ライフサイエンスコーパス: ERK1

1 ERK1/2 expression was reduced in torn (diseased) compare

2 ERK1/2 inhibition did not attenuate IL-1beta-induced CTG

3 ERK1/2 phosphorylate DLC1 on serine S129, which increase

4 ERK1/2 phosphorylation decreased after 6-hour treatments

5 he intestine, inhibition of IR-induced MPK-1/ERK1 activation, and apoptosis in the germline.

6 f extracellular signal-regulated kinase 1/2 (ERK1/2) activation and expression of a RHAMM target gene

7 d extracellular signal-regulated kinase 1/2 (ERK1/2) activity and the AKT signaling pathways required

8 ellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase in T ly

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

10 KD), the extracellular-regulated kinase 1/2 (ERK1/2) pathway, is activated and has been implicated in

11 d extracellular signal-regulated kinase 1/2 (ERK1/2) pathways, but the exact mechanism of action of L

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

13 ellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation occurred more transiently in the

14 , extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation, and real-time receptor internal

15 t extracellular-signal regulated kinase-1/2 (ERK1/2) signaling in human embryonic kidney 293 cells.

16 p38 and extracellular regulated kinases 1/2 (ERK1/2) signaling in neuroblastoma and neural crest-deri

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

18 , extracellular signal-regulated kinase 1/2 (ERK1/2), NF-kappaB, and Nrf2 activation and nuclear tran

19 g extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and Jun amino-terminal kinase (JNK), which

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

21 ar signal-regulated protein kinases 1 and 2 (ERK1/2) and NF-kappaB pathways that eventually led to th

22 tracellular signal-regulated kinase 1 and 2 (ERK1/2) and Src homology phosphatase 2 (SHP2) ensures se

23 extracellular signal-related kinase 1 and 2 (ERK1/2) pathway is a highly conserved signaling cascade

24 tracellular signal-regulated kinase 1 and 2 (ERK1/2), leading to enhanced transcription and up-regula

25 tracellular signal-regulated kinase 1 and 2 (ERK1/2), mitogen-activated protein kinases (MAPK), leadi

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

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

28 ty to induce increased intracellular Ca(2+), ERK1/2 phosphorylation, internalization, and NADPH oxida

29 vely protracted activation of the RAF-MEK1/2-ERK1/2 module, in comparison with RAF1 membrane localiza

30 f phospho-p53, total p53, cleaved caspase 3, ERK1/2 and phospho-AKT in white individuals compared to

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 (V600E)-melanocytes did not further activate ERK1/2 and cell proliferation, but rendered these phenot

35 TBL1XR1 activated ERK1/2-Sox2 signaling and was dependent on signaling via

36 association of RAF1 and that they activated ERK1/2 and ELK1.

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

38 vated anion channel that regulates PI3K-AKT, ERK1/2, mTOR signaling, muscle differentiation, myoblast

39 These findings identify amplified ERK1/2 signaling in KRAS-mutated colorectal cancer cells

40 t in response to SDF1 in ASCs with amplified ERK1/2 activation, growth factor-like immediate early ge

41 An ERK1/2 pathway inhibitor, trametinib, is currently used

42 -10 induction in B cells was regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism,

43 studies showed that V2R regulates YAP by an ERK1/2-dependent mechanism in human ADPKD cystic epithel

44 i resistance and enhances the efficacy of an ERK1/2 inhibitor in a model of acquired BRAFi + MEKi res

45 From this, an ERK1/2-controlled metastatic gene set (EMGS) was defined

46 TAAR1 activation increases Bcl-2 through an ERK1/2-dependent pathway.

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

48 get of rapamycin (TOR), phospholipase A, and ERK1, but does not require the PI3 kinase/Akt/PKB and gu

49 a similar potency to IP(1) accumulation and ERK1/2 phosphorylation, whereas Ca(2+) mobilization was

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

51 tin translocation, G protein activation, and ERK1/2 phosphorylation (pERK) while lacking activity at

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

53 GLPG1690 suppressed AKT and ERK1/2 signaling and profoundly impacted the transcripto

54 essed lower levels of phosphorylated AKT and ERK1/2; exhibited reduced foam cell formation and lipid

55 ment resulted in activation of Lyn, Akt, and ERK1/2, suggesting that GB is able to mitigate the H(2)O

56 rough activation of the protein kinase B and ERK1/2 signaling pathways.

57 Inhibitors of the p38alpha/beta and ERK1/2 MAPK pathways reduced the production of IL-5, IL-

58 Caki-1 cells, V2R agonists reduced cAMP and ERK1/2 activation, while dDAVP treatment had the reverse

59 encing in Caki-1 cells also reduced cAMP and ERK1/2 activation.

60 rate mediated by Pi transport-dependent and ERK1/2-dependent metabolic Pi sensing pathways.

61 via CXCR4, as well as activation of EGFR and ERK1/2.

62 hat results in growth factor elaboration and ERK1/2 cell cycle activation.

63 lved in the WNT, TGF-beta, JNK, HedgeHog and ERK1/2 pathways suggests the regulation of osteogenesis

64 egulation of the JAK1, STAT1, NF-kappaB, and ERK1/2 pathways.

65 mitogen-activated protein kinase kinase, and ERK1/2.

66 High intracellular cAMP levels and ERK1/2 activation were observed in human ccRCC tumors.

67 eam signaling pathways of MEK (p38(MAPK) and ERK1/2(MAPK)) were then examined, and TGF-beta1 and EGF

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

69 and IL-17 production, diminished mTORC1 and ERK1/2 activation, and impaired transcription of a subse

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

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

72 al effects on the phosphorylation of p38 and ERK1/2, with TGF-beta1 upregulating p-p38 but not pERK1/

73 ssed the phosphorylation of JNK1/2, p38, and ERK1/2 in LPS-stimulated RAW264.7 cells.

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

75 revealed an increased activation of p38- and ERK1/2-dependent signaling in EGFRvIII expressing cells,

76 exhibited increased tau phosphorylation and ERK1/2 phosphoactivation.

77 S production, Nox2 expression, p47(phox) and ERK1/2 phosphorylation, cell proliferation and IL-1beta

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

79 ration, calcium flux, cell polarization, and ERK1/2 activation, suggesting that TrkA is an important

80 activation of the MyD88 adaptor protein and ERK1/2 kinases downstream of the IL-33 receptor, IL1RL1.

81 ation sites on beta-arrestin recruitment and ERK1/2 activation.

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

83 ween beta-arrestin-dependent trafficking and ERK1/2 signaling, we investigated three naturally occurr

84 VCP, the levels of Shoc2 ubiquitination and ERK1/2 phosphorylation are imbalanced.

85 ncy and restrains commitment by antagonising ERK1/2 signalling.

86 s were tested in signal transduction assays (ERK1/2 phosphorylation, cAMP inhibition, Ca(2+) mobiliza

87 tained and tested in four functional assays: ERK1/2 phosphorylation, adenylyl cyclase inhibition, cal

88 ARP cleavage in human islets, and attenuated ERK1/2 and JNK1/2 activation in MIN6 cells.

89 Because ERK1/2 plays an important role in regulating thromboxane

90 These findings highlight differences between ERK1/2 signalling pathway activation and expression of T

91 Blockade ERK1/2 activation by PD98059 attenuated these stimulatin

92 ological inhibition of SHP2 activity blocked ERK1/2 and AKT signaling generated from exogenous stimul

93 the abundance of pro-apoptotic BIM and BMF, ERK1/2 pathway inhibition is predominantly cytostatic, r

94 emonstrate that ELK1 is required by the BRAF-ERK1/2 pathway to repress PARK2 expression and promoter

95 gulates MYC levels, which is counteracted by ERK1 activation.

96 ctor stimulation, Exo70 is phosphorylated by ERK1/2, which in turn suppresses its phosphorylation by

97 these data establish the key role played by ERK1/2 signaling in the maintenance of vascular normalcy

98 how that phosphorylation of FHOD proteins by ERK1/2 is a critical switch for nuclear positioning and

99 e with an Lmna mutation and elevated cardiac ERK1/2 activity have altered nuclear positioning.

100 e with LMNA mutation-induced cardiomyopathy, ERK1/2 mediated phosphorylation of FHOD3, an isoform hig

101 eractivation versus inhibition of both CDC42:ERK1/2 and NF-kappaB:AP-1 pro-oncogenic signaling pathwa

102 Thus combining ERK1/2 pathway inhibitors with MCL1 antagonists in melan

103 both function-selective and ATP-competitive ERK1/2 inhibitors are effective at inhibiting PDGF-media

104 leading to decreased beta-arrestin-dependent ERK1/2 activation, faster recycling of receptors to the

105 ecruitment and downstream arrestin-dependent ERK1/2 phosphorylation and internalization.

106 beta-arrestin-dependent ERK1/2 regulation is the subject of important studies be

107 PSMalpha peptides induced an FPR2-dependent ERK1/2 phosphorylation and internalization.

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

109 and subsequent CREB and G-protein-dependent ERK1/2 phosphorylation, in addition to beta-arrestin-2 r

110 lective ligands, and dependent on downstream ERK1/2 phosphorylation.

111 MNA mutations causing cardiomyopathy elevate ERK1/2 activity in the heart, and inhibition of the ERK1

112 s transduced with ARAF-S214P showed elevated ERK1/2 activity, enhanced lymphangiogenic capacity, and

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

114 eptor tyrosine kinases, prominently engaging ERK1/2 but also other pathways.

115 n soft surfaces myosin IIA deletion enhances ERK1/2 activity, while on stiff surfaces it enhances the

116 Mechanistically, FGF4-ERK1/2-RSK signalling inhibits EPHA2 via Ser/Thr phospho

117 HA2 via Ser/Thr phosphorylation, whilst FGF4-ERK1/2 disrupts a core pluripotency transcriptional circ

118 In fibroblasts, ERK1/2 activation negatively regulated nuclear movement

119 In vitro, 44 showed biased agonism for ERK1/2 phosphorylation and, in vivo, it preferentially e

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

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

122 n of MEK, but not p38, confirming a role for ERK1/2 in regulating TPO-mediated increases in TxA(2) sy

123 r kinase 2 (GRK2)-dependent beta(2) AR-G(i) -ERK1/2 cascade.

124 NP/NPR-C is dependent on activation of G(i), ERK1/2, and phosphoinositide 3-kinase gamma/Akt at a mol

125 beta-arrestin recruitment) which identified ERK1/2 phosphorylation-preferring aryloxyethyl derivativ

126 hosphorylation, accompanied by a decrease in ERK1/2 phosphorylation compared with control cells.

127 ation and IFN-beta production but defects in ERK1/2 and STAT3 activation after LPS stimulation.

128 lls promoted GZMB(+) B cell proliferation in ERK1/2-dependent manner, facilitating GZMB(+) B cell exp

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

130 f downstream prosignaling kinases, including ERK1/2 and FAK.

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

132 he noncompetitive inhibition of CCL2-induced ERK1/2 activation, independent of AT1R activity.

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

134 In hPPECs, TM2 inhibited thrombin-induced ERK1/2 phosphorylation and activation of Ras homolog gen

135 4 siRNA knockdown inhibited thrombin-induced ERK1/2 phosphorylation.

136 (ER) stress, but only atorvastatin inhibited ERK1/2(T202/Y204), Akt(Ser473), and mammalian target of

137 r cell proliferation and partially inhibited ERK1/2 phosphorylation in the injured tissue, suggesting

138 s dependent on alpha(2)M*-GRP78 interaction, ERK1/2 and CREB phosphorylation, and unfolded protein re

139 r the precise functions of the ERK isoforms (ERK1 and ERK2) in cancer progression have not been well

140 kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK)-dependent transforming growth factor-beta1

141 orylation of extracellular-regulated kinase (ERK1/2) and thromboxane (TxA(2)) synthesis was dependent

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

143 The MYC stabilizing kinase, ERK1, regulates MYC levels directly and indirectly by in

144 The related human kinases ERK1 and ERK2 also bound to arsenic in vitro, suggesting

145 ntly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected indivi

146 ts increased phosphorylation of MAP kinases (ERK1/2, p38) under hypertonic conditions.

147 the extracellular signal-regulated kinases (ERK1/2) pathway by the shedding of growth factors which

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

149 Instead, it selectively activated MAPK ERK1/2 and JNK.

150 and mitogen-activated protein kinase (MAPK) ERK1/2 activation.

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

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

153 initiates signaling through the RAS-RAF-MAPK/ERK1/2 pathway and receptor endocytosis.

154 stream signaling pathways, specifically MAPK/ERK1/2, endothelial nitric oxide synthase, and mammalian

155 rmeability by potentially involving the MAPK/ERK1/2 signaling.

156 a(2+) mobilization, activation of the MAPKs (ERK1/2 and P38), and production of cytokines (IL-13 and

157 e growth factor-1 receptor (IGF-1R)-mediated ERK1/2 signaling.

158 te similarly impaired phosphorylation of MEK/ERK1/2 and activity-induced transcription of a neuronal

159 cell-derived CCL2 stimulates tumor cell MEK1-ERK1/2-ROCK2-dependent signaling and enhances tumor cell

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

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

162 ion and consequently the signaling molecules ERK1/2 downstream of EGFR thus revealing additive effect

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

164 We demonstrate that ERK2, but not ERK1, phosphorylates the purine synthesis enzyme PFAS (p

165 We hypothesized that ERK2, but not ERK1, promotes the cancer stem cell (CSC) phenotype and

166 y functional screen identified ERK5, but not ERK1/2, as a RAS pathway effector important for DIPG gro

167 , Ezrin-Radixin-Moesin (ERM) and p53 but not ERK1/2, effects recapitulated in Cav-1 silenced (siRNA)

168 the activation of HIF-1alpha, but not Notch, ERK1/2, (PI3K)AKT, and P38 pathways.

169 in backgrounds is unstable in the absence of ERK1/2 and GSK3 inhibition.

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

171 Notably, prominent activation of ERK1/2 and ELK1 by p.Gln72Leu associates with the severe

172 S were required for full-scale activation of ERK1/2 and induction of cell proliferation by BRAF(V600E

173 8) mediates Toll-like receptor activation of ERK1/2 and p38alpha MAP kinases and is critical for regu

174 and for selecting between the activation of ERK1/2 and Src.

175 182 reduction led to increased activation of ERK1/2 in basal and challenge models, demonstrating a po

176 , deactivation of GSK3beta and activation of ERK1/2 in the striatum of ouabain-treated mice.

177 oring factors that promote the activation of ERK1/2 or Src, the kinases that lead to cell growth and

178 nduced hepatic lipogenesis via activation of ERK1/2 signaling pathway.

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

180 I (Ang II) and ROS production; activation of ERK1/2, p53, and gammaH2AX; and losses of capillaries an

181 for transducing the signal for activation of ERK1/2-RSK2 under ER stress.

182 cific changes in c-Fos level and activity of ERK1/2 and GSK3beta kinases in response to a single dose

183 se studies demonstrate that amplification of ERK1/2 signaling in KRAS-mutated colorectal cancer cells

184 Blockade of ERK1/2 reactivation following EGFR TKI treatment by comb

185 Combination of ERK1/2 pathway inhibitors with BCL2/BCL-w/BCL-X(L) inhib

186 quitous expression and multiple functions of ERK1/2, complete inhibition of ERK1/2 using ATP-competit

187 low SS (2 dyn/cm(2)), whereas inhibition of ERK1/2 attenuated peak ICAM-1 at high SS (12 dyn/cm(2)).

188 Furthermore, inhibition of ERK1/2 kinases activates IFN-kappa expression.

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

190 otein kinase B (AKT), but only inhibition of ERK1/2 phosphorylation prevented TAAR1-induced increases

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

192 functions of ERK1/2, complete inhibition of ERK1/2 using ATP-competitive inhibitors may lead to unwa

193 Treatment with pharmacologic inhibitors of ERK1/2 or PKCbeta prevented death due to spontaneous aor

194 and act as function-selective inhibitors of ERK1/2 signaling.

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

196 icted to MEKi to maintain a precise level of ERK1/2 signalling that is optimal for cell proliferation

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

198 eatment induced the phosphorylated levels of ERK1/2(Thr202/Tyr204), but not that of p38 (Thr180/Tyr18

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

200 of RNA-seq data, causally linked the loss of ERK1/2 in HUVECs in vitro to activation of TGFbeta signa

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

202 rats were characterized by overactivation of ERK1/2 (extracellular signal-regulated kinase1-/2), AKT

203 Overexpression of ERK1/2 increased the expression of lipogenic genes, and

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

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

206 orylation of SHP-1 and de-phosphorylation of ERK1/2 and p38.

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

208 m is unable to facilitate phosphorylation of ERK1/2 in cells that are devoid of beta-arrestin-1/2.

209 Rapid and prolonged phosphorylation of ERK1/2 led to sequential activation of p90RSK and CREB,

210 Phosphorylation of ERK1/2 was also elevated in PTPN7 KO platelets.

211 selectively promoted the phosphorylation of ERK1/2 without affecting JNK or p38, and contributed to

212 n significantly increased phosphorylation of ERK1/2, a pro-survival MAPK in DM and AMPK-DN mice.

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

214 with significantly lower phosphorylation of ERK1/2, AKT, STAT3, and NF-kappaB, and a concomitant red

215 ethacin did not result in phosphorylation of ERK1/2, indicating that GPVI-mediated ERK phosphorylatio

216 5 impaired M3R-stimulated phosphorylation of ERK1/2.

217 eed the MCL1:BCL-X(L) ratio is predictive of ERK1/2 pathway inhibitor synergy with MCL1 or BCL2/BCL-w

218 odeling in asthma with defined regulation of ERK1/2 signaling.

219 We sought to understand the role of ERK1/2 signaling in cells expressing a Cre allele regula

220 To define the role of ERK1/2 signaling in the quiescent endothelium, we induce

221 osphorylation magnitude and translocation of ERK1/2 between cardiac myocytes and fibroblasts.

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

223 nhibitors of MEK1/2, the kinases upstream of ERK1/2, have been critical in defining the role of the R

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

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

226 p110gamma contribute to the effect of TPO on ERK1/2 phosphorylation and TxA(2) formation.

227 y prevented the synergistic effect of TPO on ERK1/2 phosphorylation and TxA(2) synthesis.

228 viability, neutral lipid content, and AKT or ERK1/2 signaling in human TSC2-deficient cells treated w

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

230 ion levels between SUM149 cells with ERK2 or ERK1 knockdown revealed differential and in some cases o

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

232 pharmacological inhibition of BRAF-V600E or ERK1/2 in melanoma cells increases PARK2 expression.

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

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

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

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

237 e transiently in the presence of CXCR4, peak ERK1/2 phosphorylation was increased when compared with

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

239 hibited by expression of the nuclear phospho-ERK1/2-specific dual-specificity phosphatase, DUSP5.

240 and murine MEP have lower levels of phospho-ERK1/2 in iron-deficient conditions compared with contro

241 cathepsin B and C, claudin-1, phosphorylated ERK1/2, and CD44, but not with synaptopodin, in parietal

242 osphorylated histone H(3) and phosphorylated ERK1/2) in the prostate glands.

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

244 Mechanistically, PKCzeta, ERK1/2, mTOR, and PP2A are key regulators of the Myc res

245 , MEK2-deficient BMDMs exhibited a preserved ERK1/2 phosphorylation, higher HIF-1alpha and Glut1 leve

246 IL-1beta treatment induced profound ERK1/2 signalling, TGFB1 and BMP2 mRNA expression in dis

247 ) expression and activation of proliferative ERK1/2 signaling.

248 Exogenous T3 stimulates proliferative ERK1/2 signaling in apical cardiomyocytes, but not in th

249 In fibroblasts, RHAMM promoted ERK1/2 activation and MMP-9 expression, whereas in kerat

250 The RAS-ERK1/2 axis controlled expression of the cytokine ANGPT2

251 Alterations in the RAS-ERK1/2 pathway are associated with the shortest overall

252 13D) amplification is not reversible; rather ERK1/2 hyperactivation drives ZEB1-dependent epithelial-

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

254 eceptor binding, beta-arrestin2 recruitment, ERK1/2 phosphorylation, cAMP inhibition) and in vivo (an

255 er evaluation of the mechanism shows reduced ERK1/2 activation and stimulation of AMP kinase in skele

256 Src/FAK signal circuit converges to regulate ERK1/2 phosphorylation and this pathway drives cetuximab

257 on of BRAF(V600E) or KRAS(G13D) to reinstate ERK1/2 signalling.

258 Robust ERK1/2 activation following MEKi withdrawal drives a p57

259 production of sphingosine 1-phosphate (S1P), ERK1/2 and matriptase activation via S1P receptor 4 (S1P

260 However, function-selective ERK1/2 inhibitors caused fewer changes in protein expres

261 is for the development of function-selective ERK1/2 inhibitors to mitigate airway remodeling in asthm

262 signals transmitted via the essential Shoc2-ERK1/2 signaling axis.

263 lation of signaling molecules, specifically, ERK1/2 phosphorylation was attenuated by mellitin (Nox5

264 ndings indicate cooperation between the SRC, ERK1/2, and AKT kinases to reduce DLC1 Rho-GAP and tumor

265 17 also robustly stimulated ERK1/2 phosphorylation in rat cortex and showed highly p

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

267 The PI3K/AKT-TBL1XR1-ERK1/2-Sox2 axis may represent a target for the treatmen

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

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

270 We found that ERK1/2 activation involves both arrestin and Galphas, wh

271 We found that ERK1/2 was activated by TGF-beta and required to regulat

272 he recombinant receptor, TAAR1 activates the ERK1/2 pathway but not the AKT pathway to upregulate the

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

274 In the diseased cells, the ERK1/2 inhibitor (PD98059) completely blocked the IL-1be

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

276 nalization and away (cooperativity) from the ERK1/2 phosphorylation pathway, respectively.

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

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

279 Trametinib also inhibited the ERK1/2 pathway in cultured primary human renal fibroblas

280 lates mitogenic signaling pathways, like the ERK1/2 MAP kinase pathway, and innate immune signaling.

281 Stable knockdown clones of the ERK1 and ERK2 isoforms were generated in SUM149 and BT54

282 owth factor (PDGF) and the activation of the ERK1/2 are major regulators of ASM cell proliferation an

283 activity in the heart, and inhibition of the ERK1/2 kinase activity ameliorates pathology, but the do

284 protein Shoc2 amplifies the activity of the ERK1/2 pathway and is an essential modulator of a variet

285 ritical role of VCP in the regulation of the ERK1/2 pathway and reveals a previously unrecognized fun

286 d that in injured kidneys, inhibition of the ERK1/2 pathway by trametinib ameliorated mammalian targe

287 ls a previously unrecognized function of the ERK1/2 pathway in the pathogenesis of IBMPFD.

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

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

290 for the negative regulation of PARK2 via the ERK1/2-ELK1 axis.

291 lly methylated (DM) CpGs, treatment with the ERK1/2-selective inhibitor SCH772984 showed less than 40

292 cate that EGF stimulates TGF-betaRII through ERK1/2 and EGFR signaling, suggesting interplay between

293 We found that TRPC6 binds to ERK1/2 and the actin regulatory proteins, caldesmon (a c

294 All changes to ERK1/2 pathway intermediates were blocked by the TAAR1 a

295 The opto-RTKs efficiently trigger ERK1/2, PI3K/Akt, and PLCgamma signaling.

296 ctor receptor-regulated MMP-9 expression via ERK1/2, which resulted in cleavage of the ectodomain of

297 el in which TGF-beta regulates Scleraxis via ERK1/2 and then Scleraxis and Smad3 cooperate to regulat

298 Signalling via ERK1/2 and tuning by its negative regulator DUSP4 are cr

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

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