ライフサイエンスコーパス: p70S6K

1 p70S6K activation by CNTO 530, however, was selectively

2 p70S6K phosphorylation in CD4+CD25(hi) Tregs was signifi

3 p70S6K regulates protein synthesis, proliferation, and c

4 p70S6K was primarily cleaved at a noncanonical recogniti

5 p70S6K(Thr389) phosphorylation increased at 4 h post-exe

6 otic initiation factor 4E-binding protein-1, p70S6K, and ribosomal protein S6, are highly phosphoryla

7 d known targets of mTORC1 (p-mTOR Ser(2448), p70S6K, p-S6, p4EBP1) and mTORC2 (p-mTOR Ser(2481), p-AK

8 on of Bcl-2 antagonist of cell death, 4EBP1, p70S6K, and S6, as well as increases in cleaved caspase

9 target of rapamycin (mTOR) effectors 4EBP1, p70S6K, and rpS6, independent of HIF.

10 -7) M) increased Akt/mTOR/Raptor to activate p70S6K and increase proliferation, viability, and apopto

11 of dendritic spines also displayed activated p70S6K.

12 ing indicates that PA binds to and activates p70S6K, even in the absence of mTOR.

13 reases VEGF protein production by activating p70S6K in cell lines, xenografts, and in human cancers a

14 Additionally, p70S6K co-precipitated with PKC-eta, suggesting a physic

15 the presence of rapamycin without affecting p70S6K or ERK activation.

16 s common to those generated in vitro by AKT, p70S6K, MEK1, and MKK6, suggesting that these kinases ma

17 of Raf-1, inactivation of MEK1/2, ERK, Akt, p70S6K, dephosphorylation of GSK-3, and activation of c-

18 Many AGC-family kinases (AKT, p70S6K, PKC, ROCK1) seem to be regulated similarly.

19 The cooperative effects of thrombin on Akt/p70S6K phosphorylation and [(3)H]thymidine incorporation

20 of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1alpha protein transl

21 ation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nicke

22 vivo (P<0.05).However, genetically altering p70S6K activity had no impact on eIF2Bepsilon protein ab

23 lation through phosphorylation of 4EBP-1 and p70S6K.

24 protein kinasealpha (AMPKalpha)-Thr(172) and p70S6K-Thr(389), both PP2A substrates, were also increas

25 77), eNOS-Thr(495), PKC-betaII-Ser(660), and p70S6K-Ser(411) was evaluated.

26 ANG II induced phosphorylation of Akt and p70S6K and EGFR, which was abrogated by knockdown of c-S

27 incorporation as well as late-phase Akt and p70S6K phosphorylation in ASM cultures.

28 phospho-S6RP and increased levels of Akt and p70S6K phosphorylation, upstream positive regulators of

29 Indeed, phosphorylation of both Akt and p70S6K proteins was decreased as well as the activation

30 and activation of p38 MAPK, ERK1/2, Akt, and p70S6K proteins.

31 in phosphorylated p38 MAPK, ERK1/2, Akt, and p70S6K were observed.

32 phosphorylation of JNK, p38 kinase, Akt, and p70S6K, was significantly enhanced in p53-deficient cell

33 lar regulators including AKT, AMPKalpha, and p70S6K.

34 phorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicati

35 f stress activate mTOR leading to 4E-BP1 and p70S6K phosphorylation.

36 reased phosphorylations of mTOR, 4E-BP1, and p70S6K at late times in infection (48 h postinfection [h

37 chain reaction showed that mTOR, 4E-BP1, and p70S6K mRNA are expressed in the DRG and dorsal horn.

38 of Akt, endothelial NO synthase (eNOS), and p70S6K were determined.

39 the prosurvival kinases PI3K-Akt, eNOS, and p70S6K in accordance with the RISK pathway.

40 ncrease in phosphorylation of Akt, eNOS, and p70S6K in an LY- and Wort-sensitive manner.

41 g a physical interaction between PKC-eta and p70S6K regulates the observed phosphorylation.

42 sphorylation of HSP27, p38, ERK1/2, FAK, and p70S6K was induced substantially already at lower exposu

43 , leading to activation of AKT, GSK3beta and p70S6K.

44 esting that troglitazone inhibited IGF-I and p70S6K signaling through activation of AMPK.

45 activation of Akt, AMPK (only in males) and p70S6K kinases.

46 he upregulation of activated p44/42 MAPK and p70S6K (Thr 421/Ser 424).

47 ed upregulation of activated p44/42 MAPK and p70S6K.

48 Immunohistochemistry revealed mTOR and p70S6K in the DRG neurons.

49 tivation of phosphorylation of Akt, mTOR and p70S6K in the kidney after HIR.

50 increases in protein synthesis and mTOR and p70S6K phosphorylation.

51 t, mammalian target of rapamycin (mTOR), and p70S6K.

52 wnstream targets GSK-3beta, FOXO1, mTOR, and p70S6K.

53 of p27(kip1), FRKHL-1, MDM2, Bad, mTOR, and p70S6K.

54 6RP and constitutively active Akt, mTOR, and p70S6K.

55 Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.

56 creased phosphorylation of phospholamban and p70S6K.

57 sustained late-phase activation of PI3K and p70S6K via a pathway dependent on Gbetagamma subunits of

58 /arrestin-independent activation of PI3K and p70S6K.

59 inases, including protein kinase B (PKB) and p70S6K, whereas mTOR activity remains largely unaffected

60 1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.

61 mammalian target of rapamycin (mTOR), S6 and p70S6K and increased proliferation rates compared with w

62 HG increased phosphorylation of tuberin and p70S6K, phosphorylation of Bcl-2, expression of cytosoli

63 h GM-CSF-dependent migration, and attenuated p70S6K phosphorylation.

64 substrates, including FoxO1, GSK3alpha/beta, p70S6K, AS160, and the E3 ubiquitin ligase MDM2.

65 Both p70S6K enzymatic activity and T(421)/S(424) and T(389) p

66 ty of TRIB2 may be due to the fact that both p70S6K and Smurf1 were down-regulated and negatively cor

67 initiation factor 4E-binding protein (4E-BP)-p70S6K and nuclear factor-kappaB were critical for proli

68 l as PDGF-BB-induced ERK/CREB and mTOR/4E-BP-p70S6K activation, thereby underscoring its role in this

69 horylation of mTOR and its effectors 4E-BP1, p70S6K, rpS6, and eukaryotic initiation factor 4G.

70 ssociation with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increase

71 e in MRE11 that we show is phosphorylated by p70S6K in vitro.

72 paired phosphorylation and ubiquitination by p70S6K and Smurf1 increase the protein stability of TRIB

73 4 failed to alter the profile of cooperative p70S6K T389 phosphorylation, p70S6K kinase activity, or

74 that constitutive activation of cytoplasmic p70S6K plays a pivotal role in the pathogenesis of TSC t

75 1) containing mTOR and raptor with decreased p70S6K, 4EPB1 phosphorylation, and GLUT1 mRNA, but also

76 cepsilonRI- and Kit-induced mTORC1-dependent p70S6K phosphorylation and partially blocked the 4E-BP1

77 Mutation of Ser-83 diminished p70S6K-induced phosphorylation of TRIB2.

78 main active phosphoform of the mTOR effector p70S6K, was induced in an N-methyl-D-aspartate and phosp

79 biological pathways including the EIF2, eIF4/p70S6K, mTOR signaling and mitochondrial dysfunction pat

80 fferentially expressed genes included ezrin, p70S6K, and PKCs, which are known to have key roles in K

81 s) and CD4(+)CD25- T cells were analyzed for p70S6K phosphorylation.

82 mTOR and 19.1% (+/- 1.9%) were positive for p70S6K.

83 VEGF expression, showed significantly higher p70S6K phosphorylation as well.

84 Inhibitors of mTOR, PI3K, and Ca(++) impair p70S6K activity, whereas inhibitors of JNK and PKC stimu

85 and threonine residues are phosphorylated in p70S6K following treatment with paclitaxel.

86 om the MEK/MAPK pathway also plays a role in p70S6K activation.

87 ma from patients with PAH failed to increase p70S6K activation or to induce cell survival in vitro Op

88 atter condition was accompanied by increased p70S6K activity and phosphorylation.

89 mplexed to raptor) as indicated by increased p70S6K and 4E-BP1 phosphorylation, and activation of mTO

90 nally, patients with tumors having increased p70S6K phosphorylation showed a trend for worse disease-

91 In summary, paclitaxel is able to induce p70S6K(T421/S424) phosphorylation and decrease its activ

92 diated Gbeta1 knockdown, while IGF-1-induced p70S6K activation is markedly suppressed following trans

93 Rapamycin did not inhibit insulin induced p70S6K phosphorylation and activity in cells transfected

94 n of PKC and JNK prevents paclitaxel-induced p70S6K inactivation.

95 Our data suggest that paclitaxel-induced p70S6K(T421/S424) phosphorylation and kinase inactivatio

96 Paclitaxel-induced p70S6K(T421/S424) phosphorylation requires both de novo

97 C proliferation, did not affect PDGF-induced p70S6K phosphorylation.

98 Insulin treatment induced p70S6K, mTOR, and Akt phosphorylation, effects that were

99 he immunosuppressant FK506 failed to inhibit p70S6K activation, but was able to rescue the rapamycin-

100 d forms of mTOR and of its downstream kinase p70S6K, which indicated mTOR pathway activation.

101 ys that lead to activation of protein kinase p70S6K and to the serine phosphorylation of IRS-1.

102 apamycin despite a decrease of p70S6 kinase (p70S6K) activation by the drug in response to both cytok

103 on of its substrates including p70S6 kinase (p70S6K) and 4E-BP1 was decreased.

104 Here we clarify the role of p70S6 kinase (p70S6K) as an integrator of receptor tyrosine kinase and

105 F-I-induced phosphorylation of p70S6 kinase (p70S6K) at Thr(389), a site specifically phosphorylated

106 the detection of the ribosomal p70S6 kinase (p70S6K) in a hematopoietic cell, the neutrophil, and the

107 sphorylation of tuberin, mTOR, p70S6 kinase (p70S6K), and 4E-BP1.

108 stored by inhibiting mTORC1 or p70S6 kinase (p70S6K), downstream kinases whose activities are stimula

109 TOR) and its downstream target p70S6 kinase (p70S6K).

110 tion of a third mTOR effector, p70S6 kinase (p70S6K).

111 ylation and p70 ribosomal S6 protein kinase (p70S6K) phosphorylation and kinase activity.

112 of the ribosomal protein S6 protein kinase (p70S6K), a protein synthesis regulator, in promoting ret

113 (4E-BP1/2), p70 ribosomal S6 protein kinase (p70S6K), and their phosphorylated (active) counterparts

114 targets, 70-kDa ribosomal protein S6 kinase (p70S6K) and eukaryote initiation factor 4E binding prote

115 tivation of the ribosomal protein S6 kinase (p70S6K) and its downstream target, ribosomal protein S6

116 ycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K) and the extracellular signal-regulated kinases 1

117 n of the 70 kDa ribosomal protein S6 kinase (p70S6K) in the basal state and following insulin treatme

118 The 70-kDa ribosomal S6 kinase (p70S6K) is activated by mitogens, growth factors, and ho

119 The 70 kDa ribosomal S6 kinase (p70S6K) is important for cell growth and survival.

120 apamycin (mTOR)/ribosomal protein S6 kinase (p70S6K) pathway is considered a central regulator of pro

121 p70 S6 kinase (p70S6K) plays an important role in protein translation a

122 d phosphorylation of TRIB2 by p70 S6 kinase (p70S6K) via another domain (amino acids 69-85) that is a

123 eam target, ribosomal protein p70 S6 kinase (p70S6K), and concomitant inhibition of cell growth.

124 n, constitutive activation of p70 S6 kinase (p70S6K), and increased basal DNA synthesis.

125 nstream pathways of p70 ribosomal S6 kinase (p70S6K), eukaryotic initiation factor 4E-binding protein

126 d that Thr-389-phosphorylated p70 S6 kinase (p70S6K), the main active phosphoform of the mTOR effecto

127 -binding protein (4E-BP1) and p70 S6 kinase (p70S6K).

128 signaling molecule, ribosomal p70 S6 kinase (p70S6K).

129 nockdown of mTOR or p70 ribosomal S6 kinase (p70S6K, an effector of mTOR).

130 h by negatively regulating a protein kinase, p70S6K (S6K1), which generally requires PI3K signals for

131 pendent decrease in the level of full-length p70S6K in small cell lung cancer H69 and non-small cell

132 ressing cells stimulated with PMA maintained p70S6K phosphorylation on Thr389 and phosphorylation of

133 (which encodes the worm homolog of mammalian p70S6K) is required germline-autonomously for proper est

134 on of thrombin receptors and the p44/42 MAPK/p70S6K pathway.

135 ell proliferation mainly via FKBP12-mediated p70S6K activation.

136 d that this effect is independent of ras-MEK/p70S6K-eEF2K signaling cascades.

137 etic manipulation of the downstream molecule p70S6K specifically blocked BDNF rescue.

138 nstream mammalian target of rapamycin (mTOR)-p70S6K signalling and decreased activity of the forkhead

139 ts downstream signaling molecules Akt, mTOR, p70S6K, ERK and JNK increased markedly in 50% but not 30

140 The results indicate that although mTOR, p70S6K, and 4E-BP1 are highly expressed in the DRG and d

141 otein synthesis (Akt1, GSK3alpha,beta, mTOR, p70S6K and 4E-BP1) was observed in patients, which was p

142 In the dorsal horn, mTOR, p70S6K, and 4E-BP1 were detected in neurons, but not in

143 tion (48 hpi), the phosphorylations of mTOR, p70S6K, and 4E-BP1 are dramatically decreased by a mecha

144 lels the negative feedback loop between mTOR-p70S6K and IRS-1 that mediates rapamycin-directed IGF-IR

145 luate the possible roles of the Akt/PKB-mTOR-p70S6K-S6 and cap-dependent translation (eIF4G) pathways

146 e-dependent dendritic activation of the mTOR-p70S6K pathway is necessary for the induction phase of p

147 ase activities accompanied by activated mTOR/p70S6K signaling at varying levels, demonstrating the ga

148 ants in NIH3T3 cells strongly activated mTOR/p70S6K signaling, induced cell transformation and invasi

149 esult of cross-talk among the MAPK, Akt/mTOR/p70S6K and NF-kappaB pathways.

150 It inhibited the Akt/mTOR/p70S6K pathway and activated the ERK1/2 pathway, resulti

151 feration requires activation of the Akt/mTOR/p70S6K pathway and is associated with inhibition of LKB1

152 y linked to the octreotide mediated Akt/mTOR/p70S6K pathway deactivation and reduction of kidney infl

153 +)-dependent activation of the PI3K/Akt/mTOR/p70S6K pathway during myoblast differentiation and muscl

154 Herein, we explore the role of the Akt/mTOR/p70S6K pathway in fibronectin-induced NSCLC cell growth.

155 However, the role of the Akt/mTOR/p70S6K pathway in lung carcinoma remains unknown.

156 Importantly, the PI3K/Akt/mTOR/p70S6K pathway, which plays a crucial role in muscle gro

157 inhibited cell survival through the Akt/mTOR/p70S6K pathway, with attendant effects on key proangioge

158 tosis in myotubes by activating the Akt/mTOR/p70S6K pathway.

159 expression of IGF-1, likely via the Akt/mTOR/p70S6K signaling pathway.

160 of PTEN was sufficient to activate Akt/mTOR/p70S6K signaling.

161 lamban phosphorylation and improved Akt/mTOR/p70S6K signaling.

162 rapamycin/p70 ribosomal S6 kinase (Akt/mTOR/p70S6K) in the kidney were measured after 60 minutes of

163 -regulation, allowing cell survival and mTOR/p70S6K activation.

164 pe is dependent on constitutive Akt and mTOR/p70S6K signaling and is actively inhibited through the t

165 B' substrates in the GSK3beta, Akt, and mTOR/p70S6K signaling pathways.

166 cin/70-kDa ribosomal protein S6 kinase (mTOR/p70S6K) were not involved.

167 h causes cell death and inactivation of mTOR/p70S6K signaling.

168 activation of PKC, but not of PI3K/PKB, mTOR/p70S6K, or ERK/RSK.

169 ibitor commonly used to investigate the mTOR/p70S6K pathway, reduced the in vivo phosphorylation of s

170 maintain an efficient activation of the mTOR/p70S6K pathway.

171 ll-established downstream targets of mTORC1, p70S6K and 4EBP, do not correlate with trophoblast motil

172 FGF19 activates the mTORC1-p70S6K and extracellular signal-regulated kinase (Erk)-p

173 e that deregulation of the PI3K-AKT/ mTORC1/ p70S6K pathways, an event frequently observed in cancer,

174 ound that LIF treatment activated the mTORC1/p70S6K signaling pathway, enhanced tumor growth, inhibit

175 ion to achieve full activation of neutrophil p70S6K.

176 ut only a 40-50%, indicating that neutrophil p70S6K activity has a rapamycin-resistant component.

177 Blockade of the PI3K pathway but not p70S6K led to up-regulation of IL-17RA, and constitutive

178 r initiation combined with the activation of p70S6K (phospho-T389) and inactivation of the 4E-binding

179 nuated TGFalpha-mediated basal activation of p70S6K (S6K) specifically at Thr-389, indicating that th

180 oaded rat hearts inhibited the activation of p70S6K and 4EBP1 and subsequently augmented atrophy in t

181 ion was accompanied by reduced activation of p70S6K and of the extracellular signal-regulated kinases

182 eurons, the sites of dendritic activation of p70S6K appeared as discrete compartments along dendritic

183 Activation of p70S6K requires sequential phosphorylation of multiple s

184 A similar dendrite-wide activation of p70S6K was induced in primary hippocampal neurons by dep

185 In addition, an elevated activation of p70S6K, PKC-betaII by HDL(NYHA-IIIb), and a higher amoun

186 hat Gbeta1 participates in the activation of p70S6K, which in turn promotes the serine phosphorylatio

187 ild type Rheb1 or Rheb2 causes activation of p70S6K, while expression of Rheb1D60K mutant results in

188 ked nutrient- or serum-induced activation of p70S6K.

189 -induced phosphorylation and low activity of p70S6K mainly occurs during mitosis.

190 .2 nm) of the in vitro enzymatic activity of p70S6K.

191 lts in inhibition of basal level activity of p70S6K.

192 Simultaneous analysis of p70S6K phosphorylation by phosphoflow cytometry and West

193 Cisplatin failed to induce cleavage of p70S6K in MCF-7 cells that lack functional caspase-3, bu

194 spase-3 and that the proteolytic cleavage of p70S6K is important for cisplatin-induced apoptosis.

195 The proteolytic cleavage of p70S6K was inhibited by a broad specificity caspase inhi

196 3 in MCF-7 cells resulted in the cleavage of p70S6K.

197 ed cisplatin-induced proteolytic cleavage of p70S6K.

198 CD3(+) T cells correlated with the degree of p70S6K phosphorylation in everolimus-treated patients.

199 cyte growth through regulating expression of p70S6K.

200 to mTOR/raptor inhibition and independent of p70S6K.

201 ation and that this effect is independent of p70S6K.

202 Inhibition of p70S6K activity by exogenous expression of a dominant ne

203 Inhibition of p70S6K expression with small interfering RNA oligonucleo

204 Inhibition of p70S6K increased expression of CD200R and CCL22 indicati

205 We found that inhibition of p70S6K, downstream of TORC1, resulted in diminished Ser(

206 ivation of AMPK and subsequent inhibition of p70S6K.

207 effect, at least in part, via inhibition of p70S6K.

208 udy, we have investigated the involvement of p70S6K in DNA damage-induced apoptosis.

209 Increased levels of p70S6K have been associated with drug resistance.

210 a greater than additive effect in levels of p70S6K phosphorylated at residue T389, whereas a signifi

211 expression of a dominant negative mutant of p70S6K prevented insulin-induced cell survival, whereas,

212 ression of a rapamycin-insensitive mutant of p70S6K.

213 d the fibronectin-induced phosphorylation of p70S6K and 4E-BP1.

214 protein synthesis through phosphorylation of p70S6K and 4E-BP1.

215 way detected by decreased phosphorylation of p70S6K and increased phosphorylation of AMP-activated pr

216 Insulin-induced phosphorylation of p70S6K and mTOR was prevented by the mTOR inhibitor, rap

217 e-damaging agent, induces phosphorylation of p70S6K at threonine 421 and serine 424 (T421/S424) in a

218 Rapamycin blocked phosphorylation of p70S6K but had no affect on PDGF-induced Akt phosphoryla

219 -1 PTB also inhibited the phosphorylation of p70S6K on Thr421/Ser424 and Ser411, which may result fro

220 PC-induced phosphorylation of p70S6K was not blocked in TG betaARKct hearts; therefore

221 and T421/S424 as well as phosphorylation of p70S6K's natural substrate S6 protein in S235/S236.

222 Despite phosphorylation of p70S6K(T421/S424), paclitaxel inactivates this kinase in

223 emsirolimus inhibited the phosphorylation of p70S6K, a substrate of mTOR.

224 litazone on IGF-I-induced phosphorylation of p70S6K, suggesting that troglitazone inhibited IGF-I and

225 d enhanced expression and phosphorylation of p70S6K.

226 correlating with reduced phosphorylation of p70S6K.

227 ct on fibronectin-induced phosphorylation of p70S6K.

228 ion in monkey cells, the phosphorylations of p70S6K, S6, and eIF4G are increased early in the infecti

229 Phosphoflow cytometric quantification of p70S6K phosphorylation may play an adjunct role to pharm

230 tion was associated with marked reduction of p70S6K phosphorylation compared to healthy volunteers or

231 In addition, the down-regulation of p70S6K could be mediated, at least in part, through acti

232 HSC activation, we investigated the role of p70S6K in HSC proliferation, cell cycle control, and typ

233 lex 2 but demonstrate a lesser dependence on p70S6K than the previously identified FRAP1 feedback loo

234 Similar effects on p70S6K were observed in MIN6 beta cells with knockdown o

235 thereby releasing its inhibitory effects on p70S6K.

236 d the augmentative effect of PLD2 exerted on p70S6K activity.

237 ibutes to the cooperative effect of GPCRs on p70S6K activity and cell growth.

238 time- and dose-dependent phosphorylation on p70S6K residues Thr389 and Thr421/Ser424.

239 wnstream signal PI-3K/Akt, but not ERK1/2 or p70S6K.

240 sion did not prevent ET-induced ERK, JNK, or p70S6K phosphorylation.

241 reover, knockdown of mTOR, but not rictor or p70S6K, abrogated rapamycin's ability to increase eIF4E

242 ellular phosphorylation of mTOR complex 1 (p-p70S6K, pS6, and p-4E-BP1) and mTOR complex 2 (pAKT (S47

243 of 21 (62%) Ser2448p-mTOR, 22 of 22 (100%) p-p70S6K, and 5 of 20 (25%) p-ribosomal protein S6.

244 related with the presence of the activated p-p70S6K.

245 Inhibition of p4EBP1 and p-p70S6K and suppression of translation are the most repre

246 hibitors correlated with p-ERK, p-AKT, and p-p70S6K levels.

247 p-AKT-Ser473 and p-p70S6K-Thr389 each had a limited correlation with trastu

248 yzed the status of PTEN, p-AKT-Ser473, and p-p70S6K-Thr389 using immunohistochemistry.

249 , leading to reduced expression of p-mTOR, p-p70S6K (T389), p-4EBP (T37/46) and p-S6 (S240/244).

250 (a) expression of phosphorylated (p)-mTOR, p-p70S6K; (b) mTORC 2 in EWS and DSRCT; (c) ERK signaling

251 rs of the mTORC1 signaling pathway, namely p-p70S6K (Thr 389).

252 In addition, expression of p-p70S6K and its downstream target molecule S6, key regula

253 bserved no significant changes in pAKT+ or p-p70S6K+ beta-cells in either experiment; however, pERK+

254 ols showed significant increases in pAKT+, p-p70S6K+, and pERK+ beta-cells and a significant decrease

255 vival signaling molecules, including pAkt, p-p70S6K, and pNFkappaB.

256 29 phosphorylation is limiting in late-phase p70S6K activation by EGF and contributes to the cooperat

257 ions (p < 0.05), and the cytoplasmic phospho-p70S6K expression was most specific for and abundant in

258 ll lines demonstrated by a T421/S424 phospho-p70S6K antibody.

259 increased phosphorylated Akt, phosphorylated p70S6K, and VEGF compared with controls.

260 2 and 24 hpi), in AGMK cells, phosphorylated p70S6K was moderately increased, correlating with a sign

261 ion of phosphorylated-MEK and phosphorylated-p70S6K, the two key signaling molecules responsible for

262 of cooperative p70S6K T389 phosphorylation, p70S6K kinase activity, or ASM [(3)H]thymidine incorpora

263 e downstream targets of Gbetagamma, the PI3K/p70S6K pathway.

264 DGF-induced Akt phosphorylation, positioning p70S6K downstream of Akt.

265 kinase B (Akt)/mammalian target of Rapamycin/p70S6K pathway and the up-regulation of the Extracellula

266 tivate the AKT/mammalian target of rapamycin/p70S6K/hypoxia-inducible factor-1alpha axis in CLL-BMSCs

267 In mTORi treated RTX recipients, p70S6K phosphorylation was selectively reduced in CD4(+)

268 mTORC1 functions by regulating p70S6K/ribosomal protein S6 (RPS6) and eukaryotic transl

269 ts of apoptotic targets and largely restores p70S6K activity and cell size to normal levels.

270 concomitantly with an increase in ribosomal p70S6K enzyme activity and phosphorylation in T389 and T

271 cules examined, the response of p(T421/S424)-p70S6K phosphorylation and total eukaryotic initiation f

272 ssant, inhibited hyperphosphorylation of S6, p70S6K activation, and DNA synthesis in LAMD-SM cells.

273 S6K1 (p70S6K) is a serine kinase downstream from Akt in the in

274 DNA synthesis by demonstrating that specific p70S6K phosphorylation sites receive distinct regulatory

275 whereas inhibitors of JNK and PKC stimulate p70S6K activity.

276 elet-derived growth factor (PDGF) stimulated p70S6K phosphorylation, which was blocked by LY294002, a

277 et of rapamycin and its downstream substrate p70S6K.

278 hat the phosphorylation of the PKC substrate p70S6K kinase behaved in a similar manner.

279 ownstream signalling to the mTOR substrates, p70S6K and 4E-BP1, by increasing PI3K/Akt-mediated activ

280 sphorylation of rpS6 (ser235/36), suggesting p70S6K kinase activity was still intact.

281 essed increased levels of the Raptor target, p70S6K, which provided a basis for investigating aldoste

282 s, AMPK and Akt, and its downstream targets, p70S6K and 4E-BP1, as candidate molecules on which to ce

283 pression of CD200R and CCL22 indicating that p70S6K negatively regulates some, but not all, human M2

284 These results suggest that p70S6K is a novel substrate for caspase-3 and that the p

285 Together, these results suggest that p70S6K plays a key role in insulin stimulated retinal ne

286 In addition, the p70S6K inhibitor hamartin transduced into cells as activ

287 inding integrin alpha5beta1 also blocked the p70S6K phosphorylation in response to fibronectin.

288 TOR-independent) participation of PLD in the p70S6K pathway and implicate PA as a nexus that brings t

289 tumor cell growth involves inhibition of the p70S6K signaling pathway.

290 gnificant increase in phosphorylation of the p70S6K substrate, ribosomal protein S6.

291 and LST8 (TOR complex 1), phosphorylates the p70S6K and 4E-BP1 to promote mRNA translation.

292 In the liver, their p70S6K (S6K1) protein was significantly lower, and tumor

293 C+P could, potentially, be mediated through p70S6K, downstream of mTOR, which in turn may suppress t

294 Akt expression led to p70S6K activation, prostatic intraepithelial neoplasia (

295 Together, p70S6K plays a crucial role in HSC proliferation, collag

296 In vitro-translated p70S6K was cleaved by human recombinant caspase-3.

297 rvival, whereas, overexpression of wild type p70S6K or expression of a rapamycin resistant form of th

298 Unexpectedly, p70S6K and 4EBP1, downstream components of mTOR, were ac

299 To clarify whether p70S6K activity is varying among CD4(+) T-cell subsets,

300 fied the MAPK subnetwork of genes along with p70S6K and FRAP1 as the most prominent targets that incr