ライフサイエンスコーパス: S6K

1 S6K directly phosphorylates IRS-1 on multiple serine res

2 S6K exists as two homologues, S6K1 and S6K2, but little

3 S6K in turn acted through a negative feedback loop to re

4 s in genes encoding raga-1 (RagA) or rsks-1 (S6K) is fully suppressed by neuronal-specific rescues.

5 he mechanistic target of rapamycin complex 1-S6K pathway and the transcription factor E2F1.

6 ncrease in the activation of MEK1/2, ERK1/2, S6K, and Akt, which is coupled with a 2-3-fold increase

7 s linked to enhanced PIP(3) production via a S6K-IRS positive feedback mechanism.

8 cardiolipin could also bind to and activate S6K, albeit with different kinetics.

9 D2 mutants K444R and K758R neither activated S6K nor induced chemotaxis, intracellular PA is needed f

10 , synthesis of PA) must be present to affect S6K.

11 rowth and survival pathways mediated by AKT, S6K, STAT3, and ERK1/2 activation.

12 , sequentially inhibited phosphorylated AKT, S6K, and 4EBP1, and concurrently suppressed chemokine re

13 s that phosphorylate AMPK at this site (Akt, S6K, and ERK) did not prevent these events.

14 for adiponectin-mediated modulation of AMPK-S6K axis and more importantly, inhibition of adhesion, m

15 We also identify an S6K-mediated feedback in two long-lived mutants that sug

16 es and that this feedback loop depends on an S6K-PI3K-Ras pathway.

17 rs endothelial recovery/proliferation via an S6K-dependent mechanism.

18 wnstream Akt targets including GSK-3beta and S6K.

19 rylation or the downstream elements, AKT and S6K in platelets and their aggregation rates in both gro

20 The deletion of SCH9 (homologous to AKT and S6K), but not CR, protects against the age-dependent def

21 rinuclear region, thereby inducing 4E-BP and S6K phosphorylation.

22 rin1 show that phosphorylation of 4E-BP1 and S6K in infected cells depends on mTOR kinase.

23 In infected cells, 4E-BP1 and S6K phosphorylation is maintained when raptor or rictor

24 of the mTOR complex 1 substrates 4E-BP1 and S6K, which led to induction of the functional protein tr

25 er mTOR complex can phosphorylate 4E-BP1 and S6K.

26 causal role of EIF-4F complex, EIF4EBP, and S6K in the circulation on type 2 diabetes, based on inde

27 L expression and the activity of MEK-ERK and S6K-RPS6 cascades but also displays a potent antiprolife

28 sary for normal wound healing, with FOXO and S6K as their respective effectors.

29 e-extracellular signal-regulated kinase) and S6K-RPS6 (ribosomal protein S6 kinase-ribosomal protein

30 In sum, mTOR and S6K contribute to the apoptotic resistance of mesothelio

31 e negative feedback, it can deprive mTOR and S6K of their natural activator.

32 f PLD enzymatic activity) activates mTOR and S6K, known to inhibit apoptosis, and enhances cell migra

33 s mRNA expression levels for PLD2, mTOR, and S6K, with PLD2 preceding mTOR/S6K in time.

34 nerabilities of some targets such as Myc and S6K are found to vary significantly depending on the wei

35 failed to induce an increase in both PLD and S6K activity or phosphorylation, indicating that the enz

36 ignaling components including TOR, Rheb, and S6K.

37 Both RSK and S6K phosphorylate serine 145 of Mad1 upon serum or insul

38 alterations in the phosphorylation of S6 and S6K.

39 ments of phosphorylation of mTOR Ser2448 and S6K Thr389 showed that AMPK, by counteracting Akt under

40 Inhibition of Ret plus Raf, Src and S6K was required for optimal animal survival, whereas in

41 d AMPK activity, and decreased AKT, TOR, and S6K activities.

42 et of rapamycin) signaling proteins ULK1 and S6K.

43 B-unlike other substrates of mTORC1, such as S6K and 4E-BP1- is strictly dependent on the amino-acid-

44 ycin (mTOR) effectors of cell growth such as S6K and 4E-BP1.

45 PDK1 phosphorylation of AGC kinases such as S6K and RSK is also necessary for thymocyte development.

46 insulin-dependent Akt1 activation as well as S6K and FoxO1-3 phosphorylation, but selectively reduces

47 sulin-induced phosphorylation of Akt, AS160, S6K, and S6 was also decreased in skeletal muscle.

48 Mf and locally delivered mTOR inhibitors at S6K.

49 extent, PLD1, resulted in elevation of both S6K activity and chemokinesis, whereas PLD silencing was

50 mTORC1 branch of the pathway, as measured by S6K and eIF4EBP1 phosphorylation.

51 This effect is mediated by S6K and contributes to control mechanisms that keep SCs

52 S1, the major site of its phosphorylation by S6K in vitro, through genetic knock-in of a serine-to-al

53 ively activate mTORC1, effectively bypassing S6K-mediated feedback inhibition.

54 Conversely, S6K signaling was increased in vascular tumor cells wher

55 d under ROCK2 knockdown, including decreased S6K and phosphorylated mTOR levels.

56 ets, TSC2 and GSK3, and the TORC1 effectors, S6K and 4E-BP1, were unaffected.

57 TRBP serines 283/286 are essential for S6K-mediated TRBP phosphorylation, optimal expression of

58 PP2A, previously identified as important for S6K regulation.

59 resence of an mTOR-independent mechanism for S6K.

60 r, our findings establish critical roles for S6K and RSK in the induction of IFN-dependent biological

61 adeno-associated virus carrying a shRNA for S6K and examined the effects on steatosis and insulin re

62 Furthermore, S6K was crucial to promoting the over activation of mTOR

63 , within the hepatic compartment, mTORC1 --> S6K signaling regulates Akt largely through IRS-independ

64 cellular amino acids and activate mTORC1 --> S6K signaling.

65 rapamycin complex 1 and S6 kinase (mTORC1--> S6K) attenuates insulin-stimulated Akt activity in certa

66 ults suggest that activation of hypothalamic S6K contributes to hepatic insulin resistance in respons

67 resent evidence suggesting that hypothalamic S6K activation is involved in the pathogenesis of diet-i

68 ed growth arrest of MCF-7 cells and identify S6K as a novel downstream target of nSMase2.

69 causes an approximately 2.9-fold increase in S6K catalytic activity.

70 robust time- and dose-dependent increases in S6K enzymatic activity and Thr(421)/Ser(424) phosphoryla

71 mock-treated cells to 0.09 +/- 0.03 units in S6K-overexpressing macrophages causing stellation and ar

72 versed in cells expressing a kinase-inactive S6K mutant and was fully reversed in cells silenced with

73 other downstream Akt-mTOR targets, including S6K and 4E-BP2, was also increased by MCV sT.

74 ays a positive role in cell adhesion-induced S6K phosphorylation, whereas TSC2 is required for cell s

75 TSC2 is required for cell suspension-induced S6K inactivation.

76 ar data reveal that FL772 is able to inhibit S6K phosphorylation in yeast cells.

77 While rapamycin potently inhibits S6K activity throughout the duration of treatment, 4E-BP

78 t of rapamycin) and its target p70S6 kinase (S6K) in response to laminar and oscillatory flows.

79 )-binding protein (4E-BP1) and p70S6 kinase (S6K) in uninfected cells, and this activity is lost upon

80 carboxylase and inhibition of p70S6 kinase (S6K).

81 oprotein may activate the S6 protein kinase (S6K) through binding and E6AP-mediated degradation of th

82 f liver-specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of an adeno-associa

83 sary for long-term maintenance of S6 kinase (S6K) activity.

84 The 40S ribosomal protein S6 kinase (S6K) acts downstream of mTOR, which plays important role

85 the phosphorylation of ribosomal S6 kinase (S6K) and 4E binding protein 1 (4EBP1), targets of mTOR.

86 eased phosphorylation of ribosome S6 kinase (S6K) and BAD (Bcl-2-associated death promoter) and prote

87 the phosphorylation of ribosomal S6 kinase (S6K) and eukaryotic initiation factor 4E-binding protein

88 ssed phosphorylation of ribosomal S6 kinase (S6K) and its downstream targets S6 and eIF4B.

89 tein kinase B (PKB), p70Ribosomal S6 kinase (S6K) and p90Ribosomal S6 kinase (RSK).

90 ncreased levels of phosphorylated S6 kinase (S6K) and S6 was observed, consistent with constitutive a

91 We also demonstrate that S6 kinase (S6K) and serotonin production are involved in the postma

92 an target of rapamycin (mTOR) and S6 kinase (S6K) are highly expressed in the undifferentiated promye

93 ted the role of ribosomal protein S6 kinase (S6K) at the intersection of nutrition and the establishm

94 orylation of the mTORC1 substrate S6 kinase (S6K) at Thr389 and the mTORC2 substrate Akt at Ser473.

95 Prolonged activation of p70 S6 kinase (S6K) by insulin and nutrients leads to inhibition of ins

96 enhancing the phosphorylation of S6 kinase (S6K) in cells.

97 The 40S ribosomal protein S6 kinase (S6K) is a conserved component of signalling pathways con

98 n this paper, we demonstrate that S6 kinase (S6K) localizes to the presynaptic active zone.

99 pecific manner, by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) and results

100 ion is mediated by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) in a cell-ty

101 an target of rapamycin (mTOR) and S6 kinase (S6K) pathway is essential for cell differentiation, grow

102 ivated the PI3K/mTORC2/PKB/mTORC1/S6 kinase (S6K) pathway, but pathophysiologically high albumin conc

103 R activity based on its conserved S6 kinase (S6K) phosphorylation.

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

105 e mechanism for this involves the S6 kinase (S6K) signaling enzyme.

106 both pathways but also abrogated S6 kinase (S6K) signaling.

107 additional pathway that involves S6 kinase (S6K) through PLD2-Y(296), known to be phosphorylated by

108 precipitated endogenous ribosomal S6 kinase (S6K) with a stoichiometry of 94:1 lipid/protein.

109 emonstrated greater inhibition of S6 kinase (S6K), a downstream effector of mTOR complex 1, than eith

110 in kinases (ROCK1 and ROCK2), p70 S6 kinase (S6K), and mammalian target of rapamycin (mTOR) were incr

111 e protein (WASp), Grb2, ribosomal S6 kinase (S6K), and Rac2.

112 of its substrates, p70 ribosomal S6 kinase (S6K), but not another (protein kinase B (PKB)).

113 E-binding protein (4E-BP) and p70 S6 kinase (S6K), which is important for maintaining translation.

114 (eIF4E) expression, but inhibited S6 kinase (S6K).

115 S6 kinase (RSK) and p70 ribosomal S6 kinase (S6K).

116 ivation of the mTOR substrate p70 S6 kinase (S6K).

117 90 ribosomal kinase (RSK) and p70 S6 kinase (S6K).

118 the translation regulatory kinase S6-Kinase (S6K) through modulation of Rictor expression.

119 High fat diet (HFD) fed L-S6K-KD mice showed improved glucose tolerance and system

120 specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of an adeno-associated viru

121 enic gene expression was attenuated in the L-S6K-KD mice with decreased sterol regulatory element-bin

122 C1 substrate, Sch9 (a homologue of mammalian S6K), is recruited to the vacuole by direct interaction

123 Activated AMPK suppressed mTORC1 mediated S6K and 4EBP1 phosphorylation to decrease protein transl

124 AT3 and mammalian target of rapamycin (mTOR)-S6K-S6 signaling, with subsequent leptin resistance, obe

125 inhibition of phosphorylation of Akt, mTOR, S6K, and 4EBP in vivo.

126 tein synthesis, and phosphorylation of mTOR, S6K, and 4E-BP1 in Caco-2 cells.

127 se in IGF1 led to activation of the Akt-mTOR-S6K cascade and the inhibition of FoxO3a activity.

128 a1 and subsequent activation of the Akt-mTOR-S6K signaling pathway may underlie one of the mechanisms

129 everses the abnormal levels of the AMPK-mTOR-S6K pathway and of active translation at synapses.

130 cardiac hypertrophy, activation of the MTOR-S6K and calcineurin pathways, and expression of the hype

131 These findings implicate the mTOR-S6K pathway as a critical mediator of glial cell transfo

132 gically and genetically manipulated the mTOR-S6K pathway in glioma cells and monitored its effects on

133 n of Tiam1 controls the duration of the mTOR-S6K signaling pathway in response to mitogenic stimuli.

134 pathway-separate from the canonical TSC-mTOR-S6K pathway-that regulates browning of adipose tissue.

135 ndicate that activation of the PI3K/Akt/mTOR/S6K cascade, specifically S6K1/2, is pivotal in regulati

136 atase activity, inhibiting the PI3K/Akt/mTOR/S6K pathway to decrease transcription.

137 not wild-type SCRIB, activates the Akt/mTOR/S6K signaling pathway.

138 ntly suppressed follistatin-induced Akt/mTOR/S6K signaling.

139 y to repress the activation of PI3K/Akt/mTOR/S6K signaling.

140 s identify a critical role of Smad3/Akt/mTOR/S6K/S6RP signaling in follistatin-mediated muscle growth

141 induced autophagy by affecting the AMPK/mTOR/S6K signaling axis and had no influence on the PI3K/AKT/

142 We propose that IL-8 reverses an mTOR/S6K-led down-regulation of PLD2 expression and enables P

143 pholipase D2 (PLD2) plays a key role in mTOR/S6K mitogenic signaling.

144 gene expression abrogated IL-8-induced mTOR/S6K mRNA expression, whereas silencing of mTOR or S6K ge

145 ammalian target of rapamycin/S6 kinase (mTOR/S6K) pathway.

146 the first time the following mechanism: mTOR/S6K down-regulation-->PLD2 overexpression-->PLD2/Fes ass

147 However, the impact of PLD on mTOR/S6K gene expression is not known.

148 nical RAF/MAPK/ERK/RSK and PI3K/AKT/PDK/mTOR/S6K pathways are identified.

149 LD2, mTOR, and S6K, with PLD2 preceding mTOR/S6K in time.

150 iRNAs resulted in the inhibition of the mTOR/S6K pathway and upregulation of the AMPK kinase cascade.

151 owth and enhanced signaling through the mTOR/S6K pathway; evaluation of multiple breast cancer patien

152 results in sustained activation of the mTOR/S6K signaling and increased apoptotic cell death.

153 d p-AKT (ser473); it also activates the mTOR/S6K signaling pathway both in vitro and in vivo.

154 activity is negatively regulated by the mTOR/S6K signaling pathway.

155 in (which can target eEF2 through the mTORC1-S6K-eEF2K axis) causes tumour cells to undergo growth ar

156 ort a critical role for the Tsc1/Tsc2-mTORC1-S6K axis in the normal development of cardiovascular tis

157 (early stage of myogenesis), whereas mTORC1-S6K signaling is required for myoblast fusion (later sta

158 When phosphorylated by mTORC1/S6K, the insulin receptor substrate (IRS-1) is targeted

159 ion of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity.

160 TORC1 downstream targets, we identify mTORC1/S6K pathway as the mechanism by which mTORC1 regulates b

161 f S6K by overexpression of dominant-negative S6K or dominant-negative raptor in the MBH restored the

162 f these tumor cells was inhibited by a novel S6K inhibitor.

163 tivation results in subsequent activation of S6K and STAT3, as well as suppression (i.e., phosphoryla

164 sulin resistance that involves activation of S6K by an IKK2-dependent pathway.

165 Constitutive activation of S6K in the MBH mimicked the effect of the HFD in normal

166 ssion of insulin signaling and activation of S6K in the mediobasal hypothalamus (MBH).

167 Activation of S6K signaling in these mice improved insulin secretion i

168 oattractant via cell entry and activation of S6K to mediate the cytoskeletal actin polymerization and

169 flow, resulted in a transient activation of S6K.

170 ted the inhibition of TSC2 and activation of S6K.

171 , thereby confirming the role of mTOR and of S6K in the acquired resistance of three dimensional sphe

172 cellular expression, and a colocalization of S6K and PLD2 was observed by immunofluorescence microsco

173 Systemic deletion of S6K protects against diet-induced obesity and enhances i

174 Thus, deregulation of S6K contributes to the progression of type 2 diabetes, o

175 provide a scaffold for future development of S6K inhibitors with possible therapeutic applications.

176 erexpressing a constitutively active form of S6K under the control of the rat insulin promoter.

177 , our study shows that the two homologues of S6K have distinct effects on Akt activation and cell sur

178 This work defines the importance of S6K in regulation of beta-cell cycle, cell size, functio

179 Our results demonstrate the importance of S6K: 1) as a modulator of the hepatic response to fastin

180 -alpha (PGC1alpha), as well as inhibition of S6K, suppressed the held-up wing phenotype, myofibrillar

181 Knockdown of S6K via short interfering RNA in HAECs impaired cell pro

182 ors overexpressing SCRIB have high levels of S6K but do not harbor mutations in PTEN or PIK3CA, ident

183 Nesfatin-1 attenuated phosphorylation of S6K and S6 during brown adipocyte differentiation.

184 of CCT leads to decreased phosphorylation of S6K and S6 while increasing phosphorylation of Akt.

185 as evidenced by decreased phosphorylation of S6K, 4E-BP1, and ULK1, direct targets of the mTORC1 kina

186 mation of giant cells via phosphorylation of S6K, and mTOR regulates hypoxia and VEGF A-induced cellu

187 bosome-associated RNA and phosphorylation of S6K, both consistent with activation of mTOR.

188 tes the cell size and that FAK regulation of S6K phosphorylation is through TSC2.

189 This reliance of S6K on phosphatidic acid (PA), a curvature-inducing phos

190 Knockdown by small interference RNA of S6K, a major downstream target of mTOR, reproduced the e

191 ormal chow-fed animals, while suppression of S6K by overexpression of dominant-negative S6K or domina

192 gulation of p53 and p21, and upregulation of S6K, IGF-1 and IGF1R.

193 trast, phosphorylation of the p85 variant of S6K in response to T3 was not blocked by LY294002, wortm

194 neither ATRA effects nor nSMase2 effects on S6K phosphorylation required the ceramide-activated prot

195 ted mTORC1-dependent T389 phosphorylation on S6K (RPS6KB1) with an EC(50) of 250 pmol/L with approxim

196 diated by G(i)/Gbetagamma, but not by Akt or S6K, two kinases that control the phosphorylation of AMP

197 RNA expression, whereas silencing of mTOR or S6K gene expression resulted in large (>3-fold and >5-fo

198 (i) simultaneous overexpression of mTOR (or S6K), (ii) silencing of mTOR via dsRNA-mediated interfer

199 on PI3K by prolonged inhibition of mTORC1 or S6K is sufficient to rescue hydrophobic motif phosphoryl

200 Rapamycin or S6K knockdown increased TRAIL-induced caspase-8 cleavage

201 -large perimeter of cells that overexpressed S6K.

202 ession levels of p-TSC2, p-mTOR, p-4E-BP1, p-S6K, p-S6, and p-STAT3 were found in regions defined by

203 ly inhibited cellular biomarker of mTORC1 (P-S6K, P-4EBP1) and mTORC2 (P-AKT S473) over the biomarker

204 treatment showed elevated levels of AKT, p70 S6K, and/or phosphorylated mTOR, in addition to class II

205 Akt restored phosphorylation of mTOR and p70 S6K and matrix gene expression levels.

206 so induce the phosphorylation of Akt and p70 S6K in a manner that depends on Rac1 and its guanine nuc

207 survival insulin receptor, PI3K-Akt, and p70 S6K signaling is diminished in models of diabetic retino

208 ding to the activation of Akt, mTOR, and p70 S6K.

209 eam of both mTORC1 and mTORC2, including p70 S6K, 4E-BP1 and Akt.

210 L promotes cell proliferation, involving p70 S6K-mediated suppression of expression of programmed cel

211 -kappaB transcription and defective JNK, p70 S6K, and ERK1/2 activation.

212 ously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activated in BCR-ABL tran

213 ses (MAPK)/ribosomal protein S6 kinases (p70 S6K) pathway.

214 1 rather than activation of the Akt-mTOR-p70 S6K signaling pathway, and siRNA knockdown of Beclin-1 d

215 olving sequential engagement of the mTOR/p70 S6K pathway and downstream suppression of PDCD4 expressi

216 BL kinase inhibitors block activation of p70 S6K and downstream engagement of the S6 ribosomal protei

217 1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme.

218 Phospho-p70 S6K was detected by Western blot analysis and activity b

219 nduced PABP accumulation did not require p70 S6K, it was inhibited by the expression of a dominant-ac

220 phosphorylation of the mTORC1 substrate p70 S6K and the translational repressor 4E-BP1.

221 in the cellular model, and rapamycin, a p70(S6K) inhibitor, inhibited MMP-1 (P<0.001) and MMP-3 (P<0

222 hosphatidyl inositol 3-kinase (PI3K)/AKT/p70(S6K) signaling path on regulation of primary normal huma

223 Both Akt and p70(S6K) phosphorylate Pdcd4, allowing for binding of the E3

224 e B, glycogen synthase kinase 3beta, and p70(S6K) was impaired in DHet mouse muscle and liver and was

225 tal and phosphorylated forms of mTOR and p70(S6K)(Thr421/Ser424) are upregulated.

226 nsistent with the human cancer, AKT-mTOR-p70(S6K) signaling and vascular growth factor and its recept

227 n resistance, possibly via the AMPK/mTOR/p70(S6K) and apoptosis signal-regulating kinase 1/JNK/IRS1 p

228 lting in downstream inhibition of mTORC1-p70(S6K) signaling.

229 sistin also stimulated the activation of p70(S6K), a downstream kinase target of mTOR, and increased

230 Phosphorylation of p70(S6K), a known target of mTOR, occurred rapidly following

231 40 S ribosomal protein S6, a target of p70(S6K), and 4E-BP1, a target of mTOR, were both phosphoryl

232 Phospho-p70(S6K) was identified in the cellular model, and rapamycin

233 kinase-Akt-mammalian target of rapamycin-p70(S6K) and mitogen-activated protein/extracellular signal-

234 3K-AKT-mammalian target of the rapamycin-p70(S6K) pathway was observed in both the cytoplasmic and nu

235 ntified ULK1 able to negatively regulate p70(S6K) in starvation-induced autophagy of neuroblastoma SH

236 Akt, p27(kip1), and the PDK-1 substrate p70(S6K) were assessed.

237 these results may uncover the novel ULK1-p70(S6K) autophagic pathway, as well as miR-4487 and miR-595

238 new miR-182 target, promotes Akt(Ser473)/p70-S6K(Thr389) phosphorylation and cardiomyocyte hypertroph

239 with the activation of Akt and p70S6Kinase (S6K).

240 This new signaling set, PA-S6K-FLNA-actin, sheds light for the first time into the

241 24) phosphorylation, further supporting a PA/S6K connection.

242 activation of downstream signaling pathways S6K and eukaryotic initiation factor binding protein 1 (

243 A decrease in phopho-S6K levels, a marker of mTOR activity, was observed in m

244 es showed increased phospho-mTOR and phospho-S6K levels in the animal tumors.

245 asts and in the Ppt1-KO mice, phosphorylated-S6K-1 (p-S6K1) levels, which inversely correlate with li

246 d decreased the phosphorylation of placental S6K, S6 ribosomal protein, 4E-BP1, IRS-1, Akt, ERK-1/2,

247 The data suggest a new function for plant S6K as a repressor of cell proliferation and required fo

248 Surprisingly, FTS prevented S6K activation induced by a constitutively active mTOR m

249 In vivo, phosphorylation of the promitotic S6K in mouse thoracic aorta was much less than that in m

250 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) and results in enhanced interaction of the pro

251 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) in a cell-type-specific manner.

252 Ribosomal protein S6K (S6K) messenger RNA (mRNA) levels were increased and

253 Both EIF4EBPs and ribosomal protein S6K kinase (RP-S6K) are downstream effectors regulated b

254 stimulate phospho-Ser-302 or other putative S6K sites within IRS1, whereas ribosomal S6 protein was

255 way including mammalian target of rapamycin, S6K, and S6 ribosomal protein.

256 Further, Atf4 mutants have reduced S6K activity in liver and adipose tissues.

257 and consolidation were dependent on reduced S6K and dopaminergic signalling.

258 hese results suggest that FAK might regulate S6K activation and cell size through its interaction wit

259 PK activation to effect negative regulation, S6K was activated in a sustained manner.

260 n under nutrient-limiting conditions require S6K for repression of cell proliferation.

261 ein phosphatase 2A (PP2A) inhibition rescued S6K activity.

262 Here, we show that ribosomal S6K, which is normally considered a protein involved in

263 EIF-4G (6 SNPs), EIF4EBP2 (12 SNPs), and RP-S6K (16 SNPs).

264 cted EIF-4E, EIF-4A, EIF-4G, EIF4EBP, and RP-S6K circulating levels using Mendelian Randomization.

265 IF4EBPs and ribosomal protein S6K kinase (RP-S6K) are downstream effectors regulated by mTORC1 but co

266 downstream AGC kinases (including Akt, RSK, S6K, SGK, and PKC).

267 Ribosomal protein S6K (S6K) messenger RNA (mRNA) levels were increased and AMPK

268 Specifically, S6K colocalizes with the presynaptic protein Bruchpilot

269 ve cell viability and the genes JAK2, Stat3, S6K, JUN, FOS, Myc, and Mcl1 are effective candidates to

270 To study S6K function in plants, we isolated single- and double-k

271 e2 overexpression was sufficient to suppress S6K phosphorylation and signaling.

272 motes T cell cycle progression and sustained S6K activity.

273 We present a model in which synaptic S6K responds to local extracellular nutrient and growth

274 ensitive, in contrast to another TOR target, S6K, phosphorylation of which was rapamycin sensitive.

275 ted the PP2A B56gamma subunit, which targets S6K for inactivation and was required for CGNP prolifera

276 We then provide evidence that S6K functions downstream of presynaptic PDK1 to control

277 We found that S6K was hyperphosphorylated in ANDV-infected, hypoxia-tr

278 Equally important is that S6K is itself regulated by phospholipids, specifically p

279 that loss of PHLPP expression activates the S6K-dependent negative feedback loop and that PHLPP is a

280 ylation, optimal expression of TRBP, and the S6K-TRBP interaction in human primary cells.

281 Chemotaxis was inhibited >90% by the S6K inhibitors rapamycin and bisindolylmaleimide and by

282 f this study was to evaluate the role of the S6K arm of mammalian target of rapamycin complex 1 (mTOR

283 The combined use of the S6K inhibitor BI-D1870 with TNF-alpha inhibited the PKC-

284 decreased as the result of activation of the S6K-dependent negative feedback loop in PHLPP knockdown

285 rogenitors is dependent on activation of the S6K/eIF4B or RSK/eIF4B pathway.

286 o-3-phosphocholine (DOPC), binds directly to S6K and causes an approximately 2.9-fold increase in S6K

287 The expression ratio of PLD2 to mTOR (or to S6K) is gradually inverted upon in vitro induction of di

288 urthermore, the diversity of the response to S6K in several unrelated cell types (fibroblasts, leukoc

289 s separable from canonical mTOR signaling to S6K.

290 We have found that the AKT and TOR-S6K pathways, which are major regulators of nutrient met

291 Effects of TOR-S6K appear to be mediated by SGG/GSK3beta, a known kinas

292 m line as an in vivo model to understand TOR-S6K signaling in proliferation and differentiation and s

293 Our screen revealed that the TORC1-S6K-RPS6 signaling axis is regulated by many subcellular

294 ivo downregulation of IRS signaling by TORC1/S6K induces beta-cell insulin resistance, and that this

295 However, only TSC2, S6K, and S6 activation levels correlated significantly w

296 get of rapamycin (mTOR) pathway and utilizes S6K to regulate CCTbeta phosphorylation.

297 aimed to delineate the importance of in vivo S6K activation in the regulation of insulin signaling an

298 In vivo, S6K activity specifically marked the CGNP population tra

299 E was required for CGNP proliferation, while S6K activation drove cell cycle exit.

300 vascular tumors, such as angiosarcomas, with S6K inhibitors.