ライフサイエンスコーパス: S6 kinase

1 he protein kinase AKT, protein kinase C, and S6 kinase.

2 tion of the ribosomal regulatory protein p70-S6 kinase.

3 on of its two downstream targets, p21Cip and S6 kinase.

4 activity of its direct downstream target p70 S6 kinase.

5 tion depended on activation of p90 ribosomal S6 kinase.

6 uggesting a downstream pathway distinct from S6 kinase.

7 the expression and association of HDAC1 with S6 kinase.

8 1 pathway components AMPK, RAGA-1 and RSKS-1/S6 kinase.

9 educed phospho-IRS-1(S302) through AMPKalpha-S6 Kinase.

10 ed phosphorylation of MET, AKT and ribosomal S6 kinase.

11 processing is blocked by an inhibitor of p70 S6-kinase.

12 phosphorylates the 70-kDa ribosomal protein S6 kinase 1 (p70S6K1), which subsequently phosphorylates

13 The Ser/Thr kinase 90 kDa ribosomal protein S6 kinase 1 (p90RSK) belongs to a protein family that re

14 FNlambda activates the p90 ribosomal protein S6 kinase 1 (RSK1) and its downstream effector, initiati

15 dependent kinase 1 target kinases, ribosomal S6 kinase 1 (Rsk1) and Rsk2, produced a striking perturb

16 Ribosomal S6 kinase 1 (RSK1) belongs to a family of proteins with

17 owed that the inactive form of p90 ribosomal S6 kinase 1 (RSK1) interacts with the regulatory subunit

18 In particular, ribosomal S6 kinase 1 (RSK1) silencing increased, whereas RSK2 and

19 ells, interacts with mammalian p90 ribosomal S6 kinase 1 (RSK1), and causes a decrease in NK cell pop

20 ted kinase 2 (ERK2) phosphorylates ribosomal S6 kinase 1 (RSK1), which promotes cellular growth.

21 that OCD distortion is intrinsically due to S6 kinase 1 (S6K1) activation.

22 ltisite phosphorylation of ribosomal protein S6 kinase 1 (S6K1) alters target selection.

23 We provide evidence that S6 kinase 1 (S6K1) Aly/REF-like target (SKAR) is engaged

24 mTORC1 regulates p70 ribosomal protein S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E-b

25 Phosphorylation of the mTORC1 substrates S6 kinase 1 (S6K1) and S6 was elevated, whereas that of

26 downstream effectors, the ribosomal protein S6 kinase 1 (S6K1) and the translation initiation factor

27 port the identification of ribosomal protein S6 kinase 1 (S6K1) as a novel substrate of PHLPP.

28 complex 1 (mTORC1) and p70 ribosomal protein S6 kinase 1 (S6K1) axis.

29 We found that targeting ribosomal protein S6 kinase 1 (S6K1) in Pten-deficient cells suppressed gl

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

31 Suppression of the ribosomal protein S6 kinase 1 (S6K1) increases healthspan and lifespan in

32 ve shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivit

33 Ribosomal protein S6 kinase 1 (S6K1) is a major downstream signalling mole

34 S6 kinase 1 (S6K1) is a protein kinase involved in regul

35 The 40S ribosomal S6 kinase 1 (S6K1) is an important regulator of cell gro

36 Aberrant activation of S6 kinase 1 (S6K1) is found in many diseases, including

37 n complex 1 (mTORC1) and its effector kinase S6 kinase 1 (S6K1) is known to trigger multisite seryl p

38 p70 ribosomal protein S6 kinase 1 (S6K1) is regulated by multiple phosphorylat

39 1 (mTORC1)short right arrowribosomal protein S6 kinase 1 (S6K1) pathway decreases tumor suppressor pr

40 Leucine alone stimulated ribosomal protein s6 kinase 1 (S6K1) phosphorylation approximately 280% mo

41 The p70 ribosomal protein S6 kinase 1 (S6K1) plays a key role in cell growth and p

42 Although mTORC1-p70 ribosomal S6 kinase 1 (S6K1) signaling is critical for translation

43 We sought to perturb p70 ribosomal S6 kinase 1 (S6K1), a key translation initiation and elo

44 identified PKD3 to trigger the activation of S6 kinase 1 (S6K1), a main downstream target of the mamm

45 on mTOR signaling, the ribosomal protein S6, S6 kinase 1 (S6K1), and eukaryotic translation initiatio

46 tein (4E-BP) and activates ribosomal protein S6 kinase 1 (S6K1), both of which stimulate translation.

47 wnstream of mTORC1 include ribosomal protein S6 kinase 1 (S6K1), eukaryotic translation initiation fa

48 Within this pathway we have focused on S6 kinase 1 (S6K1), the downstream phosphorylation subst

49 via its downstream target ribosomal protein S6 kinase 1 (S6K1), which directly phosphorylates S1859

50 Overexpression of ribosomal protein S6 kinase 1 (S6k1), which encodes a downstream substrate

51 o the inhibitory effects of rapamycin and an S6 kinase 1 (S6K1)-specific inhibitor on T cell activati

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

53 a on S167 via its effector-the 40S ribosomal S6 kinase 1 (S6K1).

54 ing protein 1 (4E-BP1) and ribosomal protein S6 kinase 1 (S6K1).

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

56 rate-1 (Tyr-608), Akt (Thr-308 and Ser-473), S6 kinase 1 (Thr-389), eukaryotic initiation factor 4E b

57 phosphorylation (e.g., p70 ribosomal protein S6 kinase 1 [S6K1] and eukaryotic initiation factor 4E b

58 e putative ERK site on IRS1 (Ser(612)) or on S6 kinase 1 activity.

59 ciated with an increase in ribosomal protein S6 kinase 1 and eukaryotic initiation factor 4E-binding

60 itor implicated a role for ribosomal protein S6 kinase 1 in IL-33-induced mTOR-dependent cytokine pro

61 Furthermore, use of a ribosomal protein S6 kinase 1 inhibitor implicated a role for ribosomal pr

62 1-dependent manner in NIH 3T3 cells, whereas S6 kinase 1 is the dominant regulator in hepatocellular

63 orylation of their substrates phosphorylated S6 kinase 1 or phosphorylated S6 ribosomal protein and p

64 the mammalian target of rapamycin complex 1/S6 kinase 1 pathway downstream of nutrient signaling.

65 r signal-regulated kinase 1/2, and ribosomal S6 kinase 1 signal transduction pathways and subsequent

66 However, activation of the ribosomal S6 kinase 1 via mTOR (P < 0.02), and total upstream bind

67 lysis of divergent signaling through ERK1/2, S6 kinase 1, and 4E binding protein 1 provides insights

68 et of rapamycin complex 1, ribosomal protein S6 kinase 1, and eukaryotic translation initiation facto

69 lular signal-regulated kinase 1/2, ribosomal S6 kinase 1, or cAMP responsive element binding protein

70 d downstream activation of ribosomal protein S6 kinase 1/4E-BP1 pathway.

71 tes (mammalian target of rapamycin complex-1/S6 kinase 1/HIF-1alpha) were detected in LPS-stimulated

72 rcentage points), greater phosphorylation of S6-kinase 1 (p85 S6K1(Thr412) , 19%; p70 S6K1(Thr389) ,

73 ing protein 1 (4E-BP1) and ribosomal protein S6 kinase-1 (S6K1), whereas HIF-1alpha degradation remai

74 stream targets Akt and the ribosomal protein S6 kinase-1 (S6K1).

75 p90 ribosomal S6 kinase 2 (p90RSK2) is important in diverse cellular p

76 We identified ribosomal S6 kinase 2 (RSK2) as the kinase responsible for H2BS32

77 Herein, we found that ribosomal S6 kinase 2 (RSK2) directly phosphorylates histone H2AX

78 The ribosomal S6 kinase 2 (RSK2) is a member of the p90 ribosomal S6 k

79 The ribosomal S6 kinase 2 (RSK2) is a well-known serine/threonine kina

80 red that the ERK/MAPK effector p90 ribosomal S6 kinase 2 (RSK2) phosphorylates the 5-HT(2A) receptor

81 Here, we report that p90 ribosomal S6 kinase 2 (RSK2) promotes human HNSCC cell invasion an

82 e previously demonstrated that p90 ribosomal S6 kinase 2 (RSK2) promotes tumor metastasis.

83 otably, we showed that EGF induces ribosomal S6 kinase 2 (RSK2) ubiquitination, and knocking down TRA

84 neurons cultured from mice lacking ribosomal S6 kinase 2 (Rsk2), a model for the Coffin-Lowry syndrom

85 We found that the p90 ribosomal S6 kinase 2 (RSK2)-cAMP response element-binding protein

86 t growth factor 2 (FGF-2) signalling-induced S6 kinase 2 (S6K2) activation is necessary, but the down

87 is study, we evaluated p70 ribosomal protein S6 Kinase 2 (S6K2), a downstream effector of mTORC1, for

88 ere, we demonstrate that RSK2 (p90 ribosomal S6 kinase 2) plays a critical role in ER stress-induced

89 the MEK inhibitor PD98059, or the ribosomal S6 kinase-2 (RSK-2) inhibitor BI-D1870.

90 The RPS6KA6 gene encodes the p90 ribosomal S6 kinase-4 (RSK4) that is still largely uncharacterized

91 malian target of rapamycin/ribosomal protein S6 kinase, 70 kDa, pathway and thereby stimulate protein

92 malian target of rapamycin/ribosomal protein S6 kinase, 70 kDa, pathway, and the importance of this C

93 Ribosomal protein S6 kinase, 90 kDa, polypeptide 1 (RSK1; official name RP

94 A specific inhibitor of S6 kinase, a downstream target of mTORC1, did not block

95 Phosphorylation of ribosomal S6 kinase, a mammalian target of rapamycin (mTOR) target

96 re hypertrophied, and the phosphorylation of S6 kinase, a target of mammalian target of rapamycin (mT

97 constitutive activation of ribosomal protein S6 kinase A1 drives tumor invasion.

98 Transcriptomic analysis of ribosomal protein S6 kinase A1-activated tumors identified metabolic chang

99 ic target of rapamycin and ribosomal protein S6 kinase A1.

100 Conversely, an S6 kinase acetylation-deficient mutant induced all the a

101 Our data reveal a new function for an S6 kinase acting through an AMP kinase in regenerative g

102 We show here that S6 kinase, activated in the liver upon feeding, can phos

103 d in TLR-4-mediated 70-kDa ribosomal protein S6 kinase activation and enhanced TNF-alpha release, whe

104 oxidative stress) that are also positive for S6-kinase activation (a marker associated with aging).

105 ty of glucocorticoids to inhibit Akt and p70 S6 kinase activity and reduced glucocorticoid induction

106 tion leads to reduced mTOR activity, reduced S6 kinase activity, and activation of autophagy to reduc

107 reduced concomitant with increased HDAC1 and S6 kinase activity.

108 S6 kinase acts as a driver for renal hypertrophy and mat

109 /mammalian target of rapamycin/p70 ribosomal S6 kinase (Akt/mTOR/p70S6K) in the kidney were measured

110 ) phosphorylation of mTOR downstream targets S6 kinase and 4E-binding protein; and (4) formation of e

111 cells based on decreased phosphorylation of S6 kinase and 4E-BP1.

112 transduction to increase phosphorylation of S6 kinase and 4EBP-1.

113 d that UCH-L1 impairs mTORC1 activity toward S6 kinase and 4EBP1 while increasing mTORC2 activity tow

114 by CSPGs selectively inactivated CRMP2, APC, S6 kinase and CREB.

115 f raptor and mTOR and the downstream targets S6 kinase and eukaryotic initiation factor 4B.

116 ced phosphorylation of Akt, MAP kinases, and S6 kinase and Fos expression in the absence of Crk and C

117 is, including IFN-induced phosphorylation of S6 kinase and its effector rpS6, as well as phosphorylat

118 acetylation and enhanced phosphorylation of S6 kinase and its substrates rps6 and eEF2 kinase that l

119 ated mTORC1 activity, evidenced by decreased S6 kinase and Lipin1 phosphorylation.

120 AKT/mammalian target of rapamycin/ribosomal S6 kinase and MEK/ERK/RSK pathways because it was resist

121 HDAC1 decreased the acetylation of S6 kinase and mimicked the effects of high glucose, resu

122 1/2 and of two downstream targets (ribosomal S6 kinase and mitogen- and stress-activated protein kina

123 ase (AMPK) and upstream of ribosomal protein S6 kinase and mTOR complex 1 (TORC1), by its direct asso

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

125 Furthermore, ribosomal protein S6 kinase and S6 phosphorylation were increased.

126 ministration simultaneously activated mTORC1/S6 kinase and STAT3 signaling.

127 pS6), suggesting activation of the ribosomal S6 kinases and increased translation.

128 es ordered C-terminal phosphorylation by p70 S6 kinases and p90 ribosomal S6 kinases on four conserve

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

130 amatically inhibited insulin-stimulated Akt, S6 kinase, and 4E-BP1 phosphorylation but had little eff

131 ed IGF-1R-induced phosphorylation of PRAS40, S6 kinase, and 4EBP-1, indicating inhibition of mTORC1 a

132 ownregulation of germline targets, including S6 kinase, and by the activation of an intestinal transc

133 n-activated protein kinase kinase, ribosomal S6 kinase, and cyclin-dependent kinase 1/2 in combinatio

134 owed increased nuclear levels of phospho-p70 S6 kinase, and neurons protected with DRB and flavopirid

135 s of p70 S6 protein kinase and p90 ribosomal S6 kinase, and there is good evidence that it plays a po

136 orylation of ERK1/2, CREB, and p90 ribosomal S6 kinase, as well as a decreased level of pore formatio

137 obic motif, on the AGC kinases Akt, PKC, and S6 kinase, as well as an inhibitory site on the kinase M

138 phosphorylation levels of the AKT, MEK, and S6 kinase at concentrations as high as 10 mumol/L.

139 investigated regulation of ribosomal protein S6 kinase B1 (RPS6KB1) by AURKA and the effects of alise

140 The human kinase ribosomal protein S6 kinase beta-1 (RPS6KB1) was shown to play a role in M

141 y activation by catalyzing ribosomal protein S6 kinase beta-1 (S6K1) O-GlcNAcylation and suppressing

142 her involving the RPS6KB1 (Ribosomal protein S6 kinase beta-1) were recurrently expressed in a number

143 orylation of its downstream targets mTOR and S6 kinase, but not for Erk1/2 activation.

144 the proteasome (by MG-132) or p90 ribosomal S6 kinases (by BI-D1870) is further increased by knockdo

145 inase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun, and cAMP response element binding prot

146 These data illustrate that S6 kinase can modify PGC-1alpha and thus allow molecular

147 We demonstrate that S6 kinases can phosphorylate the extended C-terminal dom

148 uncovered a previously unrecognized role of S6 kinase deacetylation in high glucose-induced mesangia

149 To determine the mechanism of S6 kinase deacetylation, we found that trichostatin A, a

150 (AMPK)-mammalian target of rapamycin (mTOR)-S6 kinase-dependent manner in LXA4-treated KSHV-infected

151 as regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism, unlike in macrophages in

152 rapamycin (mTOR) hyperactivation, leading to S6-kinase-dependent degradation of p27.

153 for inhibition of Thr-389 phosphorylation on S6 kinases (EC(50) = 2 nM) relative to other inhibitors.

154 The p90 ribosomal S6 kinase family (RSK1-4) is a group of highly conserved

155 , in daf-16/FOXO, sir-2.1, rsks-1 (ribosomal S6 kinase), gcn-2, and aak-2 (AMPK) longevity pathway mu

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

157 RSKs (p90 ribosomal S6 kinases) have emerged as central regulators of cell m

158 ho80p/Pho85p and by the nitrogen-sensing Akt/S6 kinase homolog, Sch9p.

159 Cepsilon (PKCepsilon), as well as ribosomal S6 kinase II (RSK2), which have different specificities

160 ling molecules forkhead box O (FOXO) and p70 S6 kinase in a tissue and blood meal-specific manner.

161 sphorylation of the S6 kinase RSK (ribosomal S6 kinase) in breast cancer cells.

162 Because p70 S6 kinase is known to induce translation of mRNAs contai

163 RSK (p90 ribosomal S6 kinase) is a MAPK-activated protein kinase required f

164 of phosphorylation of ERK-1/2, p90 ribosomal S6 kinase-l and Akt, although phosphorylations occur mor

165 Upon feeding, dietary cholesterol stimulates S6 kinase-mediated phosphorylation of the Boi cytoplasmi

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

167 stress and the mammalian target of rapamycin/S6 kinase (mTOR/S6K) pathway.

168 mammalian target of rapamycin complex 1 and S6 kinase (mTORC1--> S6K) attenuates insulin-stimulated

169 rylation by p70 S6 kinases and p90 ribosomal S6 kinases on four conserved Ser residues (Ser-235, Ser-

170 > mechanistic target of rapamycin (mTOR) --> S6 kinase or MEK pathways.

171 stream of mTOR, persistent inhibition of p70 S6 kinase or S6K1 can activate Akt via a negative feedba

172 uced decreases in mTOR-regulated phospho-p70 S6 kinase (P-p70) and the p62 protein, as well as increa

173 stern blot analysis of p-mTOR, p70 ribosomal S6 kinase (p-P70S6K), p-S6RP, and p-4EBP1.

174 nd its downstream effector p70/p85 ribosomal S6 kinase (p70/85S6K).

175 ted protein kinases (MAPK)/ribosomal protein S6 kinases (p70 S6K) pathway.

176 of ERK2, activation of the ribosomal protein S6 kinase (p70S6K) and its downstream target, ribosomal

177 ered role of the mTOR complex 1 (mTORC1)/p70 S6 kinase (p70S6K) in the negative regulation of PD-L1 o

178 ion required phosphorylation of TRIB2 by p70 S6 kinase (p70S6K) via another domain (amino acids 69-85

179 its downstream target, ribosomal protein p70 S6 kinase (p70S6K), and concomitant inhibition of cell g

180 of the downstream pathways of p70 ribosomal S6 kinase (p70S6K), eukaryotic initiation factor 4E-bind

181 S6 is regulated by ERK via the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by

182 s have identified p90 subfamily of ribosomal S6 kinase (p90RSK) family kinases as key factors for gro

183 se 2 (RSK2) is a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins and plays a critic

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

185 (EGFR) that is coupled to MAPK/p90 ribosomal S6 kinase (p90RSK), but not phosphatidylinositol 3-kinas

186 of the known ERK1/2 substrate p90 ribosomal S6 kinase (p90RSK).

187 eport the critical role of the p90 ribosomal S6 kinase (p90RSK)/ERK5 complex in EC dysfunction in dia

188 S6) and the upstream kinase 90-kDa ribosomal S6 kinase (p90S6K).

189 of the mammalian target of rapamycin (mTOR)/S6 kinase pathway in a PLD- and endocytosis-dependent ma

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

191 f the PI3-kinase/mTOR Complex 1 (mTORC1)/p70 S6-kinase pathway.

192 K3) and mammalian target of rapamycin (mTOR) S6 kinase pathways, protein kinase Czeta (PKCzeta) pathw

193 -3s also reduces the level of phosphorylated S6 kinase, phosphorylated Thor/4E-BP and cyclin E (CycE)

194 The increased S6 kinase phosphorylation in Tec-deficient B cells was d

195 SV treatment also partially blocked mTOR and S6 kinase phosphorylation in TSC1/2-deficient mouse embr

196 not neuroprogenitor cells, ribosomal S6 and S6 kinase phosphorylation increased over time, despite a

197 GDC-0941, targeted the downstream ribosomal S6 kinase phosphorylation to significantly suppress 5-FU

198 rgin stimulated mTORC1 activity (measured as S6 kinase phosphorylation) to a greater extent in wild-t

199 ytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 translocatio

200 inhibition of the mTORC1 pathway reported by S6 kinase phosphorylation.

201 ted modulation of B7-H2 on GECs involves p70 S6 kinase phosphorylation.

202 or, as measured by reduced ribosomal protein S6 kinase phosphorylation.

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

204 protein kinase 2 (ERK) and ribosomal protein S6 kinase polypeptide 2 (p90RSK).

205 sphorylation of upstream S6 kinase/ribosomal S6 kinase residues.

206 horylation of AMPK and p70 ribosomal protein S6 kinase, respectively) and IL-6/IL-6 receptor signalin

207 mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated p

208 ated kinase) and S6K-RPS6 (ribosomal protein S6 kinase-ribosomal protein S6) axes.

209 d required prior phosphorylation of upstream S6 kinase/ribosomal S6 kinase residues.

210 d high glucose-stimulated phosphorylation of S6 kinase, rps6 and eEF2 kinase, and inhibited the depho

211 nents diverging, as in the case of ribosomal S6 kinase RPS6KA1.

212 PI3K/mTOR) blockade, including the ribosomal S6 kinases RPS6KA2 (RSK3) and RPS6KA6 (RSK4).

213 Ribosomal protein S6 kinase (RPS6KA3 or RSK2) was the most potent sensitiz

214 o exhibited decreased levels of phospho-Akt, S6 kinase (RPS6KB1), and phosphorylated S6 protein (RPS6

215 ed that WFA activated phosphorylation of the S6 kinase RSK (ribosomal S6 kinase) in breast cancer cel

216 ORF45, mediates sustained ERK-p90 ribosomal S6 kinase (RSK) activation during KSHV lytic replication

217 signal-regulated kinase (ERK)-p90 ribosomal S6 kinase (RSK) activation, which is induced by an immed

218 uated for their ability to inhibit ribosomal s6 kinase (RSK) activity and cancer cell proliferation.

219 o increased phosphorylation of p90-ribosomal S6 kinase (RSK) and a concomitant activation of ETS-like

220 n to induce cell signaling through ribosomal S6 kinase (RSK) and enhance protein translation.

221 While the p90 ribosomal S6 kinase (RSK) family has been implicated in multiple t

222 p90 ribosomal S6 kinase (RSK) family members are effectors for extrace

223 The ribosomal S6 kinase (RSK) family of kinases is a group of extracel

224 ndent protein kinase (PKA) and p90 ribosomal S6 kinase (RSK) in cardiomyocyte apoptosis.

225 Ribosomal S6 kinase (RSK) is a key downstream element of the MAPK

226 The p90 ribosomal S6 kinase (RSK) is one of these kinases, although its ro

227 mediated by either the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-

228 lar regulated kinase (ERK) and p90 ribosomal S6 kinase (RSK) proteins, we found several other copurif

229 the phosphorylation of Erk1/2, p90 ribosomal S6 kinase (RSK), and p38 in a temporal order.

230 ia the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by the site of elevated ph

231 We show here that the ribosomal s6 kinase (Rsk), often elevated in cancers, can suppress

232 causes sustained activation of p90 ribosomal S6 kinase (RSK), which is crucial for KSHV lytic replica

233 ent study has revealed a novel ERK/ribosomal S6 kinase (RSK)-dependent mechanism that regulates DR5 e

234 chinery through its substrate, p90 ribosomal S6 kinase (RSK).

235 ing by binding directly to the p90 ribosomal S6 kinase (RSK).

236 gative regulator of IRS-1, the p90 ribosomal S6 kinase (RSK).

237 af-1 phosphorylation by the 90-kDa ribosomal S6 kinase (Rsk).

238 of the MEK kinase (MEKK)1/ERK/p90 ribosomal S6 kinase (RSK)1-dependent C/EBPbeta signaling pathway i

239 The p90 ribosomal S6 kinases (RSK) are implicated in various cellular proc

240 5 is a robust activator of the p90 ribosomal S6 kinases (RSK), and we found that this activity is nec

241 g pathways, we have identified the ribosomal S6 kinase RSKS-1 as a new cell-autonomous inhibitor of a

242 causes sustained activation of p90 ribosomal S6 kinases (RSKs) and extracellular regulated kinase (ER

243 use model of liver-specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of an ad

244 The 40S ribosomal protein S6 kinase (S6K) acts downstream of mTOR, which plays imp

245 urther increased phosphorylation of ribosome S6 kinase (S6K) and BAD (Bcl-2-associated death promoter

246 ATRA suppressed phosphorylation of ribosomal S6 kinase (S6K) and its downstream targets S6 and eIF4B.

247 sion with increased levels of phosphorylated S6 kinase (S6K) and S6 was observed, consistent with con

248 We also demonstrate that S6 kinase (S6K) and serotonin production are involved in

249 hat mammalian target of rapamycin (mTOR) and S6 kinase (S6K) are highly expressed in the undifferenti

250 e investigated the role of ribosomal protein S6 kinase (S6K) at the intersection of nutrition and the

251 The 40S ribosomal protein S6 kinase (S6K) is a conserved component of signalling p

252 In this paper, we demonstrate that S6 kinase (S6K) localizes to the presynaptic active zone

253 hosphorylation is mediated by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) i

254 The mammalian target of rapamycin (mTOR) and S6 kinase (S6K) pathway is essential for cell differenti

255 rations activated the PI3K/mTORC2/PKB/mTORC1/S6 kinase (S6K) pathway, but pathophysiologically high a

256 bidopsis TOR activity based on its conserved S6 kinase (S6K) phosphorylation.

257 how that the mechanism for this involves the S6 kinase (S6K) signaling enzyme.

258 tivation of both pathways but also abrogated S6 kinase (S6K) signaling.

259 igration an additional pathway that involves S6 kinase (S6K) through PLD2-Y(296), known to be phospho

260 d oral Mf demonstrated greater inhibition of S6 kinase (S6K), a downstream effector of mTOR complex 1

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

262 iated protein kinases (ROCK1 and ROCK2), p70 S6 kinase (S6K), and mammalian target of rapamycin (mTOR

263 ich syndrome protein (WASp), Grb2, ribosomal S6 kinase (S6K), and Rac2.

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

265 factor 4E (eIF4E) expression, but inhibited S6 kinase (S6K).

266 g cascade includes the small GTPase Arf6 and S6 kinase (S6k).

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

268 o, decreased basal Akt and ribosomal protein S6 kinase (S6K1) activation, and decreased transformatio

269 tly PMT induces phosphorylation of ribosomal S6 kinase (S6K1) and its substrate, ribosomal S6 protein

270 we identify a role for the ribosome protein S6 kinase (S6K1) and its upstream regulator mTOR in the

271 mTOR complex 1 (mTORC1) and p70 S6 kinase (S6K1) are both involved in the development of

272 gnaling pathway, activation of p70 ribosomal S6 kinase (S6K1) through mTORC1, is also triggered by PK

273 p70 ribosomal S6 kinase (S6K1), a major substrate of the mammalian tar

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

275 micking the function of the cellular protein S6 kinase (S6KB1).

276 unction analysis of Drosophila p90 ribosomal S6 kinase (S6KII) or its mammalian homolog RSK has not b

277 Inhibition of mTORC1/S6 kinase signaling by rapamycin induced colocalization

278 ncreased activation of the intracellular Akt/S6 kinase signaling pathway upon BCR and CD40 stimulatio

279 ession as a sensitive reporter of tonic mTOR-S6 kinase signaling through a novel mouse strain, chino,

280 ian target of rapamycin (mTOR)/p70 ribosomal S6 kinase signaling was activated by A53T but not WT alp

281 racellular signal-regulated kinase-ribosomal s6 kinase signaling was downstream of YAP for cell survi

282 nduces autophagy via the suppression of mTOR/S6 kinase signaling.

283 A C-terminal acetylation-mimetic mutant of S6 kinase suppressed high glucose-stimulated phosphoryla

284 lving Sch9, an homologous kinase to metazoan S6 kinase, targets Maf1 at a subset of PKA sites.

285 subunit of protein kinase A (PKAc), ribosmal S6 kinase that controls RelA Ser 276 phosphorylation.

286 gulates the phosphorylation of p70 ribosomal S6 kinase, the major downstream target of mTOR complex 1

287 rylation of tau can be regulated through p70 S6 kinase, the well characterized immediate downstream t

288 rectionally regulated by RSK3 (p90 ribosomal S6 kinase type 3) and PP2A (protein phosphatase 2A) at s

289 As a post-translational modification, S6 kinase undergoes acetylation at the C terminus.

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

291 unlike in macrophages in which p90 ribosomal S6 kinase was not required.

292 However, phosphorylation of p70 S6 kinase was observed in the liver of all three phenoty

293 omeruli of diabetic rats, the acetylation of S6 kinase was significantly reduced concomitant with inc

294 Downstream, phosphorylation of S6-kinase was also diminished in both cell lines in a do

295 known Phlpp1 substrates, Akt2, PKC, and p70 S6 kinase, were enhanced in ex vivo cultured Phlpp1(-/-)

296 substrate mTOR, and the mTOR substrate, p70 S6 kinase, were indeed reduced in Hdac3-deficient primar

297 of processing requires the mTORC1 target p70 S6-kinase, whereas induction of mRNA bypasses this enzym

298 unique developmental functions for eIF4E and S6 kinase wherein their activity is specifically uncoupl

299 rol subjects was found for ribosomal protein S6 kinase, which did not change after CBT and did not co

300 reased phosphorylation and activation of p70 S6 kinase, which was inhibited by both DRB and flavopiri