ライフサイエンスコーパス: ERK2

1 itical residue Thr-207 (in Erk1)/Thr-188 (in Erk2).

2 r the Zn(2+)-induced sustained activation of ERK2.

3 ller ( approximately 6%) reduction caused by ERK2.

4 cellular signal-regulated kinase (ERK) 1 and ERK2.

5 ERK2 phosphatase DUSP6, thereby increasing p-ERK2.

6 using either the active or inactive form of ERK2.

7 ivation by phosphorylation of the MAP kinase ERK2.

8 to both nonphosphorylated and phosphorylated ERK2.

9 ime between the different activity states of ERK2.

10 ors, reduced local invasion, and decreased p-ERK2.

11 f extracellular signal-regulated kinase ERK1/ERK2.

12 ility to trigger the phosphorylation of ERK1/ERK2.

13 directional association of MKK4 peptide with ERK2.

14 ated ERK2, disrupting key features of active ERK2.

15 e same reaction order observed previously in ERK2.

16 AT2B directly interacts with MEK1, GIT1, and ERK2.

17 ing mode, occupying two key docking sites of ERK2.

18 ge region of the protein ATP-binding site on ERK2.

19 icity of the same DARPin towards non-cognate ERK2.

20 ct MAP kinase phosphatase activity toward 2P-ERK2.

21 through collaboration with IKK1/2, Akt, and Erk2.

22 EG) accessible to PARP1-bound phosphorylated Erk2.

23 cial and sufficient for its interaction with ERK2.

24 n molecular weight, e.g., ERK1 (44 kDa) from ERK2 (42 kDa).

25 on of Tau by extracellular-regulated kinase (ERK2), a mitogen-activated kinase (MAPK) that responds t

26 ylation of extracellular regulated kinase 2 (ERK2), a substrate of STEP that is involved in Zn(2+)-de

27 ed by the two cell types are proto-oncogenes ERK2, a component of the ERK/MAPK pathway, and VAV1, a g

28 lead to the activation of monophosphorylated ERK2, a form that is normally inactive.

29 ate that the deregulation of beta-catenin by ERK2-activated CSN6 is important for CRC development.

30 N6 expression was positively correlated with ERK2 activation and beta-catenin overexpression in CRC s

31 ERK2 activation during metabolic stress contributes to c

32 Remarkably, PEA-15 can efficiently bind the ERK2 activation loop in the critical Thr-X-Tyr region in

33 h factor stimulation and/or oncogene-induced ERK2 activation suppressed EpCAM expression, whereas gen

34 In the absence of ERK2, activation of the ribosomal protein S6 kinase (p70

35 rylation of the signal transduction molecule ERK2, activation of the transcription factor NFkappaB, a

36 f EMT occurs via cyclic oscillations in both ERK2 activity and downstream expression of EMT genes.

37 ERK2 activity and S1248 phosphorylation were greater in

38 ls became ethanol sensitive after increasing ERK2 activity by transfection with a constitutively acti

39 tenuated, the EGFR accumulates in the ER and ERK2 activity decreases.

40 e RSG-mediated augmentation of PPARgamma and ERK2 activity during Tg2576 cognitive enhancement was re

41 e (MEK) activity, yet paradoxically requires ERK2 activity.

42 The MEK1 kinase directly phosphorylates ERK2, after the activation loop of MEK1 is itself phosph

43 Finally, loss of ERK2 alone does not impair development of the dentate gy

44 ults indicate that phosphorylation of Tau by ERK2 alone is sufficient to produce the same characteris

45 The related human kinases ERK1 and ERK2 also bound to arsenic in vitro, suggesting that thi

46 Importantly, loss of ERK2 alters the intrinsic excitability of cortical neuro

47 ailable biophysical and biochemical data for ERK2, an archetypal MAPK.

48 upport the notion that the important kinases ERK2 and CaMKIIdelta can alter the passive force of myoc

49 of the predicted sensitivity of alternative ERK2 and EGFR inhibitors, with a particular highlight of

50 e small molecule BI-78D3 binds to the DRS of ERK2 and forms a covalent adduct with a conserved cystei

51 Phosphorylation by Erk2 and IKK1/2 of Ser114 and Ser446 converts Bcl3 into

52 to both nonphosphorylated and phosphorylated ERK2 and inhibited ERK2 kinase activity.

53 1, GRB2, IQGAP1, RALA, RAF-1, IKKbeta, AKT2, ERK2 and KRAS itself.

54 a is facilitated by prior phosphorylation by ERK2 and leads to its down-regulation.

55 pocket (DEF pocket), is formed subsequent to ERK2 and p38alpha activation.

56 a2, and p38gamma were involved in induction, ERK2 and p38delta played no role in TNF-alpha-dependent

57 ecifically interacts with non-phosphorylated ERK2 and prevents ERK2 phosphorylation and nuclear trans

58 rotein-protein interactions between purified ERK2 and PSD-93 in vitro.

59 el-like factor 2 (Klf2) is phosphorylated by Erk2 and that phospho-Klf2 is proteosomally degraded.

60 compromising its selectivity for pERK2 over ERK2 and to reprogram the substrate specificity of the s

61 imulates a robust and biphasic activation of ERK2 and transcription of the late response-gene Fra1 as

62 of extracellular signal regulated-kinase-2 (Erk2) and demonstrate that Fhl1 directly interferes with

63 edback (by expressing catalytically inactive ERK2) and increasing negative feedback (by Egr1-driven e

64 s linked to increased phosphorylated ERK2 (p-ERK2), and ERK2 knockdown restored cell surface CDH1 and

65 Here we show that Akt, Erk2, and IKK1/2 phosphorylate Bcl3.

66 inds to the cancer-associated MAPKs ERK1 and ERK2, and that this domain might thus offer a new tool t

67 ct quantitative differences between ERK1 and ERK2, and the effects are not restricted to osteosarcoma

68 nt for dimerization and dephosphorylation of ERK2, and we analyzed the role of dimerization in ERK1/2

69 t involve known docking recruitment sites on ERK2, and we obtain an estimate of the dissociation cons

70 we show that CPEB4 activity is regulated by ERK2- and Cdk1-mediated hyperphosphorylation.

71 These contiguous mutations in the CD site of ERK2 are both required for docking interactions but lead

72 el is that constraints to domain movement in ERK2 are overcome by phosphorylation at pTyr, which incr

73 ssary and sufficient for binding to ERK1 and ERK2, as well as to the MAPK kinases MEK1 and MEK2.

74 efficiently phosphorylated by the MAP kinase ERK2 at a consensus threonine site (T38).

75 ductive conformation relative to inactive 0P-ERK2:ATP.

76 pe HRas or KRas proteins fails to reduce PP5-ERK2 binding, indicating that the effect is specific to

77 The accurate ERK2-binding region seems to locate at an N-terminal reg

78 scription directly by binding to a consensus ERK2-binding site in the EpCAM promoter and indirectly t

79 h factor receptor (EGFR) signaling, in which ERK2 binds directly to CSN6 Leu163/Val165 and phosphoryl

80 Mechanistically, we show that ERK2 binds Shank3 and phosphorylates it at three residue

81 Erk2 binds to specific DNA sequence motifs typically acc

82 Importantly, ERK2 binds to the GP130 promoter, where it perhaps inter

83 ning a significant degree of disorder in its ERK2-bound state.

84 mulated secretion was inhibited by siRNA for ERK2 but not by siRNA for EGFR.

85 and Phe(665)) were necessary for binding to ERK2 but not for hBVR binding.

86 Interestingly, these effects require Erk2, but not Erk1 expression, and can be rescued by enf

87 Here, we show that ERK2, but not ERK1, also controls the expression and fun

88 We also demonstrate that ERK2, but not ERK1, is required to preserve epidermal in

89 We demonstrate that ERK2, but not ERK1, phosphorylates the purine synthesis

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

91 acilitate the highly specific recognition of ERK2 by Ets-1, and enable the optimal localization of it

92 The yeast MAPK Fus3 and human MAPK ERK2 can be functionally redirected if only two conditio

93 downstream kinase (RSK1) faces the enzyme's (ERK2) catalytic site.

94 acellular signal-regulated protein kinase 2, ERK2), cause a neurodevelopmental disease within the RAS

95 ERK2 E-K reverses a buried charge in the ERK2 common docking (CD) site, a region that binds activ

96 Formation of the hBVR-PKCdelta-ERK2 complex required the hBVR docking site for ERK, FXF

97 gene by a direct chromatin action of a c-Jun/ERK2 complex.

98 An X-ray structure of active 2P-ERK2 complexed with AMP-PNP reveals a shift in the Gly-r

99 X-ray structures of 2P-ERK2 complexed with Vertex-11e or GDC-0994 recapitulate

100 eveal that the formation of PP5.ERK1 and PP5.ERK2 complexes partially depends on HSP90 binding to PP5

101 tudy, we have generated ERK1 and conditional ERK2 compound knock-out mice to determine the role of ER

102 H2 promoter; p38alpha/beta2/delta, ERK1, and ERK2 contributed to cytokine dependent induction, wherea

103 in developmental assays in Drosophila, only ERK2 D-N displays a significant gain of function, reveal

104 The crystal structure of ERK2 D-N is indistinguishable from that of wild-type pro

105 rminus of Ets-1 interacts with a part of the ERK2 D-recruitment site that normally accommodates the h

106 ike the mutation of the preceding aspartate (ERK2 D321N [D-N]) known as the sevenmaker mutation, caus

107 Osr2-Cre;Erk2(fl/fl) mice, in which the Erk2 deletion is restricted to the palatal mesenchyme, d

108 sion of two PK isoforms (PKM2 and PKR) in an ERK2-dependent manner.

109 macologic inhibition or genetic knockdown of ERK2 did not alter L1 adhesion, but markedly decreased e

110 Therefore, ERK1 and ERK2 display both functionally distinct and redundant ro

111 allosteric conduit in dually phosphorylated ERK2, disrupting key features of active ERK2.

112 Here, we show that while single Erk1 or Erk2 disruption did not grossly compromise myelopoiesis,

113 We identify two main ERK2 docking sites in Tau sequence using NMR.

114 disordered kinase domain extension) and the ERK2 "docking" groove plays the major role in making an

115 ve conformational changes at distal sites on ERK2 during docking interactions.

116 Our results suggest that ERK2 dysregulation in Alzheimer disease could lead to ab

117 In contrast, the crystal structure of ERK2 E-K reveals profound structural changes, including

118 ERK2 E-K reverses a buried charge in the ERK2 common doc

119 ERK2 E-K, like the mutation of the preceding aspartate (

120 redicted resistance mutations in CDK4, CDK6, ERK2, EGFR and HER2.

121 ion is enabled by a unique bipartite mode of ERK2 engagement by Ets-1 and involves two suboptimal non

122 A mutant of ERK2, engineered to enhance conformational mobility at t

123 tracellular signal-regulated kinase ERK1 and ERK2 (ERK1/2) cascade regulates a variety of cellular pr

124 Upregulation of the ERK1 and ERK2 (ERK1/2) MAP kinase (MAPK) cascade occurs in >30% o

125 Thus, ERK1 and ERK2 exhibit both functionally distinct and redundant ro

126 the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the sternomasto

127 have a poorer prognosis than those with low ERK2-expressing tumors.

128 osterone-dependent regulation of hippocampal ERK2 expression.

129 ua, and GRIC-ERKdko placentas showed reduced ERK2 expression.

130 ted extracellular signal-regulated kinase 2 (ERK2) expression in the dentate gyrus in gonadectomized

131 bind to the mitogen-activated protein kinase ERK2 (extracellular signal-regulated kinase 2) in either

132 dies of the mitogen-activated protein kinase ERK2 (extracellular-regulated protein kinase 2) by hydro

133 rigid body interaction with a section of the ERK2 F-recruitment site through a binding mode that devi

134 The majority of residues in active ERK2 fit to a single conformational exchange process, wi

135 egion, we studied two mouse models: Wnt1-Cre;Erk2(fl/fl) and Osr2-Cre;Erk2(fl/fl).

136 Wnt1-Cre;Erk2(fl/fl) mice exhibited cleft palate, malformed tongu

137 Tongues in Wnt1-Cre;Erk2(fl/fl) mice exhibited microglossia, malposition, di

138 suggesting that palatal clefting in Wnt1-Cre;Erk2(fl/fl) mice is a secondary defect.

139 Osr2-Cre;Erk2(fl/fl) mice, in which the Erk2 deletion is restrict

140 The primary malformations in Wnt1-Cre;Erk2(fl/fl) mice, namely micrognathia and mandibular asy

141 se models: Wnt1-Cre;Erk2(fl/fl) and Osr2-Cre;Erk2(fl/fl).

142 llizygosity (Mx1Cre(+)Nf1(flox/flox)Erk1(-/-)Erk2(flox/flox)) fully protects against the development

143 Conditional deletion of Erk2 from cells of the oligodendrocyte lineage resulted

144 At the same time PEA-15 binding protects ERK2 from dephosphorylation, thus setting the stage for

145 analyzed two lines of mice lacking both ERK1/ERK2 function specifically in oligodendrocyte-lineage ce

146 lls, we conditionally disrupted the Erk1 and Erk2 genes in mouse RPE.

147 ibutes in cells expressing endogenous ERK or ERK2-GFP reporters.

148 rs enhanced dephosphorylation of recombinant ERK2-GST in an in vitro phosphatase assay.

149 Collectively, our findings unravel ERK2 guided PK-dependent metabolic changes during PMA in

150 s with TNBC tumors expressing high levels of ERK2 have a poorer prognosis than those with low ERK2-ex

151 t Galphai, cAMP-dependent pathways, and ERK1/ERK2 have key roles in morphine- and DAMGO-mediated sign

152 f the mitogen-activated protein (MAP) kinase ERK2 have shown that activation by dual phosphorylation

153 ase (MAPK) signaling (via the MAPKs ERK1 and ERK2; hereafter referred to as ERK).

154 Screening of inactive ERK2 identified a pyrrolidine analogue 1 that bound to b

155 Scar/WAVE phosphorylation does not require ERK2 in Dictyostelium or mammalian cells.

156 n and function of gp130 per se, as silencing ERK2 in human osteosarcoma U2OS cells inhibits the expre

157 Here, we report that the absence of Erk1 and Erk2 in murine hematopoietic cells leads to bone marrow

158 used mice with Cre-loxP-mediated deletion of ERK2 in Nav1.8(+) sensory neurons that are predominantly

159 ely, our study demonstrates that mutation of Erk2 in neural crest derivatives phenocopies the human P

160 dence indicates an isoform-specific role for ERK2 in pain processing and peripheral sensitization.

161 cy of ERK isoforms or a predominant role for ERK2 in pain; however, the tools to discriminate between

162 However, the function of ERK2 in primary sensory neurons has not been directly te

163 genetic knock-out lines to demonstrate that ERK2 in sensory neurons is necessary for development of

164 To dissect the isoform-specific function of ERK2 in sensory neurons, we used mice with Cre-loxP-medi

165 tion induced PARP1 binding to phosphorylated Erk2 in the chromatin of cerebral neurons caused Erk-ind

166 These results suggest an important role for ERK2 in the translational control of MBP, a myelin prote

167 pendently and together suggested the role of ERK2 in the up-regulation of both the isoforms of PK, pr

168 cise functions of the ERK isoforms (ERK1 and ERK2) in cancer progression have not been well defined.

169 of extracellular signal-regulated kinase 2 (ERK2), in turn leading to inhibition of c-Jun/activator

170 tively decreases the interaction of PP5 with ERK2, in a manner that is independent of PP5 and MAPK/ER

171 ined a germ line Erk1 mutation with Cre-loxP Erk2 inactivation in skeletal muscle to produce, for the

172 p-regulation of cyclin D1 and phosphorylated ERK2, increased cell proliferation, and migration.

173 c deletion and pharmacological inhibition of ERK2 increases Shank3 abundance in vivo.

174 Conversely, overexpression of ERK2 induced a depressive-like response, regardless of F

175 Additionally, our analysis revealed that ERK2 induced the expression of Dock10, a Rac1/Cdc42 GEF,

176 tion factor FoxO1 as a potential mediator of ERK2-induced EMT, and thus we investigated the mechanism

177 Hence, KRAS is associated with activation of ERK2, induction of FASN, and promotion of lipogenesis.

178 he MAPK pathway responsible for cell growth, ERK2 initiates the first phosphorylation event on RSK1,

179 ), but not KRas(V12), also decreases the PP5-ERK2 interaction.

180 HCLGLA inhibited PKC activation and PKCdelta/ERK2 interaction.

181 ferential responsiveness of PP5-ERK1 and PP5-ERK2 interactions to select oncogenic Ras variants and a

182 Erk2 interacts with and phosphorylates RNAPII at its ser

183 ERK2 interacts with ATG proteins via its substrate-bindi

184 Finally, we show that the ERK2-IQGAP1 interaction does not require ERK2 phosphoryl

185 Thus, the L->R shift in 2P-ERK2 is associated with movements needed to form a compe

186 Stable knockdown clones of the ERK1 and ERK2 isoforms were generated in SUM149 and BT549 TNBC ce

187 ylated and phosphorylated ERK2 and inhibited ERK2 kinase activity.

188 turn phosphorylate and activate the ERK1 and ERK2 kinases, stimulating the mitogen-activated protein

189 expression increases phosphorylation of Erk1/Erk2 kinases, which leads to an elevated activity of the

190 Those changes associated with ERK2 knockdown predominantly altered regulation of CSCs

191 increased phosphorylated ERK2 (p-ERK2), and ERK2 knockdown restored cell surface CDH1 and suppressed

192 ERK2 knockdown significantly inhibited anchorage-indepen

193 uiescent endothelium, we induced endothelial Erk2 knockout in adult Erk1(-/-) mice.

194 no proximal signaling defect was observed in Erk2 KO T cells.

195 Thus, phosphorylation and activation of ERK2 lead to a dramatic shift in conformational exchange

196 In inactive, unphosphorylated ERK2, localized conformational exchange was observed amo

197 y interact with clathrin terminal domain and ERK2 MAPK in vitro.

198 To understand the function of ERK2 (MAPK1) in the postmigratory neural crest populatin

199 multiple point mutations in ERK1 (MAPK3) and ERK2 (MAPK1) that could confer resistance to ERK or RAF/

200 1 [ERK1], extracellular regulated kinase 2 [ERK2] [MAPKs], and signal transducer and activator of tr

201 Thus, ERK2-mediated PFAS phosphorylation facilitates the incre

202 This fission is driven by Erk2-mediated phosphorylation of Drp1 on Serine 616, and

203 monstrate that Fhl1 directly interferes with Erk2-mediated titin-N2B phosphorylation.

204 oral profile was accompanied by decreases in ERK2 mRNA and protein phosphorylation within the VTA, wh

205 suggest region-specific changes of ERK1 and ERK2 mRNA expression during morphine-induced CPP.

206 duced CPP, the expression levels of ERK1 and ERK2 mRNA were altered in various brain regions.

207 n regions, the expression levels of ERK1 and ERK2 mRNA were decreased in three phases of morphine-ind

208 n the PFC, the expression levels of ERK1 and ERK2 mRNA were increased after chronic morphine injectio

209 with a vector expressing a dominant negative ERK2 mutant or a vector expressing MKP-3 inhibited the a

210 ent extracellular signal-regulated kinase 2 (ERK2) mutation occurring in cancers is E322K (E-K).

211 of the extracellular signal-regulated kinase ERK2 network that regulate neuronal excitability.

212 -based signal transduction pathway triggered ERK2-NF-kappaB activation.

213 and extracellular signal-regulated kinase 2 (ERK2) on the single-molecule mechanics of the N2B elemen

214 ERK2 or CDK5 phosphorylate the two proteins but with dif

215 expression levels between SUM149 cells with ERK2 or ERK1 knockdown revealed differential and in some

216 ever, the PKC was not a substrate for either ERK2 or hBVR.

217 of extracellular signal-regulated kinase 2 (ERK2) or its doubly phosphorylated (active) form (pERK2)

218 evels for ERK1 as well as the related kinase ERK2 over what would be predicted by mRNA levels.

219 d EMT was linked to increased phosphorylated ERK2 (p-ERK2), and ERK2 knockdown restored cell surface

220 ippocampus (ERK1: p=0.000, p=0.040, p=0.000; ERK2: p=0.000, p=0.000, p=0.000, respectively).

221 ns, including the classic EGFR-T790M and the ERK2-P58L/S/T mutations.

222 In addition, inactivation of ERK2/p90RSK signaling triggered by high SIRT6 levels inc

223 e discovered that several kinases in the MEK/ERK2 pathway destabilize Shank3 and that genetic deletio

224 anslation of Fra1 mRNA transcribed by the E2-ERK2 pathway, through the phosphorylation of the S6K1-de

225 ro, PLAC8 directly bound and inactivated the ERK2 phosphatase DUSP6, thereby increasing p-ERK2.

226 tructures of PEA-15 bound to three different ERK2 phospho-conformers.

227 Furthermore, recombinant ERK2 phosphorylated alpha- and beta-adducins and dematin

228 o kinase assays, we found that both ERK1 and ERK2 phosphorylated NIPA with high efficiency.

229 ERK2 phosphorylated SPF45 on Thr71 and Ser222 in vitro a

230 Kinase assays confirmed that ERK2 phosphorylated these sites in vitro, providing a di

231 ly, extracellular signal regulated kinase 2 (ERK2) phosphorylates ribosomal S6 kinase 1 (RSK1), which

232 ts with non-phosphorylated ERK2 and prevents ERK2 phosphorylation and nuclear translocation.

233 C2-dependent Akt Ser-473 phosphorylation and ERK2 phosphorylation but not phosphorylation of Akt on T

234 l profile of STEP61 hyperphosphorylation and ERK2 phosphorylation indicates that loss of function of

235 Our data suggest that ERK2 phosphorylation of S1248 modulates ethanol inhibiti

236 We further investigate the mechanism of ERK2 phosphorylation of Tau.

237 the ERK2-IQGAP1 interaction does not require ERK2 phosphorylation or catalytic activity and does not

238 gnetic resonance spectroscopy, we found that ERK2 phosphorylation proceeds at markedly different rate

239 ene led to a rapid and sustained increase in ERK2 phosphorylation within minutes of exposure to Zn(2+

240 ation is necessary for maintaining sustained ERK2 phosphorylation.

241 howed that Extracellular Regulated Kinase 2 (ERK2) phosphorylation of SPF45 regulates cell proliferat

242 both the isoforms of PK, proposing a role of ERK2-PK isoform axis in differentiation.

243 ellular signal-regulated kinase 1 (Erk1) and Erk2 play crucial roles in cell survival, proliferation,

244 Reconstitution studies show that Erk1 and Erk2 play redundant and kinase-dependent functions in he

245 eased occupancy of PRC2 and poised RNAPII at Erk2-PRC2-targeted developmental genes.

246 Surprisingly, Erk2-PRC2-targeted genes are specifically devoid of TFII

247 Of note, the direct binding of ERalpha-36 to ERK2 prevents its dephosphorylation by MKP3 and enhances

248 Our findings indicate that ERK2 promotes metastasis and the CSC phenotype in TNBC.

249 We further show that Erk1(R84S) and Erk2(R65S) are intrinsically active due to an unusual au

250 Strikingly, Erk2(R65S) efficiently autophosphorylates its Thr-188 ev

251 We conclude that global motions in ERK2 reflect conformational changes at the active site t

252 thus we investigated the mechanism by which ERK2 regulates FoxO1.

253 ated ERK1/2 independently of Cu or an active ERK2 restored the tumour growth of murine cells lacking

254 We found that loss of both ERK1 and ERK2 resulted in 60% fewer granule cells and near comple

255 tes extracellular signal-regulated kinase 2 (ERK2), resulting in NF-kappaB activation.

256 Consequently, loss of Erk2 severely impeded Th1 differentiation while enhancin

257 Mice doubly-deficient in Erk1 and Erk2 show rapid attrition of hematopoietic stem cells an

258 a-ERK2 ternary complex that is essential for ERK2 signal transduction and activation of genes linked

259 es suggest that the predominant role of ERK1/ERK2 signaling in vivo is in promoting rapid myelin grow

260 ignaling and that differential regulation of ERK2 signaling might contribute to genetic susceptibilit

261 In the absence of ERK1/ERK2 signaling NG2(+) oligodendrocyte progenitor cells p

262 We also demonstrate that MEK1/ERK2 signaling pathway is required for nontypeable H. in

263 reventing cancer metastasis by inhibition of Erk2 signaling via MKP3.

264 These results implicate a role for ERK2 signaling within the dentate gyrus area of the hipp

265 s promotes a switch to isoform-specific MEK1/ERK2 signaling, induction of GCN2/eIF2alpha phosphorylat

266 apoptosis responses using PERK/Akt and MEK1/ERK2 signaling, respectively.

267 nd, active K-Ras and hyperactivated Ras-ERK1/ERK2 signaling.

268 AR2 agonist treatment also repressed Akt and ERK2 signalling.

269 equivalent residue, Tyr-280/Tyr-261, in Erk1/Erk2 significantly impaired Erk1/2's catalytic activity.

270 The ERK2 site is downstream of a direct PKA site in the Rap1

271 Likewise, leucine replacement of S1248, an ERK2 substrate on the L1 cytoplasmic domain, did not dec

272 f greatly diminished stores of intracellular ERK2, suggesting a clear bias toward the incorporation o

273 the EpCAM promoter region, we observed that ERK2 suppresses EpCAM transcription directly by binding

274 its inhibition of pathological hypertrophy, ERK2(T188A) did not interfere with physiological cardiac

275 ERK2(T188A) efficiently attenuated cardiomyocyte hypertr

276 isolated cells and in mice using the mutant ERK2(T188A), which is dominant-negative for ERK(Thr188)

277 , we report on formation of an hBVR-PKCdelta-ERK2 ternary complex that is essential for ERK2 signal t

278 novel non-overlapping functions for ERK1 and ERK2 that are biologically relevant.

279 we find a recurrent active site mutation of ERK2 that drives resistance to ERK inhibitors in mono- o

280 ion T-loop of ERK1 and its closest relative, ERK2, three additional flanking phosphosites have been c

281 influenced recruitment of GIT1 or MAT2B and ERK2 to MEK1, respectively.

282 MAT2B directly promoted binding of GIT1 and ERK2 to MEK1.

283 Through binding of Erk2 to the second of its carboxyl-terminal NPXY motifs,

284 actin polymerization, activation of kinases ERK2, TORC2, and phosphatidylinositide 3-kinase, and Ras

285 revealed that upon binding of compound 4 to ERK2, Tyr34 undergoes a rotation (flip) along with a shi

286 canning functional readouts for PPARG, MAPK1/ERK2, UBE2I, SUMO1, PTEN, CALM1, CALM2, and TPK1 and wit

287 We find that ERK2, unlike ERK1, is required for peripheral sensitizat

288 and Lung Squamous Cell Cancer (LSCC) and the ERK2-VTX11e treatment for melanoma and colorectal cancer

289 ase extracellular signal-regulated kinase 2 (Erk2), we observe that certain features of the interacti

290 lobal changes of gene expression mediated by ERK2, we identified the transcription factor FoxO1 as a

291 inase 1, the dynamics of assigned methyls in ERK2 were altered throughout the conserved kinase core,

292 Both CaMKIIdelta and ERK2 were found to phosphorylate the N2B element, and si

293 hBVR and ERK2 were phosphorylated by PKCdelta; however, the PKC w

294 lation changes associated with activation of ERK2 were seen in PKA knockout cells.

295 C-0994, and AMP-PNP with active vs. inactive ERK2, where the extent of HX protection correlates with

296 (NIA), KRAS is found to activate the protein ERK2, whereas ERK1 activation is found in non-KRAS-assoc

297 n-protein interaction surfaces compared with ERK2, which is the closest ERK5 paralog.

298 ated mitogen-activated protein kinase (MAPK) ERK2, which showed stronger influence of pERK on pS6 (ph

299 G12D) allele, the presence of either Erk1 or Erk2 with intact kinase activity is sufficient to promot

300 ophosphorylated Tau by activated recombinant ERK2 with nuclear magnetic resonance spectroscopy (NMR)