ライフサイエンスコーパス: ERK1

1 ERK1/2 activation in human taste bud cells regulates fat

2 ERK1/2 acts on connective tissue growth factor (CTGF/CCN

3 ERK1/2 cascade was activated by Ca(2+) signaling via ope

4 ERK1/2-MAPK activation in oligodendrocytes and Schwann c

5 Extracellular signal-regulated kinase 1 (ERK1), a member of the extensively studied mitogen-activ

6 inase extracellular-signal related kinase 1 (ERK1).

7 These results suggest that: (1) ERK1/2 are critical for slow-twitch fiber growth; (2) a

8 d extracellular signal-regulated kinase 1/2 (ERK1/2) activation in macrophages; however, these events

9 extracellular signal-regulated kinases 1/2 (ERK1/2) and AKT, as well as down-regulation of octamer-b

10 f extracellular signal-regulated kinase 1/2 (ERK1/2) is increased in the retinal pigment epithelium (

11 d extracellular signal-regulated kinase 1/2 (ERK1/2) pathways.

12 e extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway using both pharmacological inh

13 f extracellular signal-regulated kinase 1/2 (ERK1/2) was G protein-, but not beta-arrestin-, dependen

14 f extracellular signal-regulated kinase 1/2 (ERK1/2), the upstream kinase-regulating Mnk1/2, also sen

15 d extracellular signal-regulated kinase 1/2 (ERK1/2), which phosphorylate and stabilize p53.

16 y extracellular signal-regulated kinase 1/2 (ERK1/2)-regulated phosphorylation of the signal transduc

17 f extracellular-signal regulated kinase 1/2 (ERK1/2).

18 lar signal regulated protein kinase 1 and 2 (ERK1/2) activation.

19 lar signal-regulated protein kinase 1 and 2 (ERK1/2) activity.

20 racellular signal-regulated kinases 1 and 2 (ERK1/2) in preexisting OLs of adult mice is sufficient t

21 acellular regulated protein kinases 1 and 2 (ERK1/2) increased significantly post exposure.

22 racellular signal-regulated kinases 1 and 2 (ERK1/2) or p38 in response to cellular stress and extrac

23 racellular signal-regulated kinases 1 and 2 (ERK1/2) were activated and MLK3 exhibited reduced electr

24 racellular signal regulated kinases 1 and 2 (ERK1/2).

25 ar signal-regulated protein kinases 1 and 2 (ERK1/2).

26 Phosphate induction of MEK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is r

27 duced via CD36 the phosphorylation of MEK1/2-ERK1/2-ETS-like transcription factor-1 cascade, which re

28 ity (PAM), is controlled by c-Src and MEK1/2-ERK1/2.

29 inase/extracellular regulated kinase (MEK1/2/ERK1/2) cascade is involved in the replication of severa

30 with U0126, a specific inhibitor for MEK1/2/ERK1/2, whereas MEK2 did not affect CSFV replication aft

31 c reduction of Adcy1 normalizes the aberrant ERK1/2- and PI3K-mediated signalling, attenuates excessi

32 the elevated Adcy1 translation and abnormal ERK1/2 signalling and behavioural symptoms in FXS.

33 -binding protein and p300 both can acetylate ERK1/2.

34 Acetylated ERK1 exhibits reduced enzymatic activity toward the tran

35 Activated ERK1/2 induces cFos phosphorylation, stimulating the tra

36 atalytic activity and stability of activated ERK1.

37 l growth factor (EGF) stimulation, activated ERK1/2 is recruited to immediate early genes and phospho

38 Prolonged H2O2 treatment activated ERK1/2 and promoted invasion of colon cancer cells, whic

39 Active ERK1 phosphorylated kinase dead FLAG-MLK3 in vitro, wher

40 translocation of ERK1/2, and arrests active ERK1/2 in the cytoplasm.

41 An increase in active ERK1/2 was also detected, consistent with DM leading to

42 that acetylation status of Lys-72 may affect ERK1 ATP binding.

43 yntomodulin-mediated cAMP formation and also ERK1/2 phosphorylation.

44 -10 induction in B cells was regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism,

45 We report that DUSP5, an ERK1/2 phosphatase, was induced in epididymal white adip

46 sults suggest oxidative stress stimulates an ERK1/2-dependent phosphorylation of MLK3 on Ser(705) and

47 Paradoxically, this sustained MEK1/2 and ERK1/2 activation was dependent on the active EGFR kinas

48 inhibit LPS-induced activation of JNK1/2 and ERK1/2 and remarkably disrupted the TLR4 dimerization in

49 revealed that EGF-activated EGFR, MEK1/2 and ERK1/2 co-localize on endosomes.

50 in melanoma cells, thus reducing MEK1/2 and ERK1/2 signaling, inhibiting melanoma cell growth and in

51 ation of the ETS upstream kinases MEK1/2 and ERK1/2, resulting in enhanced ETS factor activity and th

52 sible for continuous signaling to MEK1/2 and ERK1/2.

53 growth factor receptor (FGFR) activation and ERK1/2 phosphorylation, both at baseline and following F

54 vival was a consequence of disrupted AKT and ERK1/2 (MAPK3/1) signaling, as evidenced by reduced phos

55 and FAK expression, activating PI3K/AKT and ERK1/2 FAK-downstream pathways in MCL.

56 s an essential upstream activator of Akt and ERK1/2 in glutamate-treated SCs.

57 5-1.0 microM NMDA robustly activated Akt and ERK1/2.

58 K inhibition blocks downstream PI3K/AKT- and ERK1/2-mediated phosphorylation.

59 tion of cyclin-dependent kinase 5 (Cdk5) and ERK1/2.

60 es HDAC6 activity, we propose that HDAC6 and ERK1 may form a positive feed-forward loop, which might

61 JNKs and ERK1/2 also phosphorylated p21 at S130 and T57, which mi

62 e kinase kinase that then activates MKK7 and ERK1/2 MAP kinases.

63 t of cocaine seeking and enhanced mTORC1 and ERK1/2 activity.

64 seeking, which may be mediated by mTORC1 and ERK1/2 signaling.

65 lso modulated the phosphorylation of p38 and ERK1/2 MAPKs in BV2 cells, which was required for NO pro

66 ling cascades (STAT1, STAT3, STAT5, p38, and ERK1/2), redirection of macrophage activation toward a p

67 Inhibition of p38alpha and ERK1/2 or p53 mutations could abolish the inhibitory eff

68 igration by a pathway that required PI3K and ERK1/2.

69 two donors to simultaneously measure PKA and ERK1&2 kinase activities in the same cellular localizati

70 The simultaneous recording of PKA and ERK1&2 kinase activities reveals concomitant EGF-mediate

71 58), which promotes MLK3-dependent B-Raf and ERK1/2 activation; this positive feedback loop enhances

72 nvironment of neuroblastoma and to STAT3 and ERK1/2 as mediators of their activity.

73 al pathways mediated by AKT, S6K, STAT3, and ERK1/2 activation.

74 phospho-c-Jun, and Etv5/ERM in wild type and ERK1/2 deficient lenses supports their roles as nuclear

75 ed T-X-Y motif in conventional MAPKs such as ERK1/2.

76 We argue that BDNF-ERK1/2 in the mOFC is a key regulator of "online" goal-d

77 MEK1/2 inhibitor trametinib rapidly blocked ERK1/2 phosphorylation, decreased cytosolic and nuclear

78 Here, we report that both ERK1 and -2 are acetylated and that HDAC6 promotes ERK1

79 Briefly, we found that both ERK1 and -2 physically interact with HDAC6.

80 suggests a mechanism of mTORC1 activation by ERK1/2 in an Akt-independent manner in oligodendrocytes.

81 asmin generation, but instead is mediated by ERK1/2-regulated STAT3 phosphorylation, astrocytic throm

82 by NPM genetic knockout or knockdown caused ERK1/2 (extracellular signal-regulated protein kinases 1

83 betaRI co-localization and subsequent CD44V6/ERK1/EGR1 signaling.

84 CLL cells show low IgG levels, constitutive ERK1/2 activation, and fail to either release intracellu

85 that RvD2 enhanced phosphorylation of CREB, ERK1/2, and STAT3 in WT but not DRV2-KO macrophages.

86 the kinase domain of DAPk1 to form Bik-DAPk1-ERK1/2-Bak complex.

87 of HDAC6, suggesting that HDAC6 deacetylates ERK1/2.

88 , and CD56(lo)CD16(+) NK cells and decreased ERK1/2, MAPK-activated protein kinase 2, and STAT1 phosp

89 d FLAG-MLK3-S705A-S758A expression decreased ERK1/2 activation in H2O2-treated cells.

90 erestingly, compounds 7d and 8d demonstrated ERK1/2 phosphorylation mediated via beta-arrestin unlike

91 ion of PiT1 or PiT2 blunted the Pi-dependent ERK1/2-mediated phosphorylation and subsequent gene up-r

92 esults suggest that Gbetagamma/PKC-dependent ERK1/2 activation and heterologous desensitization of ch

93 lug attenuated Kras-induced ADM development, ERK1/2 phosphorylation and proliferation.

94 llular lumican is associated with diminished ERK1/2 phosphorylation and increased p38 phosphorylation

95 Integrator depletion diminishes ERK1/2 transcriptional responsiveness and cellular growt

96 minin receptor (LR/37/67 kDa) and downstream ERK1/2, PI3K/AKT and FAK signalling pathways.

97 from tdTomato-C5aR2 mice blocked C5a-driven ERK1/2 phosphorylation, demonstrating functionality of C

98 amycin-insensitive (phosphorylation of eEF2, ERK1/2 and UBF; gene expression of the myostatin target

99 ncreased soft agar colony size, and elevated ERK1/2 phosphorylation were observed.

100 d, which was restored to normal by elevating ERK1/2 activity in these mice.

101 ork analysis identified MAPK3, which encodes ERK1 MAP kinase, as the most topologically important hub

102 Endogenous ERK1/2 acetylation levels increased upon treatment with

103 , endogenous MLK3 associated with endogenous ERK1/2 and B-Raf.

104 udied are the fibroblast growth factor (FGF)-ERK1/2 pathway, PI3K-AKT, the leukemia inhibitory factor

105 Specific inhibitors for ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP

106 ion females show elevated protein levels for ERK1 as well as the related kinase ERK2 over what would

107 how increased activation in the striatum for ERK1, both at baseline and in response to sucrose, a sig

108 ve been confirmed (T198, T207, and Y210 from ERK1) by high-throughput mass spectrometry.

109 Furthermore, ERK1/2, p38 and JNK MAPKs, but not PI3K, were individual

110 In the CP/CPPS group, ERK1/2 phosphorylation levels were increased in the amyg

111 protein synthesis levels, thus highlighting ERK1/2 as a potential therapeutic target for the treatme

112 activating RAS mutations and hyperactivated ERK1/2 signaling observed in many human tumors and the l

113 This increase in ERK1 phosphorylation is coupled with a decrease in the a

114 egulation of these molecules was observed in ERK1/2 knock-out mice.

115 predicts the existence of VEGF threshold in ERK1/2 activation that can be continuously tuned by cell

116 ulation of HER2 signaling cascade, including ERK1/2, FAK, AKT and PAK1 as well as regulation of the g

117 tes a number of signaling pathways including ERK1/2.

118 igodendrocyte/myelin compartment to increase ERK1/2 activation, which ultimately targets Myrf, as wel

119 he proposed GPR30 agonist G-1 also increased ERK1/2 activity, but this increase was only observed at

120 nced mGluR5 endocytosis as well as increased ERK1/2, AKT, and Ca(2+) signaling in primary cortical ne

121 other and her offspring, including increased ERK1/2, MAPK-activated protein kinase 2, rpS6, and CREB

122 how that GPR30 also constitutively increases ERK1/2 activity.

123 ese results, we propose that GPR30 increases ERK1/2 activity via two Gi/o-mediated mechanisms, a PDZ-

124 ails to achieve normal thickness, increasing ERK1/2 activity in oligodendrocytes is of obvious therap

125 in recruitment desensitized U50,488H-induced ERK1/2 response.

126 cific ligation of C5aR2 inhibits C5a-induced ERK1/2 activation, strengthening the view that C5aR2 reg

127 f kinases are required for phosphate-induced ERK1/2 phosphorylation in cultured hypertrophic chondroc

128 n of C-Raf does not impair phosphate-induced ERK1/2 phosphorylation in vitro, but leads to rickets by

129 AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both hu

130 Inhibiting ERK1/2 conferred protection against mutant LRRK2-induced

131 whereby AGGF1 blocks ER stress by inhibiting ERK1/2 activation and the transcriptional repressor ZEB1

132 mic reticulum stress signaling by inhibiting ERK1/2 activation, which reduces the level of transcript

133 tive oxygen species (ROS) and p38 MAPK, JNK, ERK1/2, and NFkappaB-dependent pathways.

134 ry effect on extracellular regulated kinase (ERK1/2) was blocked by the Src family kinase inhibitor P

135 RAS-MEK-extracellular signal-related kinase (ERK1/2) pathway, are an underlying cause of >70% of huma

136 We show that the MAP kinases ERK1/2 phosphorylate TC21 and R-Ras on this C-terminal s

137 ylation and activation of all 3 MAP kinases (ERK1/2, c-Jun kinase, and p38 MAP kinase).

138 that extracellular signal-regulated kinases (ERK1/2) respond to insulin stimulation and integrate ins

139 the transcription factor ELK1, a well-known ERK1 substrate.

140 ation at serine 260 through the Ras-Raf-MAPK ERK1/2 activation is responsible for resistance to the g

141 ome, metabolome, and activation of p38 MAPK, ERK1/2, Akt, and p70S6K proteins.

142 , no differences in phosphorylated p38 MAPK, ERK1/2, Akt, and p70S6K were observed.

143 ly endosomes are accelerated, mitogenic MAPK-ERK1/2 signals are rapidly terminated, and proliferation

144 se/extracellular signal-related kinase (MAPK/ERK1/2) phosphorylation (pERK) in layers 2-3 and 5-6 of

145 interrogate the complexity in cAMP/PKA-MAPK/ERK1&2 crosstalk by using multi-parameter biosensing exp

146 IQGAP1 binds to the cancer-associated MAPKs ERK1 and ERK2, and that this domain might thus offer a n

147 PHB1 is essential for CRAF-mediated ERK1/2 activation through direct binding to CRAF.

148 erses the transient increase of EGF-mediated ERK1&2 kinase activity while reinforcing PKA activation.

149 from closed to open conformation induced MEK-ERK1/2-dependent Tyr-447 phosphorylation.

150 nt on the coactivation of JAK2/STAT3 and MEK/ERK1/2 in neuroblastoma cells.

151 At the plasma membrane, ERK1/2-mediated phosphorylation and 14-3-3 protein bindi

152 Interestingly, an acetylation-mimicking ERK1 mutant (K72Q) exhibited less phosphorylation than t

153 owever, whether HDAC6 reciprocally modulates ERK1 activity is unknown.

154 e is a primary subcellular target for muscle ERK1/2 function in vivo.

155 ectly into crush-injured rat sciatic nerves, ERK1/2 phosphorylation was observed in myelinated and no

156 ulation of signaling pathways AKT, NFkappaB, ERK1/2 and JAK/STAT.

157 -kappaB, and to a lesser extent p38, but not ERK1/2 activity, blocked TLR2-driven NGF up-regulation a

158 Here, we report that JNKs, but not ERK1/2 or CAK, can be direct CDK4-activating kinases for

159 Notably, ERK1/2 pathway inhibitors are used in cancer therapy, wi

160 We propose that after the activation of ERK1 by MEK1, subsequent slower phosphorylation of the f

161 contrast, females do not show activation of ERK1 in response to sucrose, but notably hemideletion fe

162 depends on the MK2/3-mediated activation of ERK1/2 and PI3K signaling.

163 Activation of ERK1/2 by ceramide, known to increase lysine acetylation

164 f macrophage chemotaxis, while activation of ERK1/2 by EGF alone did not inhibit fMLF-mediated migrat

165 182 reduction led to increased activation of ERK1/2 in basal and challenge models, demonstrating a po

166 Activation of ERK1/2 is experimentally shown to involve sphingosine ki

167 nation, we show that sustained activation of ERK1/2 renders them able to do so.

168 signaling participates in the activation of ERK1/2 signaling in LMNA cardiomyopathy.

169 ression of Sema3c in cNCCs via activation of ERK1/2 signaling.

170 dentified robust and sustained activation of ERK1/2 upon CD82 overexpression that results in enhanced

171 ect on chemoattractant-induced activation of ERK1/2, JNK and PI3K pathways, but only the MEK inhibito

172 Herein we show that activation of ERK1/2, p38 and JNK mitogen activated protein kinases (M

173 hanges were attributable to an activation of ERK1/2-RSK3 signaling, mediated through beta-arrestin, w

174 high efficacy agonist, NECA, in an assay of ERK1/2 phosphorylation assay.

175 sis upon drug withdrawal as a consequence of ERK1/2 hyperactivation.

176 alcium-dependent translocation downstream of ERK1/2.

177 ncogenic Nras, leading to hyperactivation of ERK1/2 signaling.

178 regulator of inflammation, via inhibition of ERK1/2 activation.

179 Inhibition of ERK1/2 impaired NPNT-induced endothelial cell migration,

180 Inhibition of ERK1/2 in Tsc2 (-/-) cells-a model of TS-rescues GSK3bet

181 Inhibition of ERK1/2 phosphorylation or knockdown of ROCK1 expectedly

182 For inhibition of ERK1/2 phosphorylation with a specific inhibitor reduced

183 USP5 functions in the feedback inhibition of ERK1/2 signaling in response to TNFalpha, which resulted

184 Inhibitors of ERK1/2 and JNK kinases abolished and significantly decre

185 t inhibiting MEK1/2, the upstream kinases of ERK1/2 signaling, alters multifactorial components of th

186 Targeted knockdown of ERK1/2 by small interfering RNA or PD0325901 (MEK1/2 inh

187 Similar levels of ERK1/2 activation were induced by all strains carrying a

188 tigen expression, as well as basal levels of ERK1/2 phosphorylation.

189 t both moderate and hyperactivated levels of ERK1/2 when upregulation commenced during developmental

190 horylation sites in the activation T-loop of ERK1 and its closest relative, ERK2, three additional fl

191 The loss of ERK1/2 activity resulted in a significant decrease in th

192 ceptors, the phosphorylation of mediators of ERK1/2 and p38 pathways and STAT3 (S727) were observed.

193 Therefore, therapeutic modulation of ERK1/2 activity in demyelinating disease or peripheral n

194 impedes IQGAP1-dependent phosphorylation of ERK1/2 (pERK1/2).

195 rogen-dependent decreased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex v

196 re related with decreased phosphorylation of ERK1/2 and expression of Rho-associated coiled-coil cont

197 inhibition decreases the phosphorylation of ERK1/2 and inhibitory kappaBalpha (IkappaBalpha), as wel

198 involving activation and phosphorylation of ERK1/2 and JNK1.

199 that displayed increased phosphorylation of ERK1/2 but not AKT.

200 Ras activation and phosphorylation of ERK1/2 downstream of Ras are both greatly increased in N

201 reover, XML inhibited the phosphorylation of ERK1/2, AKT and GSK3beta, subsequently inhibiting protei

202 cultured in vitro and the phosphorylation of ERK1/2, AKT, GSK3beta and protein expression of GATA4 in

203 receptor endocytosis and phosphorylation of ERK1/2, an effect that is dependent upon the interaction

204 -OHE2 stimulated biphasic phosphorylation of ERK1/2, slow p38 and JNK phosphorylation over time, and

205 ctivate calcium-dependent phosphorylation of ERK1/2, thereby activating the cyclin B transcription th

206 5 impaired M3R-stimulated phosphorylation of ERK1/2.

207 Because the T207 and Y210 phosphosites of ERK1 are highly conserved within the eukaryotic protein

208 We thus uncover a role of ERK1 in the regulation of furin activity by supporting a

209 To decipher the role of ERK1/2 in RPE cells, we conditionally disrupted the Erk1

210 We evaluated the role of ERK1/2 on the expression of peroxisome proliferator-acti

211 inhibition of the phosphorylation status of ERK1/2.

212 with activation of p38(MAPK), suppression of ERK1/2, and loss of c-Fos.

213 ction, inhibits the nuclear translocation of ERK1/2, and arrests active ERK1/2 in the cytoplasm.

214 that targeting the nuclear translocation of ERK1/2, in combination with MEK inhibitors can be used f

215 ERK cascade is the nuclear translocation of ERK1/2, which is important mainly for the induction of p

216 we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaff

217 and the current through the CRAC channels on ERK1/2 activation dynamics, highlighting the critical ro

218 nisms, and investigate their consequences on ERK1/2 activation.

219 ibiting eIF4E phosphorylation with Mnk1/2 or ERK1/2 inhibitors.

220 phosphorylation but not cGMP accumulation or ERK1/2 phosphorylation although prior addition of ML290

221 bility to activate calcium signalling and/or ERK1/2 phosphorylation via PAR2.

222 -induced phosphorylation of Akt, p38 MAPK or ERK1/2.

223 tion and survival such as SGK1, PKA, PKC, or ERK1/2.

224 l-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1/2 siRNA knockdown blocked the H2O2-induced shift of

225 eased cGMP accumulation but did not affect p-ERK1/2 and given chronically activated MMP-2 expression

226 ay proteins, including the kinases CK2 and p-ERK1/2 and the signaling scaffold KSR1.

227 subjects, we observed decreased p-AKT and p-ERK1/2 compared to controls, as well as a depleted neura

228 The Western blot data shown for p-ERK1/2 and actin are not from this set, but rather a sim

229 although prior addition of ML290 increased p-ERK1/2 responses to relaxin.

230 ed both cAMP and cGMP accumulation but not p-ERK1/2.

231 or advanced glycation end products (RAGE), p-ERK1/2, nuclear NF-kappaB p65, and proinflammatory cytok

232 of IL-1R-associated kinase 1 (IRAK-1), p38, ERK1/2 MAPKs, and p65 NF-kappaB, suggesting that the R75

233 TLR2 activation increased p38, ERK1/2, and p65 activity and increased p65 translocation

234 mal in the absence of ELK1 binding partners, ERK1/2 and serum-response factor.

235 tion of canonical growth signalling pathways ERK1/2 and AKT.

236 D2/3, phospho-STAT3, P65, FOXO1, and phospho-ERK1/2) of key pathways commonly affected in NSCLC.

237 This was associated with decreased phospho-ERK1/2 immunoreactivity in the hypertrophic chondrocyte

238 to propionate-mediated regulation of phospho-ERK1/2 MAP kinase signaling in FFA2-expressing 293 cells

239 ling had no effect on phospho-AKT or phospho-ERK1/2 levels, indicating that VEGF mediates cell surviv

240 easured by decreased phospho-VEGFR2, phospho-ERK1/2 and phospho-p38-MAPK levels.

241 and its receptors as well as phosphorylated ERK1/2 are observed.

242 CXCR4-mediated expression of phosphorylated ERK1/2 and ultimately reduced cancer cell functions such

243 indicated similar increase of phosphorylated ERK1/2 in all types of liver tumors, but nuclear localiz

244 mGluR5 and receptor-mediated phosphorylated-ERK1/2, Arc/Arg3.1 and c-fos.

245 wed the highest expression of phosphorylated-ERK1/2 and Akt S473 proteins of all four investigated an

246 signal-regulated kinase 1/2 phosphorylation (ERK1/2).

247 the migration-associated proteins: PKCdelta, ERK1/2 and p38 mitogen-activated protein kinase in HEK 2

248 ore, we found that P2Y2R activation promoted ERK1/2 phosphorylation through Src, leading to Fra-1 act

249 nd -2 are acetylated and that HDAC6 promotes ERK1 activity via deacetylation.

250 zation of activated PAR4 is linked to proper ERK1/2 and Akt activation.

251 used to assess the expressions of BDNF, Ras, ERK1/2, and c-fox levels.

252 BSJYD inhibited the expression of BDNF, Ras, ERK1/2, and c-fox mRNA in LVH.

253 t malignancies characterized by elevated RAS-ERK1/2 signaling.

254 P-bound, active K-Ras and hyperactivated Ras-ERK1/ERK2 signaling.

255 es to elicit long-term inhibition of the RAS-ERK1/2 signaling pathway add to the importance of discov

256 ulators of major cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT

257 reased phosphorylation of AKT, EGF receptor, ERK1/2, JNK1/2/3, and c-Jun.

258 Y210, but not T198, in negatively regulating ERK1 catalytic activity.

259 that C6 ceramide increases serum-stimulated ERK1/2 activation in a manner dependent on the ERK1/2 sc

260 , our findings suggest that HDAC6 stimulates ERK1 activity.

261 n calcium release from intracellular stores, ERK1/2 activation, and long term changes in synaptic act

262 As such, ERK1/2 down-regulates mitochondrial function directly by

263 served including activation of pro-surviving ERK1/2 kinase and inhibited expression of pro-apoptotic

264 Considering that ERK1/2 pathway regulates cellular processes by phosphory

265 Then we demonstrate that ERK1/2 activation is mediated by beta-arrestin 1 from re

266 Previously, we found that ERK1, a downstream kinase in the mitogen-activated prote

267 We identify that ERK1/2 MAPK acts downstream of PREX1 and contributes to

268 Along with our previous report that ERK1 promotes HDAC6 activity, we propose that HDAC6 and

269 vity in these mice, strongly suggesting that ERK1/2 are key transducers of FGFR2 signals for myelin g

270 The ERK1/2 MAPK signalling module integrates extracellular c

271 epithelial-to-mesenchymal transition and the ERK1/2 signaling pathway inversely affected by miR-519d

272 Blocking the ERK1/2-dependent upregulation of MCU conferred protectio

273 he NTS-derived peptide (EPE) that blocks the ERK1/2-importin7 interaction, inhibits the nuclear trans

274 h the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1/2 siRNA knockdown blocke

275 Our results identify the ERK1/2 pathway as a direct regulator of the visual cycle

276 nd pharmacological approaches implicated the ERK1/2 pathway as a critical regulator of CCN3-dependent

277 dicated Lys-72 as an acetylation site in the ERK1 N terminus, adjacent to Lys-71, which binds to ATP,

278 ited the TAC-induced HF via inactivating the ERK1/2, AKT/GSK3beta, and GATA4 signaling pathway.

279 Moreover, the ERK1/2 phosphorylation could be rescued by overexpressin

280 CU and MICU1 was caused by activation of the ERK1/2 (MAPK3/1) pathway.

281 actor receptor, leading to activation of the ERK1/2 and STAT3 pathways and up-regulation of the inhib

282 This resulted in an inhibition of the ERK1/2 protein kinase- and NF-kappaB transcription facto

283 ssion of ATP signaling and activation of the ERK1/2 signaling pathway.

284 K1/2 activation in a manner dependent on the ERK1/2 scaffold IQGAP1.

285 g and Col II in NP cell cultures through the ERK1/2/NF-kB signaling pathway.

286 to the regulation of PN-1 expression via the ERK1/2/NF-kB signaling pathway and the role of PN-1 in t

287 s compelling evidence linking FGFR2 with the ERK1/2-MAPK pathway, which converges with the PI3K/Akt/m

288 ohol disrupted lipopolysaccharide (LPS)-TLR4-ERK1/2-cyclin D1 signaling and inhibited upregulation of

289 eins in glutamate-treated SCs in addition to ERK1/2 and Akt, including p70 S6-kinase, glycogen syntha

290 ically evaluate which IQGAP1 domains bind to ERK1/2.

291 both necessary and sufficient for binding to ERK1 and ERK2, as well as to the MAPK kinases MEK1 and M

292 re ineffective in shutting down signaling to ERK1/2.

293 This was rescued by upregulating ERK1/2 activity in these mice, strongly suggesting that

294 c therapeutic interventions targeting VEGFR2-ERK1/2 axis.

295 a(2+) mobilization, as well as signaling via ERK1/2 and the small GTPase Rac1); however, CXCL14 bound

296 hosphorylation and nuclear translocation via ERK1/2 and P38 signaling.

297 found to activate the protein ERK2, whereas ERK1 activation is found in non-KRAS-associated human lu

298 ated kinase dead FLAG-MLK3 in vitro, whereas ERK1 phosphorylation of kinase dead FLAG-MLK3-S705A-S758

299 the activation of FPR2 was accompanied with ERK1/2 phosphorylation, which could be attenuated by FPR

300 cytes in response to TNFalpha, parallel with ERK1/2 dephosphorylation.