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

3 ERK2 phosphatase DUSP6, thereby increasing p-ERK2.

4 using either the active or inactive form of ERK2.

5 ivation by phosphorylation of the MAP kinase ERK2.

6 to both nonphosphorylated and phosphorylated ERK2.

7 ime between the different activity states of ERK2.

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

9 f extracellular signal-regulated kinase ERK1/ERK2.

10 ility to trigger the phosphorylation of ERK1/ERK2.

11 ated ERK2, disrupting key features of active ERK2.

12 e same reaction order observed previously in ERK2.

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

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

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

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

17 ivation of PKCdelta and its interaction with ERK2.

18 n levels were decreased by overexpression of ERK2.

19 on ventral tegmental area Ca(v)1.3 LTCCs and ERK2.

20 EG) accessible to PARP1-bound phosphorylated Erk2.

21 cial and sufficient for its interaction with ERK2.

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

23 ller ( approximately 6%) reduction caused by 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 lead to the activation of monophosphorylated ERK2, a form that is normally inactive.

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

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

30 ERK2 activation during metabolic stress contributes to c

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

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

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

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

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

36 ERK2 activity and S1248 phosphorylation were greater in

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

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

39 Functionally, reducing ERK2 activity within the dentate gyrus induced anhedonia

40 implex virus-mediated gene transfer to block ERK2 activity within the VTA, we rescued the MPH and FLX

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

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

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

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

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

50 1, GRB2, IQGAP1, RALA, RAF-1, IKKbeta, AKT2, ERK2 and KRAS itself.

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

52 gene (MVADeltaC11R) reduced both MVA-induced ERK2 and NF-kappaB activation in 293T cells or the kerat

53 at least one apical trigger in this pathway: ERK2 and NF-kappaB activation was diminished when MVA in

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

55 its both the interaction of DUSP9/MKP-4 with ERK2 and p38alpha in vivo and its ability to dephosphory

56 abrogates the binding of DUSP9/MKP-4 to both ERK2 and p38alpha MAP kinases.

57 time, the docking interactions of HePTP with ERK2 and p38alpha.

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

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

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

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

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

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

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

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

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

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

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

69 so find that the activation profiles of ACA, ERK2, and TORC2 change in the course of development, wit

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

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

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

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

74 -activated protein kinases (MAPKs), ERK1 and ERK2, are critical intracellular signaling molecules imp

75 In this study, we identified ERK2 as the kinase responsible for this critical initial

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

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

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

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

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

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

82 Erk2 binds to specific DNA sequence motifs typically acc

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

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

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

86 argeting either ERK1 or ERK2, we showed that ERK2 but not ERK1 mediated NIPA inactivation at G(2)/M.

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

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

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

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

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

92 val of extracellular Ca(2+) and depletion of ERK2 by siRNA.

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

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

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

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

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

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

99 Analysis of the same ERK2 construct with the nonphysiological His(6) tag show

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

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

102 Furthermore, the anti-ERK2 DARPin is seen to inhibit ERK phosphorylation as it

103 Similarly, in vitro ERK1/ERK2-deficient oligodendrocytes differentiated normally

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

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

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

107 of extracellular signal regulated kinase 2 (ERK2) directly to chromatin at the ESR1 gene locus in a

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

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

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

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

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

113 gnal-regulated protein kinases 1 and 2 (ERK1/ERK2), downstream mediators of mitogen-activated protein

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

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

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

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

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

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

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

121 osterone-dependent regulation of hippocampal ERK2 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 tracellular signal-regulated protein kinase, ERK2, fully activated by phosphorylation and without a H

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

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

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

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

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

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

144 Our results demonstrate that ERK2-HePTP interactions primarily involve the D-motif, w

145 Our data show that the resting state ERK2:HePTP complex adopts a highly extended, dynamic con

146 ructures of the resting and active states of ERK2:HePTP complexes.

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

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

149 ly described divergent functions of ERK1 and ERK2 in cell cycle regulation, which may be due in part

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

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

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

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

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

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

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

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

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

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

160 In this study, we deleted Erk2 in the developing mouse cortex from GFAP-expressing

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

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

163 Moreover, the synaptic pool of ERK2 in these neurons can be selectively activated by am

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

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

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

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

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

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

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

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

172 HCLGLA inhibited PKC activation and PKCdelta/ERK2 interaction.

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

174 Erk2 interacts with and phosphorylates RNAPII at its ser

175 ERK2 interacts with ATG proteins via its substrate-bindi

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

177 reverse genetic study, we show that the MAPK Erk2 is not essential for T cell proliferation in the pr

178 Phosphorylated ERK2 is seen to increase by incubation of the COS-7 cell

179 This kinase, especially ERK2 isoform, noticeably resides in peripheral structure

180 ylated and phosphorylated ERK2 and inhibited ERK2 kinase activity.

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

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

183 ERK2 knockdown led to a delay at the G(2)/M transition,

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

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

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

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

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

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

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

191 1 [ERK1], extracellular regulated kinase 2 [ERK2] [MAPKs], and signal transducer and activator of tr

192 with Fhl1 and residues that are dependent on Erk2-mediated phosphorylation in situ.

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

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

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

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

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

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

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

200 A constitutive ERK2 mutant induces stable expression of Snail1, N-cadhe

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

202 hese effects were observed in single ERK1 or ERK2 mutants.

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

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

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

206 ERK2 or CDK5 phosphorylate the two proteins but with dif

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

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

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

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

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

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

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

214 rentially incorporated the activated form of ERK2 (pERK2) into the tegument.

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

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

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

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

219 In phosphorylation assays, active ERK2 phosphorylated PSD-93.

220 ERK2 phosphorylated SPF45 on Thr71 and Ser222 in vitro a

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

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

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

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

225 ection of amphetamine induced an increase in ERK2 phosphorylation in the synaptic fraction of striata

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

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

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

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

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

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

232 C- or L-SIGN was shown to stimulate ERK1 and ERK2 phosphorylation, with statistically significant inc

233 , while the drug did not alter extrasynaptic ERK2 phosphorylation.

234 ation is necessary for maintaining sustained ERK2 phosphorylation.

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

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

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

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

239 ERK2 possesses the ability to interact with PSD-93 and p

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

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

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

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

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

245 pplementation, whereas the overexpression of ERK2 rescued this behavior in gonadectomized rats.

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

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

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

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

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

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

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

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

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

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

256 ellular signal-regulated kinase 1 (ERK1) and ERK2 signaling pathway.

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

258 reventing cancer metastasis by inhibition of Erk2 signaling via MKP3.Oncogene advance online publicat

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

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

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

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

263 AR2 agonist treatment also repressed Akt and ERK2 signalling.

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

265 ciated viral vectors expressing Ca(v)1.3 and ERK2 siRNA further indicate that recruitment of the Ca(v

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

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

268 in cancer, as a novel coimmunoprecipitating ERK2 substrate.

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

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

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

272 ERK2(T188A) efficiently attenuated cardiomyocyte hypertr

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

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

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

276 red extracellular signal-regulated kinase 2 (ERK2) that can utilize ATP analogs, we have identified t

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

278 ect and specific binding of norathyriol with ERK2 through a cocrystal structural analysis.

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

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

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

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

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

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

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

286 At synaptic sites, ERK2 was noticeably more abundant than ERK1.

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

288 expression of shRNA targeting either ERK1 or ERK2, we showed that ERK2 but not ERK1 mediated NIPA ina

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

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

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

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

293 found that two common ERK isoforms (ERK1 and ERK2) were concentrated more in extrasynaptic fractions

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

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

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

297 ation velocity data for a 15 muM solution of ERK2 with an enhanced van Holde-Weischet method determin

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

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

300 coefficient (s) to be ~3.22 S for activated ERK2 with or without 10 mM MgCl(2).