simultaneous inhibition of the MEK/ERK pathway enhanced ER stress-induced apoptosis via a c

149 via inhibition of SKP2 and targeting the MEK/ERK pathway enhanced the cytostatic effect of CDK4/6 inh

150 sitive cells were dependent upon the RAF/MEK/ERK pathway for growth and did not activate the PI3K pat

151 gnaling in multiple steps of the Ras/Raf/MEK/ERK pathway, further emphasizing the importance of MAT2B

152 syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofacial,

153 The MAPK/ERK pathway has a critical role in PNS development.

154 RAS/KRAS, upstream regulators of the RAF/MEK/ERK pathway, have been reported in pulmonary, but not in

155 lthough EGFR stimulates the IQGAP1-PI3K and -ERK pathways, here we show that IQGAP1-PI3K controls mig

156 light the potential of modulating the mGluR5-Erk pathway in a developmental stage-specific manner to

157 ivation, but sustained activation of the MEK-ERK pathway in a TSC1/TSC2/TBC1D7 protein complex and mT

158 lished a critical importance for the Raf/MEK/ERK pathway in ADM induction.

159 d MUC5AC upregulation by inhibiting the MAPK ERK pathway in an MKP-1-dependent manner.

160 Our results indicate that targeting the E2-ERK pathway in combination with the mTORC1 pathway may b

161 auses oxidative stress and activates the MEK/ERK pathway in cultured cells and furthermore provides c

162 ults emphasize the distinct role of the MAPK/ERK pathway in developmental myelination versus remyelin

163 ization and for functional signaling via the ERK pathway in early Xenopus embryos.

164 Stimulation of the ERK pathway in Gnb5(-/-) cells by epidermal growth facto

165 c reticulum (ER) stress response and the MEK/ERK pathway in inducing apoptosis in TNBC cells.

166 Nifetepimine down-regulated the MEK/ERK pathway in MDAMB-231 and MDAMB-468 cells and resulte

167 These studies identify the Ras-Erk pathway in neurofibromin-deficient macrophages as th

168 ble cross talk between eIF2alpha and the MEK/ERK pathway in neuropathic nerves.SIGNIFICANCE STATEMENT

169 MEKK2 is a novel component of a noncanonical ERK pathway in osteoblasts that mediates aberrant ERK ac

170 Thus, MEKK2 functions as a MAP3K in the ERK pathway in osteoblasts, offering a potential new the

171 pression is decreased with activation of the ERK pathway in primary cancer specimens in vivo and in c

172 Moreover, dual inhibition of the EGFR-MEK-ERK pathway in RAS mutant organoids induced a transient

173 elated to the epidermal growth factor (EGFR)/ERK pathway in SORLA transgenic mouse hippocampus from b

174 ritical cell-autonomous role for the NF1-RAS-ERK pathway in the appropriate regulation of cerebellar

175 1-4) are MEK kinases that reactivate the MEK/ERK pathway in the presence of RAF inhibitors.

176 s have implicated the involvement of the MEK/ERK pathway in the reduction of DNA methyltransferase (D

177 onsible for regulation of the Rac1/C-RAF/MEK/ERK pathway in these cells.

178 Thus, genetic blockade of the ERK pathway in Tpl2(-/-) macrophages enhances Th1 polari

179 associated with augmented activation of the ERK pathway in vitro and in hearts in vivo.

180 obustly stimulated the PI3K/Akt/mTOR and MEK/ERK pathways in CD56bright compared with CD56dim NK cell

181 ream activator of both the PI3K/Akt and MAPK/ERK pathways in liver cancer cells, and Nqo1 ablation bl

182 g through VEGF receptor 2 (VEGFR2), Akt, and ERK pathways in lungs and primary endothelial cells and

183 hanistic target of rapamycin (mTOR), and MEK/ERK pathways in the regulation of RPE phagocytosis, conf

184 , despite inhibition of the HER2 and the RAS-ERK pathways in tumor cells.

185 EGFR)-extracellular signal-regulated kinase (ERK) pathway in a reactive oxygen species (ROS)-dependen

186 (MEK)-extracellular signal-regulated kinase (ERK) pathway in HCL by exposing in vitro primary leukemi

187 o the extracellular signal-regulated kinase (ERK) pathway in medium spiny neurons (MSNs) of the stria

188 ase Ras-extracellular signal-related kinase (Erk) pathway in the brain and normalizes deficits in LTP

189 sion molecules through the NF-kappaB and MEK/Erk pathways, in particular by preventing the proteasome

190 We have recently shown that the Ras-Raf-ERK pathway induces HO-1 to promote survival of renal ca

191 ovides a biochemical framework for selective ERK pathway inhibition by targeting the SHOC2 holophosph

192 tent with ERK reactivation and/or incomplete ERK pathway inhibition in response to EGFR inhibitor mon

193 rrogated the well-described mechanism of MEK/ERK pathway inhibitor addiction in solid tumors and foun

194 come chemically by oral administration of an ERK pathway inhibitor or genetically via the specific lo

195 n this regulation, and the addition of a MEK/Erk pathway inhibitor significantly enhanced the PD-L1 A

196 the p38 MAPK inhibitor SB283580 but not the ERK pathway inhibitor UO126 significantly reduced Hsp70

197 by treating the mice with U0126, a specific ERK pathway inhibitor, showing that, in vivo, the delete

198 LPS-stimulation, which was prevented by the ERK pathway inhibitor.

199 /mTOR pathway, along with cobimetinib, a MEK/ERK pathway inhibitor.

200 creased in macrophages in the presence of an ERK pathway inhibitor.

201 istance mechanisms that hamper classical RAS-ERK pathway inhibitors.

202 g the extracellular signal-regulated kinase (Erk) pathway intact.

203 The RAS-RAF-MEK-ERK pathway is a key driver of proliferation and surviva

204 show that cancer cells in which the RAF/MEK/ERK pathway is activated are particularly sensitive to t

205 We show that the nutrient responsive ERK pathway is both induced by and restricts disparate a

206 The RAS/ERK pathway is commonly activated in carcinomas and prom

207 Our results demonstrate that the Ras/Erk pathway is decoded by both dynamic filters and logic

208 The RAS-RAF-MEK-ERK pathway is deregulated in over 90% of malignant mela

209 Regulation of the ERK pathway is intimately involved in determining whethe

210 relationship with respect to the Gq, Gs, and ERK pathways is detailed.

211 The extracellular signal-regulated kinase (ERK) pathway is an essential component of developmental

212 tracellular signal-regulated kinase (Raf/MEK/ERK) pathway is functionally linked to nuclear export of

213 e RAS-extracellular signal-regulated kinase (ERK) pathway is implicated in breast cancer pathogenesis

214 inase/extracellular receptor kinase (RAS/MEK/ERK) pathway is preferentially activated in naive and ce

215 We found that the Ras-ERK pathway, is not only essential for long-term potenti

216 D2014 did not activate AKT but activated the ERK pathway, leading to a moderate MKP-1 induction.

217 urther, IL-8 upregulation activates the MAPK/ERK pathway, leading to ERK phosphorylation and enolase

218 Inhibition of AKT and ERK pathways led to up-regulation of splicing factor exp

219 r progression to NEPC, whereas IL-8 and MAPK/ERK pathways may be promising targets for therapeutic in

220 ) and extracellular signal-regulated kinase (ERK) pathways mediated the sustained inhibitory actions

221 ic cAMP sensor-Rapgef2 --> B-Raf --> MEK --> ERK pathway mediating neuritogenesis in NS-1 cells.

222 l cells, we find that activation of the MAPK/ERK pathway mirrors the rapid and dynamic induction of D

223 genic Ras, a potent activator of the Raf/MEK/ERK pathway, on the activity of SK1 and sphingolipid met

224 tion, forestalls tumorigenesis driven by RAS-ERK pathway oncogenes.

225 re associated with genes involved in the MEK-ERK pathway, one of the most frequently disrupted pathwa

226 liferation is effectively silenced only when ERK pathway output falls below a threshold of ~10%, indi

227 e was constitutive activation of the Ras/Raf/ERK pathway p-ERK 1/2 (Thr202/Tyr204) expression in the

228 t signaling abnormalities in the PLC/IP3/PKC/ERK pathway (phospholipase C/inositol 1,4,5-triphosphate

229 n of extracellular signal regulated kinases (ERK) pathway plays an important role in left ventricular

230 oup-specific enhancer regulation of the MAPK/ERK pathway predicts sensitivity to MEK inhibition.

231 at deleting Ptpn11, which links FGF with the ERK pathway, prevents inferior colliculus formation by d

232 eans to treat NF1, the broad blockade of the ERK pathway produced by this strategy is potentially ass

233 einnervation.SIGNIFICANCE STATEMENT The MAPK/ERK pathway promotes developmental myelination and its s

234 The RAS/RAF/MEK/ERK pathway promotes gliogenesis but the kinetic role of

235 transcription and glutaminolysis through MEK/ERK pathway, providing new insight into oncogenic altera

236 Our observations suggest that the ERK pathway, rather than the mTOR pathway, most likely p

237 show that resistance to BRAFi is mediated by ERK pathway reactivation.

238 that TGF-beta1 induced activation of the MEK/ERK pathway reduces IL-13Ralpha2 expression induced by I

239 tyrosine kinases (RTK) and PI3K/Akt and MAPK/ERK pathways, regulate these phenotypic transitions.

240 The MEK-ERK pathway regulates CRNA by elevating the levels of cy

241 Here we show that activation of the RAS/MEK/ERK pathway regulates G-CSF expression through the Ets t

242 y the extracellular signal-regulated kinase (ERK) pathway regulates a mechanism of dedifferentiation

243 RAF1/extracellular signal-regulated kinase (ERK) pathway regulates arterial morphogenesis and arteri

244 ERK pathway regulating cell growth is synergistically re

245 ulation of the metabolic pathways by the RAS-ERK pathway remain elusive.

246 e, targeting the downstream PI3K and RAF/MEK/ERK pathways represents a promising approach to treat RA

247 MAPK signaling pathway and the p38, JNK, and ERK pathways, respectively.

248 genetic or pharmacological inhibition of the ERK pathway restored EpCAM expression.

249 neonatal administration of inhibitors of the ERK pathway reversed the morphological defects.

250 Inhibitors of the FGF receptor (Fgfr) and ERK pathways reversed the skewed lineage specification o

251 The Akt and ERK pathways serve as important targets in CSCs.

252 Because the ERK pathway serves as a crucial point of convergence for

253 activates PKCdelta, contributing to impaired ERK pathway signaling in lupus T cells.

254 te for the phospho-inhibition of Ras/Raf/MEK/ERK pathway signaling that is mediated by the stress-act

255 -binding protein (RREB1), which sustains Ras/ERK pathway signaling through repressing miR-143/145 exp

256 kinases are essential for normal Ras-Raf-MEK-ERK pathway signaling, and activating mutations in compo

257 uscle cell proliferation following decreased ERK pathway signaling.

258 ibition of the p38 MAPK pathway, but not the Erk pathway, significantly impaired neutrophil migration

259 lex with paradoxical components, coordinates ERK pathway spatiotemporal dynamics with polarity and th

260 GE2 from CM, and pre-treatment with a p44/42 ERK pathway-specific inhibitor, resulted in a complete i

261 In addition, we show that this Galpha12-ARAF-ERK pathway stimulates RFFL transcription through the tr

262 ciated with somatic mutations in the RAS-MEK-ERK pathway such as BRAF(V600E), suggests a possible rol

263 and this is increased by IL-33 through ST2R-ERK pathway, suggesting a mechanism for enhanced airway

264 ltaneous inhibition of the PI3K/Akt and MAPK/ERK pathways, suppressed the expression of glycolysis an

265 rization, leading to more potent and durable ERK pathway suppression that promotes BIM-dependent apop

266 dentify RASA1 and SPRED1 mRNAs as latent RAS-ERK pathway suppressors that can be upregulated in tumor

267 ed for activation of the proapoptotic Ca(2+)-Erk pathway that is selectively activated during B cell-

268 Signal transduction through the RAF-MEK-ERK pathway, the first described mitogen-associated prot

269 FR activation and stimulation of the Ras/Mek/Erk pathway, the latter activity of which was conserved

270 As a central element within the RAS/ERK pathway, the serine/threonine kinase BRAF plays a ke

271 miR-132 increased activity of the STAT3 and ERK pathways, thereby promoting keratinocyte growth.

272 )/STAT3 signaling reaches across to the MAPK/ERK pathway through MYC and MAX to sustain pluripotency.

273 nsulin-like receptor signals through the RAS-ERK pathway to drive meiotic prophase I progression and

274 an indispensable role in activating the MEK/ERK pathway to drive tumorigenesis.

275 of which would otherwise stimulate the MAPK/ERK pathway to promote NE differentiation of prostate ca

276 , followed by chemical inhibition of the Ras/ERK pathway to reprogram the sperm-oocyte decision.

277 trate that EGFR signaling activates the MAPK/ERK pathway to stimulate the expression of EGR2, which i

278 ative extracellular signal-regulated kinase (ERK) pathway; to our surprise, this negative cross-regul

279 phorylation of MEK/ERK, silencing of RAF-MEK-ERK pathway transcriptional output, loss of the HCL-spec

280 dephosphorylation, silencing of the BRAF-MEK-ERK pathway transcriptional output, loss of the HCL-spec

281 ur data show that weak activation of the Mek/Erk pathway underpins RASopathies, but in cancer, (L597V

282 blocker noggin inhibits the canonical FGF-to-ERK pathway upstream of FRS2 activation and also prevent

283 ists of the protein kinase C (PKC)-dependent ERK pathway via atypical PKC isoforms PKCzeta and PKCiot

284 ows for reversible activation of the RAF/MEK/ERK pathway via plasma membrane recruitment of RAF1 base

285 In contrast, the ERK pathway was activated by small-magnitude stretching

286 Targeting of the MEK-ERK pathway was effective in fusion-positive Schwann cel

287 its ability to stabilize neovessels when the Erk pathway was inhibited pharmacologically.

288 lecule between antigen receptors and the Ras/Erk pathway, was identified as a target for neddylation.

289 Specifically, the Akt and ERK pathways were activated in BCSC at early time points

290 ion induced growth arrest partly via the MEK/ERK pathway, whereas it induced cell death by causing mi

291 igh activity levels of the components of the ERK pathway, which are essential for initial-segment dif

292 induced type II cell differentiation via the ERK pathway, which was rescued by overexpression of a co

293 s cytotoxicity in HK-2 cells through ROS and ERK pathways, which highlight the preventive avenues in

294 d gene-based association analysis of the RTK/ERK pathway with aggressive prostate cancer in a cohort

295 cuss strategies of targeting the RAS-RAF-MEK-ERK pathway with emphasis on MEK inhibition, either alon

296 ole for MLKs as direct activators of the MEK/ERK pathway with implications for melanomagenesis and re

297 ion of genetic variants and genes in the RTK/ERK pathway with prostate cancer aggressiveness, and hig

298 in led to a rapid activation of both AKT and ERK pathways with a subsequent increase in MKP-1 express

299 receptor that can activate both the Rho and ERK pathways, with the N-terminal and C-terminal regions

300 ubular epithelial cells through the PI3K and ERK pathways without increasing glucose uptake.