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

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

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

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

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

16 nhibited phosphorylation of MAPK / Erk, AKT, p70S6K and 4EBP-1.

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 of FGF receptor 4 (FGFR4)-dependent ERK/AKT-p70S6K-S6 signaling activation in HNSCC cells, and addit

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

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

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

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

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

25 way protein expression (raptor, 4e-bp-1, and p70S6K proteins) along with enhanced muscle power (speci

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

27 K-1/2, PDK1, mTOR, PTEN, GSK-3alphabeta, and p70S6K.

28 eam of BDNF, including mTOR, ERK, 4EBP1, and p70S6K.

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

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

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

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

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

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

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

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

37 lar regulators including AKT, AMPKalpha, and p70S6K.

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

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

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

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

42 ted with phosphorylation of AKT, 4E-BP1, and p70S6K, independent of the loss of PTEN or mutation of P

43 am effectors, such as PI3K, Akt, 4E-BP1, and p70S6K, which are important for cellular growth and surv

44 e activation of eIF2, regulation of eIF4 and p70S6K signaling, and mTOR signaling pathways.

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

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

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

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

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

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

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

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

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

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

55 Immunohistochemistry revealed mTOR and p70S6K in the DRG neurons.

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

57 increases in protein synthesis and mTOR and p70S6K phosphorylation.

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

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

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

61 6RP and constitutively active Akt, mTOR, and p70S6K.

62 unohistochemistry (IHC) for pS6, p4EBP1, and p70S6K, known effectors and readouts of mTORC1 activatio

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

64 creased phosphorylation of phospholamban and p70S6K.

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

66 /arrestin-independent activation of PI3K and p70S6K.

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

68 1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.

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

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

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

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

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

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

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

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

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

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

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

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

81 4 failed to alter the profile of cooperative p70S6K T389 phosphorylation, p70S6K kinase activity, or

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 (4E-BP1/2), p70 ribosomal S6 protein kinase (p70S6K), and their phosphorylated (active) counterparts

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

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

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

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

123 f the mTOR complex 1 (mTORC1)/p70 S6 kinase (p70S6K) in the negative regulation of PD-L1 on cancer ce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 ell proliferation mainly via FKBP12-mediated p70S6K activation.

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

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

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

144 tion and survival proteins (BDNF, Akt, mTOR, p70S6K, ERK and CREB) in the cerebral cortex and hippoca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 ondrial peroxiredoxin, inactivating AKT/mTOR/p70S6K signaling, and inducing autophagic cell death in

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

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

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

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

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

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

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

173 ities associated with the activation of mTOR/p70S6K signaling in HEK293T cells.

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

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

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

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

178 in NIH3T3 cells strongly activated the mTOR/p70S6K signaling pathway and induced morphologic transfo

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

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

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

182 Elevation of PD-L1 by inhibition of mTORC1/p70S6K signaling is likely due to suppression of beta-Tr

183 er immunotherapy through co-targeting mTORC1/p70S6K signaling.

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

185 ion to achieve full activation of neutrophil p70S6K.

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

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

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

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

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

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

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

193 Activation of p70S6K requires sequential phosphorylation of multiple s

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

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

196 Simultaneous analysis of p70S6K phosphorylation by phosphoflow cytometry and West

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

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

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

200 3 in MCF-7 cells resulted in the cleavage of p70S6K.

201 ed cisplatin-induced proteolytic cleavage of p70S6K.

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

203 cyte growth through regulating expression of p70S6K.

204 to mTOR/raptor inhibition and independent of p70S6K.

205 ation and that this effect is independent of p70S6K.

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

207 Inhibition of p70S6K expression with small interfering RNA oligonucleo

208 Inhibition of p70S6K increased expression of CD200R and CCL22 indicati

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

210 ivation of AMPK and subsequent inhibition of p70S6K.

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

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

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

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

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

216 ression of a rapamycin-insensitive mutant of p70S6K.

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

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

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

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

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

222 -1 PTB also inhibited the phosphorylation of p70S6K on Thr421/Ser424 and Ser411, which may result fro

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

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

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

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

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

228 d enhanced expression and phosphorylation of p70S6K.

229 correlating with reduced phosphorylation of p70S6K.

230 ct on fibronectin-induced phosphorylation of p70S6K.

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

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

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

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

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

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

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

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

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

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

241 ay with mTOR inhibitors, raptor knockdown or p70S6K inhibitors elevated PD-L1 levels in some lung and

242 D-L1, because inhibition of either mTORC1 or p70S6K facilitated beta-TrCP degradation accompanied wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 29 phosphorylation is limiting in late-phase p70S6K activation by EGF and contributes to the cooperat

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

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

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

262 2 and 24 hpi), in AGMK cells, phosphorylated p70S6K was moderately increased, correlating with a sign

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

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

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

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

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

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

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

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

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

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

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

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

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

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 While a major mTORC1 substrate, p70S6K, is required for myotube fusion and hypertrophy,

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

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

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

283 ng the mammalian target of rapamycin targets p70S6K and 4EBP1, with decreased cytokine production and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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