ライフサイエンスコーパス: p90(rsk)

1 nase (p70(S6K)) and p90 ribosomal S6 kinase (p90(RSK)).

2 ated protein kinase activity (a substrate of p90(rsk)).

3 ivation and release of the downstream target p90RSK.

4 hibition of MEK-dependent phosphorylation of p90RSK.

5 etely blocked H(2)O(2)-induced activation of p90RSK.

6 (2)-mediated activation of ERK1/2 but not of p90RSK.

7 tein kinase 2 (MAPKAP-K2), 3pK/MAPKAP-K3 and p90RSK.

8 tion and activation of the mitogenic kinase, p90RSK.

9 ctivating the prosurvival kinases Erk1/2 and p90RSK.

10 channels in HEK 293 cells were inhibited by p90RSK.

11 otein BAD (BCL2-antagonist of cell death) by p90RSK.

12 overexpressing dominant negative p90RSK (DN-p90RSK).

13 ng a dominant negative form of p90RSK (Ad-DN-p90RSK).

14 wn ERK1/2 substrate p90 ribosomal S6 kinase (p90RSK).

15 d ribosomal protein S6 kinase polypeptide 2 (p90RSK).

16 ation of the ERK1 and the 90-kDa rpS6 kinase p90(rsk).

17 nstitutively active form of the MAPK target, p90(Rsk).

18 bition and CSF-dependent metaphase arrest by p90(Rsk).

19 d that the ERK-mediated effect may occur via p90(rsk).

20 activates both endogenous and overexpressed p90(rsk).

21 vity was transmitted to a downstream target, p90(rsk).

22 not of another putative IkappaBalpha kinase, p90(rsk).

23 ation of mitogen-activated protein kinase or p90(RSK).

24 this site was co-eluted with the S6 kinase, p90(rsk).

25 rophoretic mobility shifts in immunoreactive p90(rsk).

26 l-regulated kinase 1/2, protein kinase A, or p90(RSK).

27 6 abolished phosphorylation of both NHE1 and p90(RSK).

28 ated the presence of the full-length form of p90(rsk-1) in the mouse and showed no conclusive evidenc

29 tudy indicates the presence of a full-length p90(rsk-1) mRNA in mouse tissues that is homologous to t

30 By comparison, expression of rat p90(rsk-1) resulted in significant kinase activity.

31 , of Shc, ERK1/2, and its dependent protein, p90RSK-1 (p90 ribosomal S6 kinase 1 or RSK-1), was aboli

32 anslocation of the ERK1/2-dependent protein, p90RSK-1 (RSK-1).

33 a concurrent elevation of phosphorylation of p90(RSK), a known NHE1 kinase.

34 tutively active mutant of the protein kinase p90(Rsk), a MAP kinase target.

35 ADP also stimulated phosphorylation of p90RSK, a downstream substrate of phosphorylated ERK1/2,

36 by an accompanying loss in the activation of p90RSK, a key downstream target of MAPK, whereas the NF-

37 mong the polyribosome bound proteins are the p90rsk-activating kinase ERK-2 and a known p90rsk substr

38 cade can prevent cell death through ERK2 and p90(Rsk) activation and phosphorylation of apoptotic and

39 ivated Ras (peak at 2-5 min), which preceded p90RSK activation (peak at 20 min).

40 ic Src kinase family inhibitor, PP1, blocked p90RSK activation by H(2)O(2) in a concentration-depende

41 2) p90RSK activation by H(2)O(2) was significantly reduced

42 ogen peroxide, a mediator of induced cardiac p90RSK activation in ischemia/reperfusion injury and dia

43 We previously demonstrated increased p90RSK activation in the diabetic heart.

44 the present study, we determined the role of p90RSK activation in the modulation of voltage-gated K+

45 ion of this work, we now investigate whether p90RSK activation inhibits ERK5-mediated CHIP activation

46 p90RSK activation inhibits ERK5/CHIP association and CHI

47 and CHIP competes for ERK5 binding and that p90RSK activation is critical for inhibiting ERK5/CHIP i

48 These findings indicate that p90RSK activation is critical for reactive oxygen specie

49 An essential role for Fyn and Ras in p90RSK activation was suggested by five findings.

50 of carbachol on H508 cell proliferation and p90RSK activation.

51 use epidermal cells by targeting the MEK/ERK/p90RSK/activator protein-1 signaling pathway.

52 mitogen-activated protein kinase (MAPK), and p90(rsk) activities were indexed on the basis of analysi

53 t failed to prevent the increases in ERK and p90(rsk) activities.

54 increased J(H), as well as cellular ERK and p90(rsk) activities.

55 duced increases in J(H) and cellular ERK and p90(rsk) activities.

56 substrate RRLSSLRA evidenced an increase in p90(rsk) activity (3.4-fold).

57 90(RSK) Ser(381) phosphorylation, as well as p90(RSK) activity.

58 mannin- sensitive manner, but did not affect p90(RSK) activity.

59 tein kinase 1 or 90-kDa ribosomal S6 kinase (p90RSK) activity.

60 p90RSK activity and PRECE mRNA were both increased by st

61 Mice with increased cardiac p90RSK activity due to transgenic expression of p90RSK (

62 H(2)O(2) (200 microM) stimulated ERK1/2 and p90RSK activity in lymphocytes, endothelial cells, and f

63 p90RSK activity was increased in diabetic mouse vessels,

64 virus containing a dominant negative form of p90RSK (Ad-DN-p90RSK).

65 duced activation of MAP kinases p70/85(S6K), p90(RSK), Akt, and protein kinase A.

66 tive isoforms of protein kinase-C, p70S6K or p90rsk (all of which phosphorylate CREB at Ser133 in vit

67 element-binding protein (phospho-CREB) and -p90(RSK) and activation of p34(cdc2) and stress-activate

68 n of the ERK1/2 catalytic activity readouts, p90(RSK) and ELK1, as well as the cell type-specific cha

69 p90(RSK) and family members RSK-2 and RSK-3 are activate

70 proteins, including Bub1, are downstream of p90(Rsk) and may be effectors of APC inhibition and CSF-

71 Recently, the authors reported ERK1/2, p90(RSK) and NHE1 phosphorylation after 2 hours.

72 dentity) to the two protein kinase families, p90(RSK) and p70(RSK).

73 of ERK, JNK, p38 and the downstream elements p90(rsk) and PP-1 in vivo suggest that JNK, but neither

74 ulated kinase (ERK1/2), ribosomal S6 kinase (p90RSK) and Akt, molecules implicated in cell survival.

75 microM), inhibited the activation of ERK and p90RSK and abolished the stimulation of NHE activity by

76 ibits ERK5/CHIP association, suggesting that p90RSK and CHIP competes for ERK5 binding and that p90RS

77 p90RSK and CHIP share a common binding site in the ERK5

78 a specific PKCbeta inhibitor, inhibited both p90RSK and cTnI (Ser(23/24)) phosphorylation by H2O2.

79 2 also inhibited serum-induced activation of p90RSK and decreased phosphorylation of pro-apoptotic pr

80 RK5-S496 as being directly phosphorylated by p90RSK and demonstrated that an ERK5-S496A mutant signif

81 n and Ras in H(2)O(2)-mediated activation of p90RSK and establish redox-sensitive regulation of Ras a

82 Finally, BaP treatment activated p90RSK and its downstream target CDK1.

83 increase in phosphorylation of the ERK 1/2, p90RSK and Mnk 1 proteins (P < 0.05) in the YM.

84 ression depends on ERK signals that activate p90Rsk and Msk1, which in turn phosphorylate CREB, a key

85 on was completely blocked by an inhibitor of p90RSK and partially attenuated by an inhibitor of Rho k

86 er cells leads to hyperactivation of the Erk/p90RSK and PI3K/Akt pathways and, consequently, the phos

87 to concerted activation of two pathways, ERK/p90RSK and PI3K/AKT, which converge to phosphorylate and

88 lated phosphorylation of MEK1/2, ERK1/2, and p90RSK and prevented cellular hypertrophy, sarcomere reo

89 EGF activates ERK/p90RSK and Rho/Rho kinase signaling in A431 and DiFi col

90 EGF activated the EGF receptor/ERK/p90RSK and Rho/Rho kinase signaling pathways.

91 tracellular signal-regulated protein kinase, p90RSK and STAT3a, demonstrating activation of the VEGF

92 es such as mitogen-activated protein kinase, p90(Rsk), and p70S6 kinase (p70(S6k)) that mediate reorg

93 stream effectors activator protein 1, ELK-1, p90RSK, and activating transcription factor 2 was also o

94 IGF-1 stimulation of MEK, Erk, p90Rsk, and Akt were accordingly augmented.

95 Moreover, ERK1/2, p90RSK, and Akt were synergistically activated by SDF-1

96 GN apoptosis by repressing unique MEK5/ERK5, p90Rsk, and Akt-dependent prosurvival pathways, ultimate

97 bition of Rac suppresses distinct MEK5/ERK5, p90Rsk, and Akt-dependent signaling cascades known to re

98 extracellular signal-regulated kinase (ERK), p90RSK, and cyclic AMP-regulated-binding protein (CREB).

99 The TPA-induced phosphorylation of ERK1/2, p90RSK, and Elk, but not MEK or c-Jun N-terminal kinase,

100 to the downstream phosphorylation of Erk1/2, p90RSK, and GSK3beta, followed by the induction of cycli

101 ed novel signaling cascade involving Erk1/2, p90RSK, and p38, which leads to the accumulation of thes

102 llular signal-regulated kinase 1/2 (Erk1/2), p90RSK, and phosphorylation of Bad.

103 d myofibroblasts through an LRP-1-, Erk1/2-, p90RSK-, and Bad-dependent mechanism.

104 as through MEK1/2 and ERK1/2 to the effector P90(RSK) are activated in both perinatal Pkd1 and adult

105 trates that I kappa B kinases (IKKs) but not p90rsk are selectively activated following CD23 cross-li

106 These findings establish p90(RSK) as a serum-stimulated NHE-1 kinase and a mediat

107 ablish redox-sensitive regulation of Ras and p90RSK as a new function for Fyn.

108 When activated, p90RSK associated with ERK5, and this association inhibi

109 lts show that UVA-induced phosphorylation of p90(RSK) at Ser(381) through ERKs and JNKs, but not p38

110 ysis showed that Kv4.3 was phosphorylated by p90RSK at 2 conserved sites, Ser516 and Ser550.

111 ecanoylphorbol-13-acetate strongly activated p90(RSK) but only weakly stimulated p70(S6K).

112 hibition of phosphorylation of ERK substrate p90RSK but also demonstrated inhibition of ERK1,2 phosph

113 orylate their cytoplasmic targets, including p90(RSK), but fail to translocate into the nucleus or to

114 is coupled to MAPK/p90 ribosomal S6 kinase (p90RSK), but not phosphatidylinositol 3-kinase (PI3K)/AK

115 p90RSK, but not ERK1/2 activation, was increased in PKCb

116 These findings suggest that p90(RSK) can function in a PKC-dependent pathway to prom

117 In Xenopus, the Mos-MEK1-MAPK-p90(Rsk) cascade utilizes spindle-assembly-checkpoint co

118 and becomes activated by the Ras-Raf-MEK-ERK-p90(RSK) cascade.

119 ique 33-nucleotide deletion not found in the p90(rsk) clones from any other species that have been ex

120 p90RSK could phosphorylate cTnI in vitro with high subst

121 usly characterized ERK substrates, c-Myc and p90RSK, demonstrating the utility of this method for ide

122 romotes alpha5beta1 inactivation through the p90RSK-dependent phosphorylation of FLNa.

123 In addition, p90RSK directly phosphorylated ERK5 S496 and reduced end

124 erotic mice overexpressing dominant negative p90RSK (DN-p90RSK).

125 T-p90RSK-Tg) and a dominant-negative form of p90RSK (DN-p90RSK-Tg).

126 ritical role of the p90 ribosomal S6 kinase (p90RSK)/ERK5 complex in EC dysfunction in diabetes melli

127 Our study highlights the importance of the p90RSK/ERK5 module as a critical mediator of EC dysfunct

128 p90RSK expression significantly inhibited Kv4.3- and Kv4

129 tified p90 subfamily of ribosomal S6 kinase (p90RSK) family kinases as key factors for growth and pro

130 is a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins and plays a critical role in

131 and a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins.

132 We sought to evaluate inhibitors of p90RSK family members: BI-D1870 and BRD7389, for their a

133 rylation of downstream substrates, including p90RSK, FKHR, and BAD.

134 iferative signaling events involving Erk1/2, p90RSK, GSK3beta phosphorylation, and cyclin D1 inductio

135 The protein kinase p90(Rsk) has previously been implicated as a key target

136 p90RSK2 (also referred to as MAPKAP-K1b, or p90rsk) immunoprecipitated the active 90-kDa kinase from

137 Moreover, S6 kinase activity and p90(rsk) immunoreactivity co-immunoprecipitate with L1 f

138 s Raf-1, ERK2, and the previously identified p90(rsk) in brain.

139 However, the activity of p90(rsk) in cytokine-starved cells increased dramaticall

140 Overexpression of p90(rsk) in Xenopus embryos leads to increased steady-st

141 To confirm the role of p90RSK in cTnI phosphorylation in vivo, we generated ade

142 This study demonstrates the critical role of p90RSK in hyperglycemia-mediated myocardial PRECE induct

143 These data suggest a role for p90RSK in inhibiting CHIP activity and promoting cardiac

144 n of CREB, IRS, PKB, FoxO1, p44/42 MAPK, and p90RSK in INS-1 (832/13) cells and isolated rat islets,

145 herosclerosis, EC-specific overexpression of p90RSK increased EC dysfunction and lipid accumulation i

146 These findings establish p90RSK inhibition as a therapeutic strategy in treatment

147 Fluoromethylketone, a specific p90RSK inhibitor, abolished hydrogen peroxide effects.

148 omethyl ketone-methoxyethylamine, a specific p90RSK inhibitor, ameliorated EC-leukocyte recruitment a

149 vitro, and transfection with kinase-inactive p90(RSK) inhibits serum-induced phosphorylation of NHE-1

150 cific depletion of ERK5 or overexpression of p90RSK inhibits CHIP activity and accelerates cardiac ap

151 In turn, p90(rsk) interacts with the IkappaB kinase 2 (IKK-2) cat

152 her CSF-dependent metaphase arrest caused by p90(Rsk) involves components of the spindle assembly che

153 p90(rsk) is a distal member of the mitogen-activated pro

154 We show that p90(rsk) is a downstream target of fibroblast growth fac

155 Thus, p90(rsk) is present in mature hemopoietic cells, but the

156 onclusion that the first catalytic domain of p90(rsk) is responsible for its enzymatic activity towar

157 Thus, p90(Rsk) is sufficient not only to partially inhibit APC

158 p90 ribosomal S6 kinase (p90RSK) is activated in cardiomyopathies caused by condi

159 , Pdk1 activation of the downstream effector p90RSK is also increased by the combined presence of mut

160 phosphorylation sites, we hypothesized that p90RSK is downstream from PKCbeta II and can be a cTnI (

161 Under these conditions p90RSK is no longer bound to CBP, thereby promoting CBP-

162 ition, we show that p90 ribosomal S6 kinase (p90(RSK)) is a key NHE-1 kinase since p90(RSK) phosphory

163 trated that the Ikappakappa complex, but not p90(rsk), is activated by HIV infection and mediates HIV

164 so demonstrate that the IKK complex, but not p90(rsk), is responsible for the in vivo phosphorylation

165 Moreover, a single substrate of MAPK, p90(Rsk), is sufficient to activate Bub1 in vitro and in

166 Moreover, one substrate of MAP kinase, p90(Rsk), is sufficient to mediate these effects during

167 The p90(rsk) isoform rapidly activated by insulin is identif

168 and p38 kinase, inhibited phosphorylation of p90(RSK), JNKs, and p38 kinase, but not ERKs.

169 endogenous FGF signaling, leads to decreased p90(rsk) kinase activity.

170 1 activation was independent of Akt, PKA, or p90RSK kinase activity.

171 The family of p90-kDa ribosomal S6 kinases (p90(RSK)/MAPKAP-K1) are activated via phosphorylation.

172 Our findings link p90Rsk-mediated modulation of Hdm2 nuclear to cytoplasmi

173 We propose that p90RSK-mediated SENP2-T368 phosphorylation is a master s

174 S signaling to LKB1 and RASGRP3, via ERK and p90RSK, might be involved in liver carcinogenesis and be

175 f MAPK signalling cascade proteins (ERK 1/2, p90RSK, Mnk 1, eIF4E, p38 MAPK, JNK/SAPK, MKP 1) at rest

176 onversely, the OM had a decrease in ERK 1/2, p90RSK, Mnk 1, p38 MAPK and JNK/SAPK phosphorylation (P

177 d higher resting phosphorylation of ERK 1/2, p90RSK, Mnk 1, p38 MAPK and JNK/SAPK proteins versus YM

178 hese 33 nucleotides were introduced into the p90(rsk-mo-1) cDNA, the expressed protein showed signifi

179 n of the 33-nucleotide region missing in the p90(rsk-mo-1) clone from the p90(rsk-rat-1) cDNA abolish

180 er species and suggests that the deletion in p90(rsk-mo-1) may be a cloning artifact.

181 dermal growth factor, the immunoprecipitated p90(rsk-mo-1) protein showed no measurable kinase activi

182 When p90(rsk-mo-1) was expressed in Cos-7 cells that were sub

183 The clone p90(rsk-mo-1), isolated by others from a mouse library,

184 As a result, unphosphorylated p90RSK no longer binds to nor inhibits CBP.

185 es mellitus, had effects similar to those of p90RSK on Kv4.3- or Kv4.3- and KChIP2-encoded channels.

186 ignificant activation of Erk1/Erk2 Kinase or p90Rsk only in the wt cells.

187 ve inhibitor of p38 kinase, had no effect on p90(RSK) or JNKs phosphorylation.

188 t on UVA-induced Ser(381) phosphorylation of p90(RSK) or kinase activity.

189 Overexpression of either p90RSK or an ERK5 fragment (aa571-807) inhibits ERK5/CHI

190 sc68376, the specific inhibitors for Erk1/2, p90RSK, or p38, respectively.

191 Instead, p90(rsk) overexpression increases the levels of beta-cat

192 e mice abolished the protective effect of DN-p90RSK overexpression.

193 RSK activity due to transgenic expression of p90RSK (p90RSK-Tg) had prolongation of QT intervals and

194 nd sustained activation of the MEK1/2-ERK1/2-p90RSK pathway, resulting in increased phosphorylation o

195 OSNs through Ca2+ activation of the ERK/MAPK/p90rsk pathway.

196 se results suggest that activation of ERK1/2-p90(RSK) pathways following in vitro ischemia phosphoryl

197 extracellular signal-regulated kinase (Erk)-p90RSK pathways independently to regulate S6 in an addit

198 p38 MAPK/MSK-1 and protein kinase C/p90RSK pathways mediate CREB phosphorylation.

199 ation via both Akt-mTOR-p70/85S6K and ERK1/2-p90RSK pathways.

200 ownstream effector, p90 ribosomal S6 kinase (p90RSK), phosphorylate transcription factors involved in

201 Moreover, purified p90(Rsk) phosphorylates Bub1 in vitro and increases its

202 inase (p90(RSK)) is a key NHE-1 kinase since p90(RSK) phosphorylates NHE-1 serine 703 stoichiometrica

203 UVA-induced p90(RSK) phosphorylation and kinase activity were marked

204 We provide evidence that UVA-induced p90(RSK) phosphorylation and kinase activity were time-

205 utant of JNK1 inhibited UVA-induced JNKs and p90(RSK) phosphorylation and kinase activity, but had no

206 ver, radiation-induced increases in CREB and p90RSK phosphorylation and activation of Stat3 and Egr-1

207 K1 phosphorylation, and decreased downstream p90Rsk phosphorylation and activity; yet ES cell prolife

208 ating Erk1/2 signaling, leading to increased p90RSK phosphorylation and the induction of immediate-ea

209 contained in putative consensus sequences of p90RSK phosphorylation sites, we hypothesized that p90RS

210 pathway including B-Raf kinase, ERK1/2, and p90RSK phosphorylation.

211 We hypothesize that FGF and p90(rsk) play heretofore unsuspected roles in modulating

212 We found that the inhibition of p90RSK prevented H2O2-mediated cTnI (Ser(23/24)) phospho

213 rotein levels, whereas constitutively active p90Rsk promoted the nuclear export of Hdm2.

214 missing in the p90(rsk-mo-1) clone from the p90(rsk-rat-1) cDNA abolished kinase activity in the res

215 e-polymerase chain reaction, indicating that p90RSK regulates voltage-gated K+ channels through postt

216 phosphorylation of the cytoplasmic substrate p90RSK remains unaltered.

217 ly active target of MAPK, the protein kinase p90(Rsk), restores the activation of Bub1 in the presenc

218 or its subsequent phosphorylation at Ser9 by p90RSK, resulting in inactivation of GSK-3beta and upreg

219 p42/44(MAPK) and also the phosphorylation of p90(RSK) (ribosomal subunit S6 kinase), which mirrored t

220 ibosomal S6 kinase 2 (RSK2), a member of the p90(RSK) (RSK) family of proteins, is a widely expressed

221 To determine whether this 90-kD kinase was p90rsk (RSK), VSMCs were stimulated with 100 nmol/L angi

222 channel activities in HEK 293 cells, whereas p90RSK's effects were blocked by amino acid mutation(s)

223 nism may be distinct from either p70(RSK) or p90(RSK)s.

224 These data indicate clearly that p90(RSK) Ser(381) may be phosphorylated by activation of

225 ant negative mutant of ERK2 blocked ERKs and p90(RSK) Ser(381) phosphorylation, as well as p90(RSK) a

226 the mitogen-activated protein kinase (MAPK)/p90(rsk) signaling cascade in a p53-independent fashion.

227 racellular signal-regulated protein kinase 1-p90(rsk) signaling pathway.

228 In addition, inactivation of ERK2/p90RSK signaling triggered by high SIRT6 levels increase

229 examined the ERK/90-kDa ribosomal S6 kinase (p90(RSK)) signaling pathways.

230 p90(RSK) stimulates binding of Bad to 14-3-3 and blocks

231 e p90rsk-activating kinase ERK-2 and a known p90rsk substrate, glycogen synthase kinase 3beta, which

232 lockade of Erk1/2 activation or knockdown of p90RSK suppressed tPA-induced GSK3beta phosphorylation,

233 5, Kv2.1, and KChIP2 from ventricles between p90RSK-Tg and nontransgenic littermate control mice were

234 We investigated the role of the RAS in WT-p90RSK-Tg animals after ischemia/reperfusion with the us

235 ia in non-Tg littermate controls, whereas DN-p90RSK-Tg animals exposed to streptozotocin did not have

236 ac function after ischemia/reperfusion in WT-p90RSK-Tg isolated mouse hearts was significantly impair

237 At 8 months of age, WT-p90RSK-Tg mice developed cardiac dysfunction.

238 ogen protein reduction after perfusion in WT-p90RSK-Tg mice, suggesting an increase of angiotensinoge

239 of prorenin-converting enzyme (PRECE) in WT-p90RSK-Tg mice.

240 cleavage and subsequent RAS activation in WT-p90RSK-Tg mice.

241 diac function and reduced infarct size in WT-p90RSK-Tg mice.

242 rent (I(SS)) were significantly decreased in p90RSK-Tg mouse ventricular myocytes.

243 ion of wild-type p90 ribosomal S6 kinase (WT-p90RSK-Tg) and a dominant-negative form of p90RSK (DN-p9

244 vity due to transgenic expression of p90RSK (p90RSK-Tg) had prolongation of QT intervals and of ventr

245 ) and a dominant-negative form of p90RSK (DN-p90RSK-Tg).

246 tivates p70(S6K) through effects on calcium, p90(RSK) through effects on protein kinase C.

247 -regulatory GSK-3 residue serine 9, we found p90(rsk) to be a potential upstream regulator of GSK-3.

248 dy, we determined whether H(2)O(2) activates p90RSK to gain insight into signal transduction mechanis

249 endent translocation of multifunction kinase p90rsk to polyribosomes; concomitantly, there is enhance

250 y-dependent translation via translocation of p90rsk to ribosomes.

251 Next, we generated cardiac-specific p90RSK transgenic mice and observed that cTnI (Ser(23/24

252 stigation of ERK and its downstream effector p90RSK, two putative NHE1 kinases, revealed time-depende

253 oss-linking and results in the activation of p90Rsk via a MAP kinase-independent pathway in DT40Lyn-

254 ted with p90(RSK) when stimulated by UVA and p90(RSK) was a substrate for ERK2 and JNK2, but not p38

255 p90(rsk) was also detected in the GM-CSF-dependent eryth

256 tion of mitogen-activated protein kinase and p90(RSK) was not inhibited but was enhanced by BAPTA-AM.

257 The ribosomal S6 kinase p90(rsk) was studied in mature and proliferating hemopoi

258 evation of free beta-catenin levels, ectopic p90(rsk) was unable to rescue dorsal cell fate in embryo

259 The phosphorylation and activation of p90Rsk was ablated in Syk-deficient B cells but unaffect

260 This effect was independent of Akt, ERK, or p90Rsk, well established kinases for Ser(112) in Bad.

261 s expressing a constitutively active form of p90(Rsk) were able to reaccumulate cyclin B, hyperphosph

262 but not p38 kinase, immunoprecipitated with p90(RSK) when stimulated by UVA and p90(RSK) was a subst

263 activity of the cytoplasmic target of ERKs, p90(RSK), which in turn phosphorylates the pro-apoptotic

264 ted by MAPK activation of the protein kinase p90(Rsk), which leads to inhibition of the APC.

265 effector of PKCs is p90 ribosomal S6 kinase (p90RSK), which plays an important role in cell growth by

266 f Src and ERK1/2 is p90 ribosomal S6 kinase (p90RSK), which plays an important role in cell growth by

267 CSF arrest is mediated by the protein kinase p90Rsk, which is phosphorylated and activated by MAPK, a

268 d-flow activated the serine/threonine kinase p90RSK, which subsequently phosphorylated threonine 368

269 d phosphorylation by kinases such as PKA and p90RSK, which transduce neurite outgrowth-promoting cues

270 Expression of constitutively active p90Rsk with E1A, oncogenic H-Ras, and hTERT resulted in

271 Activation of the LPAR/SRC/EGFR/MAPK/p90RSK/YB-1 axis leads to production of the EGFR ligand