ライフサイエンスコーパス: ERK

1 ERK activation downstream of Ras was found to stabilize

2 ERK inhibition restores FoxO1, gluconeogenic enzyme expr

3 ERK reactivation was also observed following inhibition

4 ERK-mediated phosphorylation of ERG is required for ERG

5 ERK/MAPK deletion in D1R-MSNs (direct pathway) resulted

6 The mutants activate ERK signalling by different mechanisms that dictate thei

7 ht chain and HSPA5/BIP expression, activated ERK and antiapoptotic signaling, and conferred relative

8 creased levels of phosphorylated (activated) ERK compared with healthy pancreatic tissue.

9 ber 10B (Wnt10b)/beta-catenin and adipogenic ERK/MAPK signaling pathways.

10 is of a broad set of GPCRs without affecting ERK MAP kinase activation.

11 e causes a conformational change that allows ERK phosphorylation at a second serine residue, Ser-96.

12 We investigated the relationship among ERK signaling, histone modifications, and transcription

13 K1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activat

14 h the MKP DUSP5 both inactivates and anchors ERK in the nucleus, it paradoxically increases and prolo

15 ial associated with modulation of PAK1/2 and ERK/JNK MAPK signaling and F-actin dynamics.

16 ting integrin alphavbeta6, MMP-2, MMP-9, and ERK phosphorylation by HT29.

17 genitors deficient in MeCP2 restored AKT and ERK activation, respectively, and ameliorated the observ

18 TGF-beta1 inhibited IL-33-mediated Akt and ERK phosphorylation as well as NF-kappaB- and AP-1-media

19 rf2 inhibition via the regulation of Akt and ERK phosphorylation in the diabetic heart.

20 nsulin-stimulated phosphorylation of Akt and ERK, as well as the association of phosphatidylinositol

21 es Ca(2+) and activates protein kinase C and ERK, suggesting the involvement of a G protein-coupled r

22 afenib rapidly leads to RAF dimerization and ERK activation in HCCs, which contributes to treatment e

23 itors blocks growth, basal dimerization, and ERK activation in these cells.

24 The transactivation of RAF dimers and ERK signaling promotes HCC cell survival, prevents apopt

25 taarr is dispensable for V2R endocytosis and ERK activation and therefore provide novel insights into

26 2R mutant exhibits efficient endocytosis and ERK activation upon agonist stimulation.

27 translational implications as both EpCAM and ERK are currently being targeted in human clinical trial

28 ble-negative feedback loop between EpCAM and ERK that contributes to the regulation of EMT.

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

30 nal through PTH1R to induce calcium flux and ERK phosphorylation but not cyclic AMP production or CRE

31 iated phosphorylation of GluN2A, GluN2B, and ERK.

32 ting LMP1-induced noncanonical NF-kappaB and ERK activation.

33 in striatopallidal neurons enhances LID and ERK phosphorylation.

34 Similar effects were elicited by MEK and ERK inhibitors but not AKT or Rac inhibitors.

35 loop that encompasses RAS and RAF, MEK, and ERK that inhibits SOS via phosphorylation.

36 of the Akt/mammalian target of rapamycin and ERK signaling pathways in multiple cellular contexts, in

37 tion and the TGF-beta-induced AKT, SMAD- and ERK-dependent phosphorylations, and conversely, down-reg

38 and cell migration through decreased SRC and ERK activation.

39 nges and activated focal adhesion kinase and ERKs 1/2, and decreased Src kinases and aquaporins 3 and

40 We found that LF-W271A blocked ERK phosphorylation and growth in a melanoma cell line,

41 anges, we found that Hsp90 inhibition blocks ERK MAPK activation in the periaqueductal gray and cauda

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

43 e ESCs grown in 2i but abrogated in serum by ERK-dependent phosphorylation.

44 on, and inhibit apoptosis, thereby bypassing ERK.

45 last phenotype to TGFbeta1-stimulated CD44V6/ERK/EGR1 signaling.

46 Additionally, combined ERK and p65 NFkappaB inhibitors reduced p27 expression a

47 ndocytosis of EGF receptors with concomitant ERK attenuation, which stabilizes BIM.

48 ition (AMPARs) and subsequent consolidation (ERK) of learned associations.

49 EVI1 silencing had no effect on constitutive ERK activity in HER2(+) breast carcinoma cells.

50 gene-specific roles for DUSP5 in controlling ERK signaling and cell fate.

51 doxically increases and prolongs cytoplasmic ERK activity.

52 carvedilol-mediated beta-arrestin-dependent ERK activation is significantly reduced in PI3KgammaKO M

53 restin scaffolds and activates MEK-dependent ERK.

54 TCF Elk-1 mutants showed that TCF-dependent ERK-induced histone modifications required Elk-1 to be p

55 led to rapid and sustained TGFBR1-dependent ERK phosphorylation in benign pancreatic duct cells.

56 nisms for maintaining RAS activation despite ERK-dependent feedback.

57 ads to enhanced activation of its downstream ERK cascade without EGF stimulation.

58 nduce chemokines and to stimulate downstream ERK signaling in monocytes.

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

60 Conversely, enhanced ERK activity via Nf1 gene deletion extends the response

61 c kinases FLT3 and JAK2, leading to enhanced ERK and STAT3 signaling.

62 Forced activation of an FGF-ERK-ETV axis that is crucial to BG induction specificall

63 ed discrepancies relating to the role of FGF/ERK signalling in PrE versus EPI specification between m

64 Although FRS adapters are dispensable for ERK-1/2 activation, they are required for AKT activation

65 Our data further show a critical role for ERK in maintaining the excitability and plasticity of D2

66 Two auxiliary negative feedback loops, from ERK to MEK and RAF, placed downstream of the positive fe

67 Upstream from ERK, we show that PTP4A1 directly interacts with SRC and

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

69 We found that heightened ERK signaling activity in aRG is tightly linked to the t

70 d increased phosphorylation of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells across two in vi

71 se improved sensors, we succeeded in imaging ERK and PKA activation in single dendritic spines during

72 R-MSNs.SIGNIFICANCE STATEMENT Alterations in ERK/MAPK activity are associated with drug abuse, as wel

73 ion of integrin attachments, and resulted in ERK-mediated attenuation of chemokine signaling.

74 specificity phosphatases (DUSPs) inactivate ERK 1/2 through dephosphorylation and can thus inhibit i

75 lved multiple signaling molecules, including ERK, Akt, and Janus kinases (Jaks), especially those tha

76 PKD-associated signaling pathways, including ERK, mTOR, and Akt signaling, via PTPN13-mediated phosph

77 -type CRAF is enhanced, leading to increased ERK signalling.

78 depleted cells was associated with increased ERK mediated cPLA2(S505) phosphorylation.

79 ity in females, but not males, by increasing ERK signaling and pyramidal neuron excitability.

80 t, DUSP5 deletion causes BRAF(V600E)-induced ERK hyperactivation and cellular senescence.

81 fied critical molecular mechanisms involving ERK-mediated ERG activation that could be exploited for

82 ngs indicate that Thr(264) in TRPV3 is a key ERK phosphorylation site mediating EGFR-induced sensitiz

83 tion of the mitogen-activated protein kinase ERK in a positive feedback loop.

84 reated with a direct inhibitor of the kinase ERK, either alone or in combination with other ERK signa

85 that extracellular signal-regulated kinase (ERK 1/2) activation (i.e. phosphorylation) links tumor n

86 PK or extracellular signal-regulated kinase (ERK) 1/2 MAPK (upstream activators of MSK1) reduced MOR

87 icits extracellular signal-regulated kinase (ERK) activation and dendritic spine formation through Ra

88 le in extracellular signal-regulated kinase (ERK) activation following G-protein coupled receptor (GP

89 es of extracellular signal-regulated kinase (ERK) activation, an early and a late phase.

90 f MEK/extracellular signal-regulated kinase (ERK) activity is a key feature in cancer, high-magnitude

91 Extracellular signal-regulated kinase (ERK) and protein kinase A (PKA) play important roles in

92 tated extracellular signal-regulated kinase (ERK) antigen, the action of antigen-specific cytotoxic T

93 of an extracellular signal-regulated kinase (ERK) cascade.

94 f the extracellular signal-regulated kinase (ERK) cascade.

95 l and extracellular signal regulated kinase (ERK) in the cytosol and nucleus.

96 nd an extracellular signal-regulated kinase (ERK) inhibitor.

97 that extracellular signal-regulated kinase (ERK) inhibitors are likely to provide benefit, albeit wi

98 e Ras/extracellular signal-regulated kinase (ERK) protein signaling cascade within the brain is cruci

99 lated extracellular signal-regulated kinase (ERK) signaling drives cancer growth.

100 F/MEK/extracellular signal-regulated kinase (ERK) signaling pathway.

101 (FGF)-extracellular signal-regulated kinase (ERK) signalling is involved in segregation of the EPI an

102 R for extracellular signal-regulated kinase (ERK) to allow easy implementation in vivo.

103 JNK), extracellular signal-regulated kinase (ERK), and Akt (occurring within 15 min).

104 c and extracellular signal-regulated kinase (ERK).

105 on of extracellular signal-regulated kinase (ERK).

106 ) and extracellular signal-regulated kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated pro

107 ulate extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase and protein kinase

108 1 or extracellular signal-regulated kinases (ERK) 1/2 or by pertussis toxin.

109 and extracellular signal-regulated kinases (ERK).

110 inase) after DOX treatment reversed the late ERK activation.

111 -1 (SHP-1) and limits the activation of MAPK ERK and p38 that are required for assembly of the NADPH

112 MEK (mitogen-activated protein kinase (MAPK)/ERK kinase) after DOX treatment reversed the late ERK ac

113 chanistically, PRDM15 modulates WNT and MAPK-ERK signaling by directly promoting the expression of Rs

114 ption of upstream regulators of WNT and MAPK-ERK signaling to safeguard naive pluripotency.

115 twork acting downstream of LIF, WNT and MAPK-ERK to stabilize mouse embryonic stem cells (ESCs) in th

116 f the receptor and generates additional MAPK/ERK signalling, protecting cancer cells against anti-IGF

117 agamma-metalloproteinase/EGFR-dependent MAPK/ERK signaling cascades.

118 /extracellular signal-regulated kinase (MAPK/ERK) and noncanonical NF-kappaB activation were observed

119 Sustained activation of MAPK/ERK in adult SCs is therefore deleterious to successful

120 ental because acute strong induction of MAPK/ERK in adulthood induces demyelination.

121 nction MEK1DD allele produces sustained MAPK/ERK activation in adult SCs, and we determined the impac

122 this association lasts longer, sustains MAPK/ERK signalling and mitigates p53 activation.

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

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

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

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

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

128 bstrate of MEK, a central kinase in the MAPK/ERK signaling pathway.

129 Loss of intracellular D2LR-mediated ERK activation decreased neuronal activity and dendritic

130 re those complexes trigger Galphai3-mediated ERK signaling.

131 olic pathways via mitochondrial ROS mediated ERK activation.

132 ion and via reactive oxygen species mediated ERK-1/2 phosphorylation.

133 TCR-mediated ERK phosphorylation is significantly reduced in the abse

134 loss of DUSP5 exacerbated TNFalpha-mediated ERK 1/2 signaling in 3T3-L1 adipocytes and in adipose ti

135 y the regulatory effects of BCL6 on both MEK-ERK (mitogen-activated protein/extracellular signal-regu

136 Targeted therapies specific to the BRAF-MEK-ERK signaling pathway have shown great promise in the tr

137 n synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade.

138 es endocytosis, the kinase activities of MEK-ERK and CK2, and the presence of KSR1.

139 oned media did not alter CM spreading or MEK-ERK activation.

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

141 By aberrantly activating the RAF-MEK-ERK signaling pathway, BRAF-V600E shapes key biologic fe

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

143 Western blot analysis to be mediated via MEK-ERK signaling.

144 in concert with mortalin, which affects MEK/ERK activity in tumor cells.

145 ng RNAs targeting BDNF or TrkB mRNA, and MEK/ERK (U0126) or PI3 kinase/Akt (PI828) inhibitors.

146 a partial divergence between TGFbeta and MEK/ERK in early carcinogenesis.

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

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

149 ptor activation, new BDNF synthesis, and MEK/ERK signaling (the Q pathway).

150 toma cells, inhibition of JAK2/STAT3 and MEK/ERK/1/2 by ruxolitinib and trametinib potentiated tumor

151 a key feature in cancer, high-magnitude MEK/ERK activity can paradoxically induce growth inhibition.

152 itional mechanisms may exist to modulate MEK/ERK activity in favor of tumor cell proliferation.

153 KRAS and BRAF tumor cells by modulating MEK/ERK activity.

154 ase in the [Ca(2+)]c to trigger the PYK2/MEK/ERK signalling pathway as a positive feedback mechanism

155 of cross-activation between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a RasPIK3IP1PI3K sign

156 ty of EGFRvIII and activates the RAS/RAF/MEK/ERK and STAT3 pathways.

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

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

159 t as downstream effectors of the Ras/Raf/MEK/ERK signaling pathway.

160 used multi-kinase inhibitors of RAS/RAF/MEK/ERK signaling, including regorafenib and sorafenib.

161 , which we use to tune the levels of Raf/MEK/ERK signaling.

162 enic Ras-driven proliferation: MAPK (Raf/MEK/ERK) and PI3Kalpha/Akt/mTOR.

163 rotein expression can be upregulated via MEK/ERK signaling and after sciatic nerve crush and Neto2(-/

164 itiating downstream cascades, including MEK1/ERK activation and paxillin phosphorylation on S126, whi

165 Surprisingly, EpCAM appears to modulate ERK activity.

166 own complex cross-talk between the NFkappaB, ERK, and AKT pathways and multiple feedback loops.

167 established that inhibition of p38, but not ERK or JNK, rescue T cells from undergoing peripheral de

168 and activation of cytosolic PKC and nuclear ERK, which derive from endosomal CLR.

169 This is associated with accumulation of ERK-activated amoeboid microglia in mice, and is also ob

170 multaneously enhanced the late activation of ERK and blocked the increase in basal excitability.

171 e report DOX-mediated biphasic activation of ERK and the reversal of the associated changes in neuron

172 In MEFs, activation of ERK by TPA stimulation induced a common pattern of H3K9a

173 ncrease apoptosis and decrease activation of ERK in this subgroup.

174 naling molecules revealed that activation of ERK, p38, and CREB is indispensable for the induction of

175 TRAMP C2 cells and attenuated activation of ERK/MAPK and the master transcription factor NF-kappaB i

176 Analysis of ERK activity over time in the vulval precursor cells, a

177 teractions of arrestin with receptors and of ERK activation using optical reporters.

178 s quantitative and qualitative assessment of ERK activity by analysis of individual nuclei and faithf

179 cked cocaine SA-induced dephosphorylation of ERK, GluN2A, and GluN2B-containing receptors.

180 enitor cells, or pharmacologic disruption of ERK signaling, or inhibition of adult neurogenesis, each

181 in human fibroblasts through enhancement of ERK activity, which stimulates SMAD3 expression and nucl

182 hypertrophy by inhibiting the expression of ERK pathway.

183 nergistic step in sustaining the function of ERK, a nodal enzyme in multiple cellular processes.

184 , genetic evidence defining the functions of ERK/MAPK signaling in striatum-related neurophysiology a

185 Our results demonstrate the importance of ERK/MAPK signaling in governing the motor functions of t

186 Furthermore, inhibition of ERK 1/2 and c-Jun N terminal kinase (JNK) signaling atte

187 This differed for inhibitors of ERK signaling, suggesting that sequential monotherapy is

188 o presented higher phosphorylation levels of ERK-1/2 and p65/RelA (NF-kappaB) and inducible NO syntha

189 In contrast, loss of ERK/MAPK signaling in D2R-MSNs (indirect pathway) result

190 , basement membrane proteins, and members of ERK, FGF and PDGF signaling pathways, which play key rol

191 UVECs associated with the phosphorylation of ERK and AKT/eNOS, and promoted microvessel sprouting fro

192 covered that WA increased phosphorylation of ERK and p38 in HCC.

193 note, FTY720 retained the phosphorylation of ERK, together with a decreased expression of cleaved cas

194 iven cancers associated with reactivation of ERK signaling in response to targeted inhibition.

195 Here, we identified reactivation of ERK signaling within hours following treatment of FLT3/I

196 expected role for EpCAM in the regulation of ERK and define a novel double-negative feedback loop bet

197 lore its possible mechanism on regulation of ERK pathway.

198 s caused, at least in part, by the relief of ERK-mediated RAF inhibition.

199 chanisms may be correlated to restoration of ERK and AKT signaling pathways.

200 Further analyses revealed a key role of ERK leading to increased phosphorylation of p90-ribosoma

201 t delineated the cell-type-specific roles of ERK/MAPK signaling due to the reliance on globally admin

202 residue of the pT-X-pY consensus sequence of ERK and p38 into Dhb and followed the impact of dehydrat

203 it described here will facilitate studies of ERK signaling in other C. elegans contexts, and the desi

204 At the cellular level, an upregulation of ERK signaling during early phases of postnatal developme

205 hese results suggest that Rap1 activation of ERKs requires PKA phosphorylation and KSR binding.

206 IL-8 knockdown or ERK inhibition, on the other hand, abolished FOXA1 loss-

207 n CD8 single-positive thymocyte selection or ERK signaling.

208 K, either alone or in combination with other ERK signaling inhibitors.

209 Combined CagA, p-SHP-2, and p-ERK expression showed an increased positive predictive v

210 gA was closely associated with p-SHP-2 and p-ERK expression.

211 n between expression of CagA, p-SHP-2, and p-ERK in malignant B cells and tumor response to HPE was e

212 ulted in increased levels of p-Akt but not p-ERK.

213 We also examined angiogenesis (VEGFR2, p-ERK, p-PLCr1/2), hedgehog (Gli1, Ptch1, SMO), and mTOR (

214 , a marker of recycling endosomes, whereas p-ERK associates predominantly with a distinct KSR1-positi

215 udy, we showed a direct interactions of p38, ERK or IkappaBalpha with MKP-1, and demonstrated that MK

216 y, inhibition of the phosphorylation of p38, ERK or p65 decreased J82-induced MDSC trafficking and CX

217 UTP increased the phosphorylation of p38, ERK, CREB, and Ser-727 of STAT3 and induced nuclear tran

218 rylation was observed in MAPK pathways (p38, ERK, JNK) and the NF-kappaB pathway (IKKalpha/beta, NF-k

219 Multiple signaling pathways such as p38MAPK, ERK, and Wnt were found to be involved in the mechanotra

220 ly target tumors and prevent the paradoxical ERK activation could increase the feasibility of dual RA

221 It is unknown whether "paradoxical" ERK activation occurs after sorafenib therapy in HCC, an

222 nce on globally administered pharmacological ERK/MAPK inhibitors and the use of genetic models that o

223 n benign tissues of IGF2 levels with phospho-ERK and phospho-AKT levels.

224 , in particular the levels of phosphorylated ERK, and slows the growth in soft agar of HCT116 cells.

225 as Src (non-receptor tyrosine kinase), PI3K, ERK, or MAPK pathways.

226 aminobutyric acid signaling but not by a Ras-ERK blockade.

227 Targeting mevalonate activity attenuated RAS-ERK-dependent BTIC growth and self-renewal.

228 epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has identified dynamic features not evide

229 ents can be attenuated by inhibiting the Ras-ERK cascade in the adult.

230 reatment at the developmental stage with Ras-ERK inhibitors.

231 12 negative regulators of Wnt, BMP, and Ras/ERK signaling (10.9-fold enrichment, P = 2.4 x 10(-11)).

232 ating protein (RasGAP), which attenuates Ras/ERK signaling by converting active Ras is bound to guano

233 by preferentially substituting for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signaling.

234 locyte macrophage-CSF due to hyperactive RAS/ERK signaling.

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

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

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

238 s an important mechanism for fine-tuning Ras/ERK signaling as well as learning and memory in mice.

239 AKs phosphorylate CRAF and MEK to reactivate ERK.

240 hisin, the protein encoded by RS1, regulates ERK signaling and apoptosis in retinal cells.

241 ote differentiation by negatively regulating ERK MAPK and positively regulating AP1 transcription fac

242 of individual nuclei and faithfully reports ERK activity during development and neural function in d

243 confirm that this network of genes requires ERK, ERG and p300 activity.

244 Estrogen addition restored ERK phosphorylation in EVI1-silenced cells, suggesting t

245 sHA rapidly activated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in

246 The sHA/TSG-6 effect is mediated by RhoA, ERK, and PI3K/Akt signaling.

247 oiled-coil-containing protein kinase (ROCK), ERK, or PI3K.

248 Inhibition of ROCK, ERK, or PI3K/Akt blocked sHA/TSG-6-mediated AHR.

249 al-targeted GCN5L1 blunts mitochondrial ROS, ERK activation and increases FoxO1, gluconeogenic enzyme

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

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

252 The RTK/ERK signaling pathway has been implicated in prostate ca

253 ed proliferation and suppression of AKT, S6, ERK, and STAT3 activation.

254 This sensor, "ERK-nKTR," allows quantitative and qualitative assessmen

255 receptor signaling is also upregulated since ERK activation is elevated and sensitive to the inverse

256 mma resulted in rescue of insulin-stimulated ERK activation.

257 However, prior investigations into striatal ERK/MAPK functions have yielded conflicting results.

258 EGFR and RAF dimers can effectively suppress ERK-driven growth of resistant colorectal cancer.

259 splicing and found that CD44V6 then sustains ERK signaling, which is important for AP-1 activity in l

260 ne via the BCR leading to activation of SYK, ERK, and AKT and the other through MYD88 leading to acti

261 of the positive feedback, shape the temporal ERK activity profile but are dispensable for oscillation

262 The ERK/MAPK intracellular signaling pathway is hypothesized

263 ions in BRAF, NRAS and NF1 that activate the ERK cascade, account for over 80% of metastatic melanoma

264 -mediated attenuation of DUSP4 activated the ERK and p38 MAPK pathways, increased stem-like propertie

265 so impaired the PI3K/Akt while enhancing the ERK/p38MAPK/JNK pathways in LMCs.

266 y in an ALK-5-dependent manner involving the ERK/MAPK pathway.

267 hatase (MKP) DUSP2, a known regulator of the ERK and p38 MAPKs, is unique amongst the MKP family in b

268 Here, we evaluate the combination of the ERK inhibitor SCH772984 and the biguanide phenformin.

269 testing and led to the identification of the ERK inhibitor SCH772984 as a potential therapeutic agent

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

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

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

273 Inhibition of the ERK signaling pathway in serum ESCs results in the appea

274 s underscore the potential importance of the ERK/MAPK pathway in human movement disorders.

275 anscription factor activity, focusing on the ERK-regulated ternary complex factor family of SRF partn

276 r oncogenic dependency from the BCL-2 to the ERK signaling pathway.

277 ting glycolysis in endothelial cells via the ERK/Akt/HIF-1alpha pathway, thereby suggesting new thera

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

279 All this ERK signaling develops at the plasma membrane.

280 mily small GTPases, which ultimately lead to ERK, JNK, and p38 phosphorylation.

281 actor in IL-5-induced HSP70-1 in response to ERK and AKT signaling pathway.

282 vity through a cascade that was sensitive to ERK inhibitors and pertussis toxin.

283 gs B-Raf to Rap1, allowing Rap1 to couple to ERKs through B-Raf binding to Rap1 independently of its

284 However, cAMP-dependent Ras signaling to ERKs is transient and rapidly terminated by PKA phosphor

285 and Rap1 are required for cAMP signaling to ERKs.

286 etic models that only partially reduce total ERK/MAPK activity.

287 hannel Piezo1 and involves calcium-triggered ERK signalling.

288 Inhibiting BDNF's receptor, TrkB, ERK/MAP kinase activation, or NMDA receptors blocks this

289 nd sexual behavior on neural activity, using ERK phosphorylation (pERK).

290 We demonstrate that BRAF(V600E)/ERK play a critical role in binding, phosphorylating and

291 e elucidate a novel link between BRAF(V600E)/ERK signaling and Abl kinases.

292 Furthermore, VEGF/ERK signaling induces phosphorylation and activation of

293 up-regulation was initiated through EGR1 via ERK-regulated transcriptional activation.

294 iptional induction of glycolytic enzymes via ERK- and Akt-dependent translational activation of HIF-1

295 he key role of a novel crosstalk between WA, ERK/RSK, ELK1, and DR5 in HCC inhibition.

296 phocytes across both types of MVECs, whereas ERK was additionally required for TEM across dermal MVEC

297 Here, we report a mechanism whereby ERK-mediated phosphorylation of ERG at one serine residu

298 identified a positive-feedback loop in which ERK/EGR1 signaling promotes CD44V6 splicing and found th

299 Here, we generated mouse models in which ERK/MAPK signaling was completely abolished in each of t

300 AF kinase, reprograms DUSP5 into a cell-wide ERK inhibitor that facilitates cell proliferation and tr