ライフサイエンスコーパス: ERK pathway

1 ed the survival signals (mediated by Akt and ERK pathways).

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

3 -2 (SPRY2), a negative regulator of the MAPK/ERK pathway.

4 lore its possible mechanism on regulation of ERK pathway.

5 sion by Neu3 sialidase further activates the ERK pathway.

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

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

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

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

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

11 hypertrophy by inhibiting the expression of ERK pathway.

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

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

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

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

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

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

18 stimulation predominantly activates the MEK/ERK pathway.

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

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

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

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

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

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

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

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

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

28 nase activity and weak activation of the Mek/Erk pathway.

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

30 G protein-coupled receptor, GPR65, via a MEK/ERK pathway.

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

32 mediates Ca(2+)-dependent activation of the ERK pathway.

33 inds to SHC and Raf-1, two components of the ERK pathway.

34 tch-induced type II cell differentiation via ERK pathway.

35 activity and leads to stimulation of the MEK/ERK pathway.

36 e self-renewal, particularly within the MAPK/ERK pathway.

37 nocytogenes was dependent selectively on the ERK pathway.

38 curs in microglia via interaction with C-Raf/ERK pathway.

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

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

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

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

43 and JNK signaling pathways while inhibiting Erk pathway.

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

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

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

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

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

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

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

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

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

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

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

55 phA2 including inhibition of PI3/Akt and Ras/ERK pathways.

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

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

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

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

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

61 arrowextracellular signal-regulated kinase (ERK) pathways.

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

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

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

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

66 Thus, eIF3a is a negative modulator of ERK pathway activation and its biological effects.

67 ERK pathway activation in cells expressing wild-type BRA

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

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

70 (OCLN) expression resulting from Ras/Raf/MEK/ERK pathway activation led to the identification of seve

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

72 ERK pathway activation strongly enhances proliferation o

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

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

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

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

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

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

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

80 as a molecular mechanism responsible for MEK/ERK pathway activation.

81 This process requires TrkB-dependent ERK pathway activation.

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

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

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

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

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

87 monstrated that commensal bacteria stimulate ERK pathway activity via interaction with formyl peptide

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

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

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

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

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

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

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

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

96 iated in part by early inhibition of the MAP/ERK pathway and inactivation of STAT3, potentially drivi

97 terodimer uses PLC-beta3 to activate the Ras-ERK pathway and increase intracellular calcium ion conce

98 BRAF, the inhibitor PLX4720 switches off the ERK pathway and inhibits the expression of proangiogenic

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

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

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

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

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

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

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

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

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

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

109 kt/mammalian target of rapamycin and Raf/MEK/ERK pathways and from the reduction in GHRH produced by

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

111 d the extracellular signal-regulated kinase (ERK) pathway and nascent virions preferentially incorpor

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

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

114 ing the BF cholinergic circuitry through the ERK pathway, and demonstrate that the normal development

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

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

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

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

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

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

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

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

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

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

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

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

127 /extracellular signal-regulated kinase (MAPK-ERK) pathway, are significantly increased by EAPII overe

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

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

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

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

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

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

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

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

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

137 ents thus suggest that activation of the RAS/ERK pathway by Nf1 loss-of-function in osteochondroproge

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

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

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

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

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

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

144 The ERK pathway controls cell proliferation, and Aurora B pl

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

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

147 The ERK pathway defect is due to impaired phosphorylation of

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

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

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

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

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

153 Thus, targeting the Ras-Raf-ERK pathway for HO-1 overexpression may serve as novel t

154 Furthermore, we find that the Ras-MapKinase/ERK pathway functions with PUF-5/6/7 to repress specific

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

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

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

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

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

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

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

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

163 Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response

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

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

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

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

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

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

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

171 TCR ligation triggers the activation of the ERK pathway in naive cells.

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

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

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

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

176 1-4) are MEK kinases that reactivate the MEK/ERK pathway in the presence of RAF inhibitors.

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

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

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

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

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

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

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

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

187 a MEK-extracellular signal-regulated kinase (ERK) pathway in neutrophils and that the inhibition of t

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 ombined inhibition results in enhancement of ERK pathway inhibition and antitumor activity.

192 ed increase in viral titer was determined by Erk pathway inhibition with multiple Erk1/2 pathway inhi

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

194 lls with FBS and to decrease upon adding the ERK pathway inhibitor PD98509.

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

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

200 /mTOR pathway, along with cobimetinib, a MEK/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 c signaling, indicating that the RAS/RAF/MEK/ERK pathway is required downstream of EGF/EGFR to induce

211 Activation of PI3-K-AKT and ERK pathways is a complication of mTOR inhibitor therapy

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

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

214 e (MEK)/extracellular signal-related kinase (ERK) pathway is of significance.

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

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

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

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

219 ile other branches, such as the JAK/STAT and ERK pathways, make minor contributions to EGF-induced sp

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

221 This ROS/Src/Erk pathway mechanism appeared to be the same route by w

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

223 Gene expression arrays of ERK pathway members suggested a higher expression of KRA

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

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

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

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

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

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

230 The extracellular signal-regulated kinase (ERK) pathway participates in the control of numerous cel

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

232 e/extracellular signal-regulated kinase (MEK/ERK) pathway prevented HGF suppression of hepcidin in pr

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

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

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

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

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

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

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

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

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

242 ERK pathway regulating cell growth is synergistically re

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

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

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

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

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

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

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

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

251 Cdelta T(505) phosphorylation and inhibiting ERK pathway signaling similar to that observed in lupus

252 rom patients with active lupus have impaired ERK pathway signaling that decreases DNA methyltransfera

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

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

255 tion illustrate the opposing consequences of Erk pathway signaling.

256 se, DUSP3/VHR, and consequent stimulation of ERK pathway signaling.

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 ernatively, in the presence of TGF-beta, the Erk pathway suppresses a large program of gene expressio

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

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

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

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

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

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

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

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

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

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

275 MLS-2 cooperates with the EGF-Ras-ERK pathway to turn on the LIN-48/Ovo transcription fact

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

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

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

279 Inhibition of the MAPK-ERK pathway, unlike STAT5 signaling, impaired IL-2-induc

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

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

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

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

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

285 pecific inhibitors demonstrated that the MEK/ERK pathway was required for angiogenesis.

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

287 defective in activation of the PI3K and Shp2-Erk pathways, we find that Gab2 inhibits E-cadherin expr

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

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

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

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

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

293 ted the extracellular signal-related kinase (Erk) pathway, which antagonized LPA-mediated signaling e

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.