ライフサイエンスコーパス: ERK

1 ERK activation downstream of C-Raf is necessary for main

2 a negative-feedback component in which MPK-1/ERK activity targets the upstream kinase LIN-45/Raf for

3 athway in osteoblasts that mediates aberrant ERK activation after NF1 loss.

4 Amylin is also able to activate ERK signaling specifically in POMC neurons independently

5 of FGF signaling components, which activate ERK signaling and direct the exit from the ESC state.

6 In vitro, IL11 activated ERK signaling, but inhibited STAT3 activity, and caused

7 1/2 as downstream targets of virus-activated ERK signaling.

8 RK kinase, indicating that MAP3K19 activates ERK via a RAF-independent mechanism.

9 ed increase in gene expression by activating ERK and JNK; these changes in gene expression could be m

10 Our results show primarily active ERK in both the inner cell mass and trophectoderm cells

11 s were exposed to their respective agonists, ERK was the most significantly activated intracellular s

12 GFR under hypoxia led to an increase in AKT, ERK, and Rb phosphorylation as well as increased levels

13 ated oncogenic signalling pathways (PI3K-AKT/ERK), which may also involve the distinct alteration of

14 oplasmic anchors, is sufficient for allowing ERK interactions with its substrates.

15 n of p38, a pro-death MAPK, without altering ERK and JNK.

16 erall, this signaling pathway constitutes an ERK-mediated "toggle switch" that promotes pluripotency

17 This study defines an ERK-mediated molecular mechanism of dedifferentiation of

18 enerated a targeted mouse line expressing an ERK-kinase translocation reporter (KTR) that enables liv

19 ulated and translocates to the nucleus in an ERK-dependent manner in neurons treated with sSORLA.

20 e results, Mrs6 may selectively propagate an ERK-dependent signal.

21 3/6 and p38MAPK or to upregulate MEK-1/2 and ERK-1/2 in BALB/c-derived peritoneal macrophages.

22 Functional imaging to monitor Ca(2+) and ERK signals revealed a significant role of Y954 in influ

23 chanistically, Rac1 activates aldolase A and ERK signaling which up-regulates glycolysis and especial

24 in regulating growth factor induced Akt and ERK activities.

25 IM) of NADH and signaling by kinases Akt and ERK revealed that breast cancer cells utilized oxidative

26 on of proinflammatory molecules, GM-CSF, and ERK-2, promoting immune homeostasis.

27 t the plasma membrane and in the cytosol and ERK in the nucleus.

28 In addition, EGFR and ERK signaling both became more sustained when substoichi

29 36), a marker for activation of the mTOR and ERK signaling pathways.

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

31 y networks, T-cell kinetic proofreading, and ERK signalling.

32 cells, and increased activation of STAT3 and ERK during the later stages of tumorigenesis.

33 ated expression of endocan via JAK/STAT3 and ERK/ELK cascades, thus forming a positive regulatory loo

34 eveal the segregation of oncogenic STAT5 and ERK activation to competing clones.

35 STAT5 and ERK engage opposing biochemical and transcriptional prog

36 STAT5- and ERK-activating lesions are found frequently, but occur t

37 E CMs, which peak during metaphase, that are ERK dependent and Hippo independent.

38 s are bypassed for downstream events such as ERK and PKCdelta phosphorylation.

39 Key cellular mechanisms such as ERK signaling and cell-cycle synchronization differed si

40 Disruption of DBT severely attenuates ERK/MAPK signaling, p53 activation, and apoptosis in mel

41 ll differentiation, Etv deficiency augmented ERK phosphorylation without disrupting the normal lens f

42 rster Resonance Energy Transfer (FRET)-based ERK biosensors by creating a series of improved biosenso

43 nished CXCR4 agonist activity as measured by ERK phosphorylation, chemotaxis, and G(i/o)-mediated cAM

44 ular endothelial growth factor-A/C, and cAMP/ERK expression was performed.

45 In differentiated GBM cells, ERK-mediated repression of miR-199a-3p induced EGR1 prot

46 EGFR activation kinetics, and consequently ERK signaling dynamics, were switched from transient to

47 evidence for an additional step controlling ERK's access to substrates.

48 these negative regulators of MAPK to dampen ERK activity, leading to sustained CIC-DUX4 expression.

49 ed that this reduces viability and decreases ERK and JNK pathway activation.

50 ing NCS-Rapgef2 expression on cAMP-dependent ERK->Egr-1/Zif268 signaling in cultured neuroendocrine c

51 Ablation of cocaine-dependent ERK activation by elimination of NCS-Rapgef2 occurred wi

52 ul hypersensitivity through GPR160-dependent ERK and cAMP response element-binding protein (CREB).

53 required for D1 dopamine receptor-dependent ERK phosphorylation in mouse brain.

54 Therapeutic targeting of YBX1-dependent ERK signalling in combination with JAK2 inhibition could

55 are resistant to cancer drugs and diminished ERK signaling.

56 epolarization-dependent C-Raf and downstream ERK activity maintain a depolarized RMP and nociceptor h

57 In search for downstream ERK effectors activated by sSORLA, we identified upregul

58 -iTrkB are capable of reproducing downstream ERK and Akt signaling only in the presence of tdnano.

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

60 sing markers of pluripotency through an EGFR-ERK-EGR1-dependent axis.

61 EGFR-interacting protein that activates EGFR/ERK/Fos signaling to enhance neurite outgrowth and regen

62 Induction of EGR1 by EGFR/ERK signaling promoted cell conversion from a less aggre

63 des PCSCs growth and metastasis via the EGFR/ERK/FOXA2/SOX9 axis.

64 resulted in reduced activation of Akt, FAK, ERK, and p38 signaling pathways, which are coordinately

65 FGF/ERK signaling is crucial for the patterning and prolifer

66 inner cell mass (ICM), all cells relayed FGF/ERK signals with varying durations and magnitude.

67 Thus, reduced FGFR2/ERK signaling apparently leads to abnormal urothelial re

68 mice had reduced fibrosis, lesser fibroblast ERK activation, and diminished immune cell STAT3 phospho

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

70 partments, it is important to understand how ERK activity is temporally regulated at specific subcell

71 (2020) identify ERK-mediated phosphorylation of the m(6)A methyltransfer

72 motifs to measure spatiotemporal changes in ERK activity.

73 loyed to identify gene expression changes in ERK isoform knockdown clones.

74 he same phosphorylation can also be found in ERK-activated human cancer cells and contribute to tumor

75 Y1173 phosphorylation, which is involved in ERK activation in cultured neurons.

76 ocaine on protein phosphorylation, including ERK/MAPK-targets like gephyrin, and modulates the synapt

77 cre recombinase, eliminated cocaine-induced ERK phosphorylation and Egr-1/Zif268 upregulation in D1-

78 ence after injury, implicating wound-induced ERK activity in this response.

79 The compounds can inhibit ERK phosphorylation at higher concentrations by engaging

80 the Ras, Rho, and Rab families and inhibits ERK activity, resulting in endoplasmic reticulum (ER) st

81 Interestingly, ERK was heavily activated in both patients, highlighting

82 rved in vitro, is Rab11a-dependent, involves ERK-MAPK-signalling and is inhibited by antibodies again

83 auses splicing-dependent alterations of JAK2-ERK signalling and the maintenance of JAK2(V617F) malign

84 and 3) suppress the phosphorylation of JNK, ERK, and p38 MAPK signaling pathways.

85 cells (via activation of the protein kinase ERK)(5-8).

86 opioid-induced phosphorylation of the kinase ERK and increased abundance of the kinase RSK in the dor

87 MAPK)/extracellular-signal-regulated kinase (ERK) (MEK) 1/2, which has been approved for treatment of

88 lated extracellular signal-regulated kinase (ERK) (pERK) levels.

89 that extracellular signal-regulated kinase (ERK) 1/2 cascade is the most significantly upregulated g

90 on of extracellular signal-regulated kinase (ERK) 5 signaling, which has recently been implicated in

91 atory extracellular signal-regulated kinase (ERK) activity, which can be eliminated by TACE knockout,

92 f the extracellular signal-regulated kinase (ERK) and JUN N-terminal kinase (JNK) signaling pathways,

93 on of extracellular signal-regulated kinase (ERK) and of cell growth than SHP099, a potent SHP2 inhib

94 on of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcriptio

95 on of extracellular signal-regulated kinase (ERK) in NF1 (-/-) Schwann cells.

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

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

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

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

100 inase extracellular signal-regulated kinase (ERK) prevents stem cell persistence after injury, implic

101 MAPK)/extracellular signal-regulated kinase (ERK) signaling pathways play central roles in cancer cel

102 aired extracellular signal-regulated kinase (ERK) signaling, delayed ESC cell cycle progression, and

103 ol of extracellular signal-regulated kinase (ERK) signalling.

104 ereas extracellular signal-regulated kinase (ERK), which is essential for host cell viability, remain

105 mmon, extracellular-signal regulated kinase (ERK)-dependent cascade.

106 arent extracellular signal-regulated kinase (ERK)-driven proliferation of mostly keratin 5 (KRT5)(+)/

107 ering extracellular signal-regulated kinase (ERK)-mediated PKM2 translocation into the nucleus.

108 (MEK)/extracellular signal-regulated kinase (ERK).

109 K and extracellular signal-regulated kinase (ERK).

110 (MAPK)/extracellular signal-related kinase (ERK) (MEK) biology and our observation that 6-OH-BDE-47

111 -driven extracellular signal-related kinase (ERK) signaling in dendritic cells (DCs) versus macrophag

112 of Ras/extracellular signal-related kinase (ERK) signaling with the genetic loss of the receptor tyr

113 signaling molecules Src (Src family kinase), ERK (extracellular signal-related kinase), and VASP (vas

114 t cells, phosphorylation of protein kinases, ERK and SYK, was decreased.

115 tive role in CMT1B Schwann cells by limiting ERK/c-Jun hyperactivation.

116 We investigated the mechanism that makes ERK resistant to NleD cleavage.

117 rough immunoregulation by blunting the MAPK (ERK, JNK)-mediated priming signal of the NLRP3 inflammas

118 Genetic and pharmacologic MAPK-ERK activation through DUSP6 inhibition leads to CIC-DUX

119 C-DUX4 targets that negatively regulate MAPK-ERK signaling.

120 s that the EDN1-EDNR axis activates the MAPK-ERK signaling pathway that is vital to the cancer cell s

121 eceptor TSPAN12 at cell membranes in an MAPK/ERK kinase (MEK)/ERK-dependent manner.

122 detected mainly in spinal neurons, and MAPK/ERK kinase inhibitors significantly inhibited chronic it

123 mplicated in the resistance to BRAF and MAPK/ERK kinase inhibitors.

124 cogene Ser/Thr protein kinase (RAF) and MAPK/ERK kinase, indicating that MAP3K19 activates ERK via a

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

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

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

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

129 to carcinomas by elevating p38MAPK and MAPK/ERK signaling.

130 carcinogenesis by elevating p38MAPK and MAPK/ERK signaling.

131 Virion-associated MAPK/ERK-2-mediated phosphorylation of Vpx plays a critical r

132 inase that directly phosphorylates both MAPK/ERK kinase (MEK) and MAPK kinase 7 (MKK7).

133 to induce the activation of downstream MAPK/ERK and PI3K/Akt signaling as well as the neurite outgro

134 increased phosphorylation of downstream MAPK/ERK kinase (MEK)/extracellular signal-regulated kinase (

135 dually phosphorylated ERK (dpERK) from MAPK/ERK kinase (MEK), a kinase that phosphorylates ERK, and

136 Interestingly, MAPK/ERK-2 packaging defective SIV failed to promote the effi

137 R2 kinase activity in the canonical RAF/MAPK/ERK/RSK and PI3K/AKT/PDK/mTOR/S6K pathways are identifie

138 mport of viral genome and suggests that MAPK/ERK-2-mediated Vpx phosphorylation is important for its

139 the BRAF inhibitor vemurafenib and the MAPK/ERK kinase inhibitor cobimetinib.

140 The MAPK/ERK kinase MEK is a shared effector of the frequent canc

141 s ABCB1 stability and transcription via MAPK/ERK and p53.

142 ermal interface, spatial segregation of mean ERK activity and pulses was observed.

143 K kinase translocation reporter and measured ERK activity in single cells of live embryos.

144 however, in many tumors BRAF dimers mediate ERK signaling.

145 chemokine-like receptor 1 (CMKLR1)-mediated ERK signaling and altered intracellular calcium mobiliza

146 t cell membranes in an MAPK/ERK kinase (MEK)/ERK-dependent manner.

147 Inhibition or knockdown of MEK, ERK or RSK1 caused impaired vRNP export and reduced prog

148 trical activity, pre-synaptic functions, MEK-ERK signaling, and axonal guidance.

149 resistance phenomenon, well-described in MEK-ERK-driven solid tumors, in which drug-target overexpres

150 Mechanistically, increased MEK-ERK signaling activity and mortalin function converged o

151 stream mitogen-activated protein kinase (MEK-ERK) signaling to alter cell mechanics and enhance mitot

152 therapeutic strategy in B-Raf-mutant or MEK-ERK-driven tumors.

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

154 The RAS-RAF-MEK-ERK signaling axis is frequently activated in human canc

155 distinct feedback mechanisms in the Raf-MEK-ERK signaling network, with the receptors themselves act

156 chimeric protein DeltaRaf-1:ER and that MEK-ERK-sensitive regulation of the peptide-binding domain i

157 city, at least in part, by impairing the MEK-ERK axis of MAPK signal transduction.

158 Specifically, whereas MEK-ERK activity increased mitochondrial permeability by pro

159 MEK/ERK and NFkappaB inhibitors were used to assess the regu

160 MEK/ERK inhibition also drove oligodendrocyte formation in h

161 on of ELK1 at Ser 383 through activating MEK/ERK signaling.

162 lug, a process that is dependent on both MEK/ERK signaling and ATF4.

163 and class II MHC mismatch and blocked by MEK/ERK and NFkappaB inhibition.

164 ty crosstalk mediated by NMDAR-dependent MEK/ERK signaling.

165 expression, and that K-Ras(G12V)-driven MEK/ERK activity is necessary for this lethality.

166 a transcriptional factor downstream from MEK/ERK, binds to the promoter region of VE-cadherin (chip a

167 is often upregulated and mislocalized in MEK/ERK-deregulated tumors.

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

169 al screening revealed that inhibition of MEK/ERK signaling overcame the HIF1a-mediated block in oligo

170 gnaling as well as via the activation of MEK/ERK.

171 r resistance by inducing reactivation of MEK/ERK/MYC signaling.

172 d SOS1-inhibition markedly inhibited Raf/MEK/ERK and PI3K/AKT signaling.

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

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

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

176 ect transforming effect via constant RAS/MEK/ERK signaling, an inflammation-related effect of KRAS co

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

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

179 s, but rather a dramatic increase of the MEK/ERK/c-Jun pathway accompanied by a reduction in expressi

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

181 bryonic stem cells (mESCs) cultured with MEK/ERK and GSK3beta (2i) inhibitors transition to ground st

182 VEGF that results in phosphorylation of MEK1/ERK and activation of ERG leading to expression of VE-ca

183 Furthermore, EGF-induced plasma membrane ERK activity involves Rap1, a noncanonical activator, an

184 behavior is mediated by asymmetric mitosis, ERK activity, cell-cycle duration, and DNA repair capaci

185 st growth factor 19 (FGF19), acting via mTOR/ERK signaling and TFEB phosphorylation, feedback inhibit

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

187 ion are rapidly reinstated in the absence of ERK activation, revealing that inductive signaling must

188 proinflammatory molecules and activation of ERK (extracellular signal-regulated kinase) 5/p38 pathwa

189 impact of each variant on the activation of ERK (extracellular signal-regulated kinase), AKT (protei

190 ef2 in the NAc is required for activation of ERK and Egr-1/Zif268 in D1 dopaminoceptive neurons after

191 This scenario describes the activation of ERK, a highly conserved cell-signaling enzyme.

192 In macrophages, blockade of ERK signaling by pharmacologic or genetic approaches inh

193 In DCs, blockade of ERK signaling similarly inhibited IL-10 expression but d

194 Given the wide distrubtion of ERK susbtrates across different subcellular compartments

195 sions depend on the duration and dynamics of ERK signaling.

196 h microglial contractility, dysregulation of ERK signaling, excessive TGFbeta1 expression and abnorma

197 pression, which is opposite to the effect of ERK signaling blockade on IL-12/23p40 in macrophages.

198 ur study reveals an unrecognized function of ERK in regulating m(6)A methylation.

199 1, and lag-3/sel-8, which encode homologs of ERK/MAPK and core components of the Notch-dependent tran

200 targets offering a more narrow inhibition of ERK activation downstream of NF1 loss in the skeleton, f

201 Pharmacological inhibition of ERK induced differentiation only when cells were in the

202 ere abolished upon intrathecal inhibition of ERK, RSK, or protein synthesis.

203 ifically, we demonstrate that interaction of ERK with its substrate Capicua (Cic) is controlled at th

204 Capicua (Cic) is controlled at the level of ERK phosphorylation, whereby Cic binds to dpERK much str

205 erm cells displayed higher overall levels of ERK activity, while pluripotent epiblast cells exhibited

206 ops of JNK and p38 but not the rigid loop of ERK.

207 FGF receptor mutants that displayed loss of ERK signaling and defective cell differentiation, Etv de

208 ticles and Pam3Cys led to phosphorylation of ERK (extracellular signal-regulated kinase), JNK, and p3

209 tic model to dissect dual phosphorylation of ERK by MEK, a kinase that is mutated in a large number o

210 f mitotic events results in a short pulse of ERK inactivity in both daughter cells that correlates wi

211 er (KTR) that enables live quantification of ERK activity at single-cell resolution.

212 ieved through precise temporal regulation of ERK activity.

213 d with Pam(3)Cys-Ser-Lys(4), and the role of ERK signaling was interrogated pharmacologically with ME

214 duced activation of FAK but had no impact on ERK-1/2 activation.

215 protein has been mainly related to oncogenic ERK signaling through the RAS-SHOC2-PP1 phosphatase comp

216 TAMs by activating STAT5, NF-kappaB, and/or ERK signaling.

217 ational changes located in the polar core or ERK interaction site of beta-arr1 via direct receptor tr

218 activation, whereas pharmacological EGFR or ERK inhibition reverses sSORLA-dependent enhancement of

219 , suggesting that these waves of oscillatory ERK activity depend on autocrine/paracrine signals produ

220 CR effectors including c-Myc, NFkappaB and P-ERK, leading to cancer cell death in vitro and in xenogr

221 The mutational state of NOTCH1, p-ERK and RelB could serve as potential biomarkers of tipi

222 An immunohistochemistry study showed that p-ERK and RelB were associated as potential biomarkers of

223 perturbations to Ras, PI(4,5)P2, PI(3,4)P2, ERK, and TORC2 alter the threshold, observations that de

224 lso exhibited increased RAC1-GTP and phospho-ERK levels compared with Nf1(flox/flox);PostnCre (-) lit

225 lso exhibited increased RAC1-GTP and phospho-ERK levels compared with Nf1(flox/flox);PostnCre(-) litt

226 signaling, including phospho-AKT and phospho-ERK signaling; and decreased the invasion capability of

227 and fibrosis, angiogenesis, and cAMP/phospho-ERK expression.

228 oter also eliminated cocaine-induced phospho-ERK activation and Egr-1/Zif268 induction, but without e

229 letely free of tumors and had normal phospho-ERK activity compared with Nf1(flox/flox) ;PostnCre (+)

230 letely free of tumors and had normal phospho-ERK activity compared with Nf1(flox/flox);PostnCre(+) mi

231 ations, mediated through NCS-Rapgef2/phospho-ERK activation, independently of PKA/CREB signaling.SIGN

232 Phosphorylated ERK was observed in the interneurons expressing the rece

233 cation associated with absent phosphorylated ERK staining and decreased p53 expression versus control

234 hosphorylated AKT, and drives phosphorylated ERK-mediated KRT5(+)/KRT14(-) cell proliferation, leadin

235 sociation of activated dually phosphorylated ERK (dpERK) from MAPK/ERK kinase (MEK), a kinase that ph

236 attenuated or ablated spinal phosphorylated ERK.

237 lation of Cic and stabilizing phosphorylated ERK.

238 ogether, our work showed that phosphorylated ERK is a unique marker for itch signal transmission in t

239 K kinase (MEK), a kinase that phosphorylates ERK, and other cytoplasmic anchors, is sufficient for al

240 t to a lower threshold of excitable Ras/PI3K/ERK network, caused by various combinations of genetic i

241 This altered PRMT6-ERK-PKM2 signaling axis was further confirmed in both a

242 Our findings indicate that the PRMT6-ERK-PKM2 regulatory axis is an important determinant of

243 ing phosphorylation of EGFR family proteins, ERK, FAK, and CSC markers.

244 d distribution of basal cells with pulsatile ERK activity, and down-regulation was linked to the onse

245 Activation of a canonical EGFR-Ras-Raf-ERK cascade initiates patterning of multipotent vulval p

246 Alk signaling, including members of Ras/Raf/ERK-, Pi3K-, and STAT-pathways as well as tailless (tll)

247 ectal cancer metastatic disease, yet how RAS-ERK signaling regulates colorectal cancer metastasis rem

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

249 The RAS-ERK/MAPK (RAS-extracellular signal-regulated kinase/mito

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

251 eurite regeneration through the EGF receptor/ERK/Fos pathway, thereby demonstrating a potential neuro

252 1), five had established roles in regulating ERK-type pathways (STE4, STE7, BMH1, BMH2, MIG2) and sev

253 ty protein phosphatase negatively regulating ERK function.

254 stration of KGF to uninjured mice reproduced ERK-driven KRT5(+)/KRT14(-) proliferation seen in injure

255 otho induces phosphorylation of AKT(ser473), ERK(thr202/tyr204), and FOXO1(ser256) as well as blunts

256 Here we tracked spatiotemporal ERK MAPK dynamics in human epidermal stem cells.

257 d that Ph-like ALL cells have activated SRC, ERK, and PI3K signaling consistent with activated B cell

258 of PKA/CREB signaling.SIGNIFICANCE STATEMENT ERK phosphorylation in dopamine D1 receptor-expressing n

259 driven by overexpression of FGFR1 to sustain ERK signaling, where a subsequent combination of EGFR TK

260 ensors, we showed that EGF induces sustained ERK activity near the plasma membrane in sharp contrast

261 rent mouse models of chronic itch, sustained ERK phosphorylation was detected mainly in spinal neuron

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

263 nerve growth factor (NGF) promotes sustained ERK activation and cell differentiation.

264 Our findings demonstrate that ERK MAPK signal fluctuations link kinase activity to ste

265 We find that ERK phosphorylates METTL3 at S43/S50/S525 and WTAP at S3

266 Instead, we found that ERK signaling faithfully followed RTK dynamics when rece

267 f Nanog in embryonic stem cells reveals that ERK inhibition promotes enhanced stabilization of NANOG

268 A greater understanding of the role that ERK signaling plays in different immune cell types may i

269 n response to IL-15, CD122+Macs activate the ERK signaling cascade and enhance production of proinfla

270 s reveal that MAP3K19 directly activates the ERK and JNK cascades and highlight a role for this kinas

271 r Rho family GTPases that also activates the ERK/MAPK pathway.

272 rexpression of WT MAP3K19 activates both the ERK and JNK pathways in a panel of cancer cell lines.

273 Drosophila embryos were used to dissect the ERK-dependent control of the HMG-box repressor Capicua (

274 generated a transgenic mouse expressing the ERK kinase translocation reporter and measured ERK activ

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

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

277 ative conditioning in animals, including the ERK, PI3K, and PKC pathways.

278 While inhibitors of the ERK activating kinases MEK1/2 are promising as a means t

279 ptoAKT, to delineate the contribution of the ERK and AKT signaling pathways to neuroregeneration in l

280 n TNBC, however the precise functions of the ERK isoforms (ERK1 and ERK2) in cancer progression have

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

282 BRAF kinase, a critical effector of the ERK signaling pathway, is hyperactivated in many cancers

283 d invasive growth and phosphorylation of the ERK-type fMAPK, Kss1.

284 are proto-oncogenes ERK2, a component of the ERK/MAPK pathway, and VAV1, a guanine nucleotide exchang

285 s well-known for its ability to regulate the ERK and PI3K signaling pathways.

286 division by signal transduction through the ERK cascade and mutations leading to constitutive activi

287 fficiency of signal transduction through the ERK pathway.

288 r to induce downstream signaling through the ERK serine/threonine kinase and the Fos transcription fa

289 d invasion, mesenchymal markers (through the ERK-ZEB1-vimentin axis under certain conditions) and in

290 that blocks PI3K/Akt signaling, through the ERK/cAMP-responsive element-binding protein/c-Jun pathwa

291 duce a reporter (FUS1-HIS3) that responds to ERK-type pathways (Mating and filamentous growth or fMAP

292 sults indicate that NCS-Rapgef2 signaling to ERK in dopamine D1 receptor-expressing neurons in the NA

293 on of the mechanism of dopamine signaling to ERK that underlies plasticity in dopamine D1 receptor-ex

294 dermal growth factor (EGF) induces transient ERK activation that leads to cell proliferation, whereas

295 Furthermore, sSORLA triggers ERK activation, whereas pharmacological EGFR or ERK inhi

296 dpERK much stronger than to unphosphorylated ERK, both in vitro and in vivo.

297 ive competition of Cic with unphosphorylated ERK and contributes to efficient signal propagation.

298 ifferential affinity of Cic for dpERK versus ERK is required for both down-regulation of Cic and stab

299 signals enabling anchorage independence via ERK and PI3K bypass cascades activated in a non-IL6-depe

300 D-beige mice injected via the tail vein with ERK clones were employed to determine metastatic potenti