ライフサイエンスコーパス: p70 S6 kinase

1 ase) and mammalian target of rapamydn (mTOR)-p70 S6 kinase .

2 not by rapamycin, which blocks activation of p70(S6 kinase).

3 ivated downstream of PI 3'-kinase, involving p70 S6 kinase.

4 te cross-regulated by rapamycin and IL-7 was p70 S6 kinase.

5 nd enhances the ability of Tiam1 to activate p70 S6 kinase.

6 PI3-kinase downstream effectors PKB/Akt and p70 S6 kinase.

7 n and regulate a growth checkpoint involving p70 S6 kinase.

8 e NEK6 interferes with insulin activation of p70 S6 kinase.

9 enous EDG-1 required G(i) activation but not p70 S6 kinase.

10 ovel candidate physiologic regulators of the p70 S6 kinase.

11 t not by a kinase-inactive mTOR mutant or by p70 S6 kinase.

12 mediates that link cell surface receptors to p70 S6 kinase.

13 ression of rat SGK, but not mouse PKB or rat p70 S6 kinase.

14 ositide 3-kinase with IRS-1 or activation of p70 S6 kinase.

15 uced regulation, thus suggesting the role of p70 S6 kinase.

16 the activity of its direct downstream target p70 S6 kinase.

17 eukin-2 receptor, the protooncogene PKB, and p70 S6 kinase.

18 enic potential, but did activate p21 RAS and p70 S6 kinase.

19 cluding Fyn, Lyn, p38, ERK1/2, JNK1/2/3, and p70 S6 kinase.

20 1, and LY2584702 (p70S6Ki), an inhibitor of p70 S6 kinase.

21 orylation of the transcription factor YY2 by p70 S6 kinase.

22 apamycin (mTOR) and downstream activation of p70 S6 kinase.

23 ld be blocked by inhibitors of PI3-kinase or p70 S6-kinase.

24 -1c processing is blocked by an inhibitor of p70 S6-kinase.

25 rylation of the ribosomal regulatory protein p70-S6 kinase.

26 tion of BAD on serine(112), or activation of p70(S6) kinase.

27 wn that curcumin inhibits phosphorylation of p70 S6 kinase 1 (S6K1) and eukaryotic initiation factor

28 ely active and rapamycin-resistant mutant of p70 S6 kinase 1 (S6K1) conferred to resistance to rapamy

29 We previously showed that genetic removal of p70 S6 kinase 1 (S6K1) corrects altered protein synthesi

30 apamycin complex 1 (mTORC1) and its effector p70 S6 kinase 1 (S6K1) in the extinction of auditory thr

31 the Akt-mammalian target of rapamycin (mTOR)-p70 S6 kinase 1 (S6K1) pathway.

32 tes the mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) signaling pathway and promotes ne

33 1 to promote protein synthesis by activating p70 S6 kinase 1 (S6K1).

34 get of rapamycin complex 1 (mTORC1) known as p70 S6 kinase 1 (S6K1).

35 p70 S6 kinase-1 is known to be a positive regulator of t

36 de-dependent protein kinase-1, as well as of p70 S6 kinase-1.

37 , and a 2.2-fold increase in the activity of p70 S6 kinase, a downstream effector of mTOR.

38 ore, polymerized collagen rapidly suppresses p70 S6 kinase, a possible regulator of p27Kip1.

39 erfering RNA knockdown of the mTOR substrate p70 S6 kinase abrogated PAK1 phosphorylation and enhance

40 Taken together, the data indicate that p70 S6 kinase activates PAK1 and contributes to phosphat

41 Thus, rapamycin inhibits p70 S6 kinase activation and liver regeneration, but not

42 annot bind to Tiam1 suppresses serum-induced p70 S6 kinase activation in cells, suggesting that a Tia

43 ed receptor on PI 3-kinase/Akt signaling and p70 S6 kinase activation using Rat-1 fibroblasts stably

44 p70 S6 kinase activation was blocked by wortmannin and r

45 tussis toxin treatment inhibited S1P-induced p70 S6 kinase activation, cyclin D1 expression and proli

46 otein translation, a biologic consequence of p70 S6 kinase activation.

47 nds on mammalian target of rapamycin and the p70 S6 kinase activities.

48 ectomy induced a transient increase in liver p70 S6 kinase activity and 4E-BP1 phosphorylation as com

49 g protein 1 (4E-BP1), resulting in decreased p70 S6 kinase activity and an increase in 4E-BP1 binding

50 sponse to S1P, concomitant with induction of p70 S6 kinase activity and expression of cyclin D1.

51 bility of glucocorticoids to inhibit Akt and p70 S6 kinase activity and reduced glucocorticoid induct

52 zing radiation caused a 2-3-fold increase in p70 S6 kinase activity that was blocked pharmacologicall

53 pendent Erb-B3 signaling also contributed to p70 S6 kinase activity through recruitment and activatio

54 DQA*03011 (DQ 65-79), and rapamycin inhibit p70 S6 kinase activity, but only DQ 65-79 blocks Akt kin

55 ffects of IFNs, imatinib mesylate suppressed p70 S6 kinase activity, consistent with inhibition of BC

56 on of PI3K, which has been shown to regulate p70 S6 kinase activity.

57 in response to activators and inhibitors of p70 S6 kinase activity.

58 tivation of mTOR and downstream induction of p70 S6 kinase activity.

59 d to Akt dephosphorylation and inhibition of p70 S6 kinase activity.

60 proliferation occurred despite inhibition of p70(s6) kinase activity.

61 Moreover, up-regulation of Drosophila p70/S6 kinase activity in DILP neurons led to attenuated

62 ed neoplastic proliferation, tumor size, and p70/S6 kinase activity, but did not affect the status of

63 ycin.FKBP12 complex in vitro can protect the p70 S6 kinase against rapamycin-induced dephosphorylatio

64 kinase activity, p110(CAAX) fully stimulated p70 S6 kinase, Akt, 2-deoxyglucose uptake, and Ras, wher

65 phobic motif site FXXFS/TF/Y, e.g.,Thr412 in p70 S6 kinase (alpha 1).

66 The p70 S6 kinase, an enzyme critical for cell-cycle progres

67 o signal to the raptor-dependent substrates, p70 S6 kinase and 4E-BP.

68 of eIF4F assembly and the phosphorylation of p70 S6 kinase and 4E-BP1 and that basal MEK activity is

69 rotein synthesis, and the phosphorylation of p70 S6 kinase and 4E-BP1 independently of both phosphati

70 Phosphorylation of p70 S6 kinase and 4E-BP1 is also repressed by PI3K inhib

71 by phosphorylation of the downstream targets p70 S6 kinase and 4E-BP1, and mTOR inhibition with rapam

72 ownstream components of the pathway, such as p70 S6 kinase and 4E-BP1, are poorly understood.

73 Furthermore, we have shown that p70 S6 kinase and 4EBP-1, downstream mediators of Akt si

74 ine kinase network stimulates cytoprotective p70 S6 kinase and Akt activity in response to clinically

75 cts of low dose ionizing radiation (2 Gy) on p70 S6 kinase and Akt signaling with respect to Erb-B re

76 growth factor I also commonly increased both p70 S6 kinase and choline kinase activities.

77 -IR cells results in a rapid deactivation of p70 S6 kinase and dephosphorylation of eIF-4E BP1, which

78 Although all three proteins (4E-BP1, p70 S6 kinase and eEF2) can be regulated through the mam

79 ycin-induced dephosphorylation, and for both p70 S6 kinase and eIF-4E BP1, such protection requires t

80 We identify central p70 S6 kinase and Erk1/2 pathways as intracellular effec

81 oposide led to the dephosphorylation of both p70 S6 kinase and eukaryotic initiation factor (eIF) 4E-

82 osphorylation of two translation modulators, p70 S6 kinase and eukaryotic initiation factor 4E-bindin

83 3'-kinase pathway mediates activation of the p70 S6 kinase and inactivation of 4E-BP1, to regulate mR

84 ndicated by the decreased phosphorylation of p70 S6 kinase and of 4EBP1.

85 t in healthy kidney, whereas, phosphorylated p70 S6 kinase and p56 were present only in angiomyolipom

86 PDK1 mediates activation of PKB, p70 S6 kinase and p90 Rsk in vivo, but is not rate-limit

87 In PDK1(-/-) ES cells, PKB, p70 S6 kinase and p90 Rsk were not activated by stimuli

88 ), and the p70 and p90 ribosomal S6 kinases (p70 S6 kinase and p90 Rsk, respectively), are activated

89 glutathione S-transferase fusion proteins of p70 S6 kinase and PAK3 each isolated PP2A; and 3) PAK3 a

90 ctivating PKB and PKC isoenzymes, as well as p70 S6 kinase and perhaps PKA.

91 e initiation of protein synthesis, including p70 S6 kinase and PHAS-I, in synergy with insulin.

92 wo intermediates controlling translation are p70 S6 kinase and PHAS-I.

93 Insulin elicited full activation of p70 S6 kinase and phosphorylation of 4E-PB1 in etoposide

94 lation of AKT, 4E-BP1, eIF2alpha, AMPKalpha, p70 S6 kinase and rpS6 in muscle homogenates.

95 to be accompanied by a strong activation of p70 S6 kinase and the mitogen-activated protein kinase (

96 -kinase-mediated DNA synthesis requires both p70 S6 kinase and the P21ras/MEK pathway.

97 two other downstream effectors of PI3K, the p70 S6 kinase and the repressors of mRNA translation, 4E

98 ases revealed that PP2A co-precipitated with p70 S6 kinase and the two PAK isoforms; 2) glutathione S

99 cross-linked PP2A revealed an enrichment of p70 S6 kinase and two p21-activated kinases (PAK1 and PA

100 en stimulates translation by phosphorylating p70 S6 kinase and, consequently, the 40 S ribosomal prot

101 essive effect is due to dephosphorylation of p70 S6 kinase and/or 4E-BP1.

102 ergoes ordered C-terminal phosphorylation by p70 S6 kinases and p90 ribosomal S6 kinases on four cons

103 target of rapamycin complex 1 as assessed by p70 S6-kinase and 4E-BP1 phosphorylation.

104 ere it could activate its substrates such as p70 S6-kinase and p90 ribosomal S6 kinase that do not in

105 ing of the actin cytoskeleton, activation of p70(S6) kinase and c-jun N-terminal kinase (JNK), and re

106 eukaryotic translation regulators, including p70-S6 kinase and the eukaryotic translation initiation

107 he translational regulatory proteins 4E-BP1, p70 S6 kinase, and eIF-4E, thus providing a mechanism fo

108 o associated with reduced activation of Akt, p70 S6 kinase, and extracellular regulated kinase signal

109 l showed increased nuclear levels of phospho-p70 S6 kinase, and neurons protected with DRB and flavop

110 show constitutive phosphorylation of Akt, of p70 S6 kinase, and of the 4E-binding protein 1.

111 ase family including protein kinase B (Akt), p70 S6 kinase, and protein kinase Czeta.

112 creases in protein synthesis, phosphorylated p70 S6 kinase, and ribosomal S6 protein levels as well a

113 gulation of CYP2E1 and implicate PI3-kinase, p70 S6 kinase, and Src kinase in mediating these effects

114 s to see whether there is phosphorylation of p70 S6 kinase, and the ribosomal S6 protein in angiomyol

115 k1/2, insulin-like growth factor receptor-1, p70 S6 kinase, and transforming growth factor alpha comp

116 n with spinophilin, a scaffold that binds to p70 S6 kinase, another protein regulated by Rac.

117 p70 S6 kinase, another signaling component downstream of

118 BrdU incorporation, coinjection with an anti-p70 S6 kinase antibody effectively blocked anti-NSH2-sti

119 c initiation factor 4E binding protein-1 and p70 S6 kinase are early events that control the translat

120 ude the mitogen-activated protein kinase and p70 S6 kinase, are discussed.

121 its downstream signaling molecules, Akt and p70 S6 kinase, are required, albeit to varying degrees.

122 r-308, and concurrently activated downstream p70 S6 kinase as well as glycogen synthase kinase-3beta.

123 cruited by Pl 3-kinase for the activation of p70 S6 kinase as well as of PKB, and serves as a multifu

124 otently inhibited PDGF-induced activation of p70 S6 kinase as well as proliferation of smooth muscle

125 d levels of phosphorylated Akt and activated p70/S6 kinase associated with an increase in proliferati

126 IGF1 did not induce phosphorylation of p70 S6 kinase at its hydrophobic motif in PDK1(-/-) cell

127 Recombinant NEK6 phosphorylates p70 S6 kinase at Thr412 and other sites and activates th

128 Cdc42Hs, the Jun NH2-terminal kinase and the p70 S6 kinase, became activated.

129 A novel ribosomal S6 kinase, termed p70 S6 kinase beta (p70beta), which has a highly conserv

130 and PAK3 each isolated PP2A; and 3) PAK3 and p70 S6 kinase bound to microcystin-Sepharose (an affinit

131 in, VacA did not suppress phosphorylation of p70 S6 kinase but caused mitochondrial depolarization an

132 ha(1)-adrenergic receptor agonist, activated p70 S6 kinase but did not activate PI 3-kinase or any of

133 nsulin-like growth factor 1, which activates p70 S6 kinase but not Erk, regulation of eEF2 is blocked

134 ar or lower levels and activity of ribosomal p70 S6 kinase, but c-Myc levels were elevated in both re

135 In addition, extra Ca2+ activated p70 S6 kinase by a zinc-dependent mechanism and enhanced

136 Inhibition of 1) p70 S6 kinase by rapamycin, 2) protein kinase B by Akt i

137 These results demonstrate that activation of p70 S6 kinase by the alpha(1A)-adrenergic receptor in Ra

138 with Shc and activation of MAPK, but not the p70 S6 kinase, could be stimulated by epidermal growth f

139 nases activated by IL-2, MAP kinase/ERK2 and p70 S6 kinase, do not appear to be involved in STAT5 reg

140 Surprisingly, the slow activation of p70 S6 kinase during differentiation was not only preven

141 The proteins eIF-4E BP1 and p70 S6 kinase each undergo an insulin/mitogen-stimulated

142 creases in the phosphorylation of 4E-BP1 and p70 S6 kinase, eIF4F assembly, and protein synthesis.

143 PDK1 phosphorylates the hydrophobic motif of p70 S6 kinase either directly or by activation of anothe

144 ssion of p85 alpha PI3K followed by enhanced p70(S6) kinase, essential to protein synthesis.

145 rterial wall also stimulated the activity of p70 S6 kinase from 30 minutes to 12 hours, suggesting an

146 SCs in addition to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6

147 ile inhibitors of MEK, protein kinase C, and p70 S6 kinase had a modest effect or no effect on NF-kap

148 nM; 60 min), which blocks the activation of p70 S6 kinase, had no effect.

149 e major protein kinase that is active on the p70 S6 kinase hydrophobic regulatory site, Thr412, was p

150 d rapamycin, consistent with PI3K, mTOR, and p70 S6 kinase in a linear pathway.

151 horylation of mTOR and its downstream target p70 S6 kinase in a PKC-delta- and PI3K/Akt-dependent man

152 ignaling molecules forkhead box O (FOXO) and p70 S6 kinase in a tissue and blood meal-specific manner

153 In contrast, the acute activation of p70 S6 kinase in C2C12 myoblasts induced by phorbol este

154 Rapamycin blocked the activation of p70 S6 kinase in response to partial hepatectomy in a do

155 PKB signals are sufficient for activation of p70 S6 kinase in T cells.

156 at Thr412 and other sites and activates the p70 S6 kinase in vitro and in vivo, in a manner synergis

157 y mitogen-activated protein kinase, Akt, and p70(S6) kinase in response to insulin.

158 eveals a prominent role of neural Drosophila p70/S6 kinase in the modulation of hunger response by in

159 By contrast, rapamycin, a p70 S6-kinase inhibitor, did not rescue immature B cells

160 Upon mu-opioid receptor stimulation, p70 S6 kinase is activated and phosphorylated at threoni

161 The p70 S6 kinase is activated by diverse stimuli through a

162 proliferation, suggesting that activation of p70 S6 kinase is critical in EDG-1/G(i)-mediated cell pr

163 Because p70 S6 kinase is known to induce translation of mRNAs co

164 The p70 S6 kinase, like several other AGC family kinases, re

165 the LKB1/AMPK/TSC1/2 pathway alleviates the p70 S6 kinase-mediated negative regulation of insulin si

166 tream regulator of eIF-4E BP1 as well as the p70 S6 kinase; moreover, these two mTOR targets are regu

167 and increased ribosomal antigen and phospho-p70 S6 kinase, occurred early in the course of acute vas

168 e whether inhibition of either the ribosomal p70 S6 kinase or eukaryotic initiation factor (eIF) 4E p

169 t upstream of mTOR, persistent inhibition of p70 S6 kinase or S6K1 can activate Akt via a negative fe

170 does not require the activation of PAK, JNK, p70 S6 kinase, or Rho, but instead requires phosphatidyl

171 -induced decreases in mTOR-regulated phospho-p70 S6 kinase (P-p70) and the p62 protein, as well as in

172 This activation of the mTOR/p70 S6 kinase (p70 S6K) pathway in response to ATP is be

173 We have previously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activa

174 p70 S6 kinase (p70(S6K)) activity was also reduced.

175 de that modulates translation initiation via p70 S6 kinase (p70(s6k)) and eIF-4E binding protein 1 (4

176 icated by the FK1012-dependent activation of p70 S6 kinase (p70(S6k)) and mitogen-activated protein (

177 he increased phosphorylation in dendrites of p70 S6 kinase (p70(S6K)) at Thr3889, a major regulator o

178 Activation of p70 S6 kinase (p70(S6K)) by growth factors requires mult

179 Here, we disrupted the p70 S6 kinase (p70(s6k)) gene in murine embryonic stem c

180 The carboxyl terminus of p70 S6 kinase (p70(s6k)) has a set of Ser and Thr residu

181 racellular signal-regulated kinase (ERK) and p70 S6 kinase (p70(S6k)) in the NO-induced increase in p

182 r growth factor-dependent phosphorylation of p70 S6 kinase (p70(S6K)) in vitro, and we demonstrate th

183 p70 S6 kinase (p70(S6k)) is a mitogen-activated protein

184 The p70 S6 kinase (p70(S6k)) is a Ser/Thr kinase that plays

185 pathways to investigate the contribution of p70 S6 kinase (p70(S6K)) to Rac1 transformation and to d

186 rapamycin, an inhibitor of the activation of p70 S6 kinase (p70(S6k)), completely abolished IGF stimu

187 luding rapamycin, which blocks activation of p70 S6 kinase (p70(S6k)), PD98059, which inhibits the ac

188 kinases downstream from PI-3 kinase, Akt and p70 S6 kinase (p70(S6K)), was decreased in cells express

189 ylation and inactivation of their substrate, p70 S6 kinase (p70(S6k)).

190 edly inhibited activation of PI-3K, Akt, and p70 S6 kinase (p70(S6k)).

191 sphatidylinositol 3-kinase (PI-3K), Akt, and p70 S6 kinase (p70(S6k)).

192 inhibitor p27(Kip1) (p27) and inhibition of p70 s6 kinase (p70(s6k)).

193 ivates phosphoinositide 3-kinase (PI3-K) and p70 S6 kinase (p70S6K) and that rapamycin, a FRAP/mammal

194 togen-activated protein kinases, implicating p70 S6 kinase (p70S6k) as the relevant mediator.

195 om apoptosis, without reactivating ribosomal p70 S6 kinase (p70S6K) downstream of mTOR.

196 scovered role of the mTOR complex 1 (mTORC1)/p70 S6 kinase (p70S6K) in the negative regulation of PD-

197 p70 S6 kinase (p70s6k) is a serine/threonine kinase whic

198 p70 S6 kinase (p70S6K) is an important regulator of cell

199 p70 S6 kinase (p70S6K) plays an important role in protei

200 ination required phosphorylation of TRIB2 by p70 S6 kinase (p70S6K) via another domain (amino acids 6

201 crease of the TPA-induced phosphorylation of p70 S6 kinase (p70S6K), a protein kinase involved in the

202 of its downstream target, ribosomal protein p70 S6 kinase (p70S6K), and concomitant inhibition of ce

203 rphosphorylation, constitutive activation of p70 S6 kinase (p70S6K), and increased basal DNA synthesi

204 the protein-serine/threonine kinases Akt and p70 S6 kinase (p70S6K), are crucial effectors in oncogen

205 le protein regulated by insulin (PHAS-I) and p70 S6 kinase (p70S6k), in an insulin-independent and ra

206 ond, we observed that Thr-389-phosphorylated p70 S6 kinase (p70S6K), the main active phosphoform of t

207 volve the cell signaling molecule, ribosomal p70 S6 kinase (p70S6K).

208 ets of rapamycin, resulting in inhibition of p70 S6 kinase (p70S6K).

209 tors, the eIF4E-binding protein (4E-BP1) and p70 S6 kinase (p70S6K).

210 osphotidylinositol 3-kinase (PI-3K), Akt and p70 S6 kinase (p70S6k).

211 rovide evidence for association of PP2A with p70 S6 kinase, PAK1, and PAK3 in the context of the cell

212 was unaffected by rapamycin, an inhibitor of p70 S6 kinase pathway but abolished by the PI3K inhibito

213 her the mammalian target of rapamycin (mTOR)/p70 S6 kinase pathway is activated by RA.

214 the mammalian target of rapamycin complex 1-p70 S6 kinase pathway, a known growth regulatory pathway

215 red for IFN-inducible engagement of the mTOR/p70 S6 kinase pathway.

216 n of BCR-ABL-mediated activation of the mTOR/p70 S6 kinase pathway.

217 on of the PI3-kinase/mTOR Complex 1 (mTORC1)/p70 S6-kinase pathway.

218 , the most downstream target of the Akt-mTOR-p70-S6 kinase pathway, is a frequent event in clinical s

219 ctivated protein kinase, leaving the Akt and p70 S6 kinase pathways unperturbed.

220 t phosphorylation, concurrently with reduced p70 S6 kinase phosphorylation at Thr389 as well as IRS-1

221 Furthermore, blocking p70 S6 kinase phosphorylation with rapamycin inhibited c

222 n or LY294002 and rapamycin, an inhibitor of p70 S6 kinase phosphorylation, ameliorated the insulin-m

223 ipocytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 transloc

224 locked SCF- and/or SDF-1alpha-induced Akt or p70 S6 kinase phosphorylation.

225 ediated modulation of B7-H2 on GECs involves p70 S6 kinase phosphorylation.

226 ses, including protein kinase B (PKB)/c-Akt, p70 S6 kinase, PKC isoforms, and serum- and glucocortico

227 ion factor 4E (eIF4E)-eIF4G interactions and p70 S6 kinase polypeptide 1 (S6K1) in reconsolidation.

228 or rapamycin (which blocks the activation of p70 S6 kinase) prevented the formation of multinucleated

229 The amount of p70 S6 kinase protein in regenerating liver did not incr

230 though H(2)O(2) increased phosphorylation of p70 S6 kinase, rapamycin failed to inhibit H(2)O(2) from

231 inase family; we show that two such kinases, p70 S6 kinase (regulated via mTOR) and p90(RSK1) (activa

232 t a Tiam1/spinophilin complex contributes to p70 S6 kinase regulation by extracellular signals.

233 In contrast, mutants of p70 S6 kinase rendered intrinsically resistant to inhibi

234 and rapamycin, which inhibit MAP kinase and P70 S6 kinase, respectively, had little effect on the in

235 le, with persistent phosphorylation of mTOR, p70 S6 kinase, ribosomal protein S6, and 4EB-P1; decreas

236 diators of PI 3-kinase, the serine/threonine p70 S6-kinase (S6-kinase) and the antiapoptotic protein

237 a mouse model of liver-specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of a

238 We found that dasatinib reduced p70 S6 kinase (S6K) and ribosomal protein S6 (S6), leadi

239 isoforms largely independently of its target p70 S6 kinase (S6K) by increasing the activity of the se

240 Prolonged activation of p70 S6 kinase (S6K) by insulin and nutrients leads to in

241 mitogen-activated protein kinase (MAPK) and p70 S6 kinase (S6K) in these cells.

242 nt phosphorylation is mediated by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RS

243 n a cell type-specific manner, by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RS

244 osphorylation, mTOR-Raptor interactions, and p70 S6 kinase (S6K) phosphorylation.

245 Here, we show that p70 S6 kinase (S6k), acting downstream of the insulin re

246 ssociated protein kinases (ROCK1 and ROCK2), p70 S6 kinase (S6K), and mammalian target of rapamycin (

247 ylation of eIF4E-binding protein (4E-BP) and p70 S6 kinase (S6K), which is important for maintaining

248 heb-induced activation of the mTOR substrate p70 S6 kinase (S6K).

249 substrate of p90 ribosomal kinase (RSK) and p70 S6 kinase (S6K).

250 mTOR complex 1 (mTORC1) and p70 S6 kinase (S6K1) are both involved in the developmen

251 Phosphorylation of this motif (FLGFT389Y) in p70 S6 kinase (S6K1) is both rapamycin- and wortmannin-s

252 p70 S6 kinase (S6K1) plays a central role during nutriti

253 the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-specific manner.

254 RNA interference-mediated knockdown of TSC2, p70 S6 kinase (S6K1), raptor, or rictor demonstrates tha

255 ukaryotic initiation factor 4E and ribosomal p70 S6 kinase (S6K1).

256 ble knock-out cells for both isoforms of the p70 S6 kinase (S6k1/S6k2), a downstream effector of Akt

257 A putative downstream target of Akt, p70 S6 kinase, showed similar changes in mobility in res

258 stimulate the phosphorylation of PHAS-I and p70(s6) kinase, suggesting that the mammalian target of

259 sphorylation of tau can be regulated through p70 S6 kinase, the well characterized immediate downstre

260 nt led to decreased levels of phosphorylated p70 S6 kinase (Thr(389)) in gallbladder tissue as assess

261 (Ser-2448 and Ser-2481), phosphorylation of p70 S6 kinase (Thr-389), and ribosomal protein S6 (Ser-2

262 mplex acts to dephosphorylate/deactivate the p70 S6 kinase; thus, some mTOR mutants that have lost th

263 tiation factor 4E-binding protein (4EBP) and p70 S6 kinase to promote protein synthesis and cell size

264 ch as the translational regulators 4E-BP and p70 S6 kinase, to the TOR catalytic domain is essential

265 parallel insulin response pathways including p70 S6 kinase, ubiquitin ligase Cbl, or mitogen-activate

266 ity was determined as the phosphorylation of p70 S6 kinase, using Western blotting.

267 ant activation of an inhibitory pathway, but p70 S6 kinase was activated by osmotic stress.

268 ated, its ability to cause activation of the p70 S6 kinase was also controlled by the p70 carboxy-ter

269 The RA-dependent activation of p70 S6 kinase was also phosphatidylinositol 3' kinase (P

270 th this, thrombin-induced phosphorylation of p70 S6 kinase was defective in embryonic fibroblasts fro

271 The IFN-activated p70 S6 kinase was found to regulate phosphorylation of S

272 Such phosphorylation/activation of p70 S6 kinase was inducible in primary acute promyelocyt

273 sphorylation of downstream molecules Akt and p70 S6 kinase was inhibited.

274 eas SDF-1alpha-mediated activation of Akt or p70 S6 kinase was normal.

275 However, phosphorylation of p70 S6 kinase was observed in the liver of all three phe

276 tion with Shc and activation of MAPK and the p70 S6 kinase were insensitive to insulin stimulation.

277 n of known Phlpp1 substrates, Akt2, PKC, and p70 S6 kinase, were enhanced in ex vivo cultured Phlpp1(

278 its substrate mTOR, and the mTOR substrate, p70 S6 kinase, were indeed reduced in Hdac3-deficient pr

279 eukaryotic translation initiation factor and p70 S6 kinase, were up-regulated following NO treatment,

280 reviously to engender some activation of the p70 S6 kinase, whereas both modifications together produ

281 ibited the c-Kit signaling events of Akt and p70 S6 kinase, whereas SDF-1alpha-mediated activation of

282 ion of processing requires the mTORC1 target p70 S6-kinase, whereas induction of mRNA bypasses this e

283 y a dose-dependent activation of Akt/PKB and p70(S6) kinase, whereas the MAP kinase pathway was unaff

284 increased phosphorylation and activation of p70 S6 kinase, which was inhibited by both DRB and flavo