ライフサイエンスコーパス: RICTOR

1 through induction of PTEN and suppression of RICTOR.

2 mTORC1, and this interaction is dependent on rictor.

3 homeostasis and function of B cells require Rictor.

4 ty and decreased the association of mTOR and rictor.

5 Rheb, mTOR, or raptor, but also by siRNA for rictor.

6 tyrosine phosphatase receptor S (PTPRS), and RICTOR.

7 and P-Ser473 Akt were inhibited by siRNA for rictor.

8 ted silencing of mTORC1/2 subunits Raptor or Rictor.

9 eficient cells with re-expression of ectopic rictor.

10 ing a unique mTOR complex lacking Raptor and Rictor.

11 cytes by disrupting the assembly of mTOR and rictor.

12 we detected an interaction between FBXW7 and rictor.

13 (13 [7%]), SMARCA4 (12 [6%]), RB1 (12 [6%]), RICTOR (12 [6%]), MLL2 (12 [6%]), BRAF (11 [6%]), and BR

14 ntified a signaling pathway involving Sirt1, Rictor (a component of mTOR complex 2 [mTorc2]), Akt, an

15 HL-60 cells, we describe a pivotal role for Rictor, a component of mammalian target of rapamycin com

16 eases mTORC2 activity, and overexpression of Rictor, a component of mTORC2, prevents morphine-induced

17 Here we demonstrate that rictor, a key component of mTORC2, plays a critical role

18 we generated a conditional knockout (CKO) of Rictor, a key component of mTORC2.

19 AKT in NK92 cells, and miR-142-3p inhibited RICTOR, a key component of the mTOR complex, with second

20 A similar effect was seen when Rictor, a key mTORC2 component, was selectively silenced

21 Furthermore, inhibitory phosphorylation of rictor, a key regulatory/structural subunit of the mTORC

22 transcriptionally upregulates expression of RICTOR, a pivotal component of mTOR complex 2 (mTORC2),

23 ed by a direct interaction between STIM1 and Rictor, a specific component of mTOR complex 2.

24 or Rictor gene targeting, we discovered that Rictor ablation inhibited vascular endothelial growth fa

25 luding the NAD+-dependent sirtuins, promotes Rictor acetylation and IGF-1-mediated Akt phosphorylatio

26 cal Notch signaling dependent on the adaptor Rictor activated the kinase AKT-transcription factor Fox

27 Rictor, an essential component of mTOR complex 2 (mTORC2

28 wed that FoxOs upregulated the expression of Rictor, an essential component of MTOR complex 2, in res

29 Conditional deletion of Rictor, an essential component of mTORC2, impaired Notch

30 st, newborns with an epidermal deficiency of Rictor, an essential component of mTORC2, survive despit

31 Furthermore, siRNA-mediated knockdown of rictor, an mTORC2 partner protein, reduced mTORC1 substr

32 Loss of Rictor, an obligatory component of mTORC2, decreased thy

33 which inhibit both mTORCs, by knocking down rictor and by knocking out rictor or Sin1 but not by sil

34 AGC kinases disrupts the interaction between Rictor and Cullin-1 to impair SGK1 ubiquitination.

35 se kinase 3 (GSK3): GSK3 was associated with rictor and directly phosphorylated the Thr-1695 site in

36 f this site impaired the interaction between rictor and FBXW7, decreased rictor ubiquitination, and i

37 T, HSF1 or HuR is sufficient to downregulate Rictor and inhibit GBM growth and invasive characteristi

38 Notably, rictor and IRS-1 phosphorylation by p70S6K1 attenuate in

39 Rictor and its binding partner Sin1 are indispensable co

40 tion of antiviral responses are defective in Rictor and mLST8-KO cells.

41 C2 activity by decreasing the association of rictor and mTOR, thereby down-regulating insulin action.

42 However, it is not known whether rictor and mTORC2 regulate mast cell activation.

43 ta-cell mass was normal in mice lacking both Rictor and Pten (betaDKO), their beta-cells were larger

44 ignaling, which is reciprocally regulated by Rictor and Pten, in NKT17 lineage determination.

45 always accompanied by disassociation of mTOR/rictor and reduction of mTORC2 kinase activity.

46 hereas mTORC2 lacks Raptor and, instead, has Rictor and SIN1 as distinct essential components.

47 Our studies also demonstrate that Rictor and Sin1 play essential roles in the generation o

48 Additional work further confirmed CDK6, RICTOR, and CTSB (cathepsin B) as targets of miR-218 and

49 ap-dependent mRNA translation, whereas mTOR, rictor, and mSin1 (mTORC2) activate the survival and pro

50 key intracellular signaling molecules, AKT, RICTOR, and Rac1, to drive PCa metastasis.

51 Through additional Rptor, Rictor, and Rptor/Rictor mutant mouse models, we identif

52 hondrial complex I, IV and V; (ii) activated RICTOR; and (iii) progenitor cell markers.

53 ation of mature B lymphocytes, and establish Rictor as an important signal relay in B-cell homeostasi

54 TOR-independent companion of MTOR complex 2 (RICTOR) as the direct targets of miR-188.

55 Rictor-associated mTORC2 complex has been linked to main

56 inct complexes: Raptor-associated mTORC1 and Rictor-associated mTORC2.

57 Here, we report that Rictor associates with Cullin-1 to form a functional E3

58 ation was further supported by enhanced mTOR/RICTOR association and increased phosphorylation of addi

59 y, in hepatocytes from Gpat1(-/-) mice, mTOR-rictor association and mTORC2 activity were enhanced.

60 get of rapamycin complex (mTORC) 2 component rictor at early stages of T cell development led to aber

61 of a feedback mechanism, phosphorylation of Rictor at T1135 by multiple AGC kinases disrupts the int

62 Using an in vivo model, a down-regulation of rictor at the BTB was also detected during adjudin-induc

63 le inhibition of mTORC1 (Raptor) and mTORC2 (Rictor), attenuated migration and invasion of CRCs.

64 Conditional deletion of Rictor before lymphoid specification impaired generation

65 The inhibition of mTOR/rictor binding and mTORC2 activity coincided with the le

66 xperiments, SGK1 interacted selectively with rictor but not with raptor, suggesting selective recruit

67 Knockdown of rictor, but not raptor, also decreased mSREBP1.

68 Depletion of mTOR and Rictor, but not Raptor, impairs actin polymerization, le

69 n of mammalian target of rapamycin (mTOR) or rictor, but not raptor, implicating mTORC2 as the target

70 In Tsc2-deficient cells, the elevation of Rictor by FoxO increases mTORC2 assembly and activity at

71 Indeed, the knockdown of rictor by RNAi was found to perturb the Sertoli cell TJ-

72 Finally, knockdown of Rictor by small interfering RNAs enhanced Treg induction

73 Our study reveals that rictor by suppressing RhoGDI2 promotes activity of the R

74 In the absence of Rictor, CD4(+) T cells proliferate normally in limiting

75 ors can induce AKT (S473) phosphorylation in Rictor(-/-) cells, and this effect is insensitive to mTO

76 Rictor CKO mice are hyperactive and have reduced anxiety

77 Rictor CKO mice have small brains and bodies, normal lif

78 -immunoprecipitate mTOR with both Raptor and Rictor, components of mTOR complexes 1 and 2 (mTORC1 and

79 ve CD4(+) T cells, and the mTORC2 component, Rictor, contained a functional target site for miR-15b/1

80 Here, we demonstrate that Rictor contains two distinct central regions critical fo

81 These findings indicate that the Rictor/Cullin-1 E3 ligase activity is regulated by a spe

82 Loss of Rictor/Cullin-1-mediated ubiquitination leads to increas

83 e that proinflammatory cytokines produced by Rictor(-/-) DC after LPS stimulation are key in promotin

84 Accordingly, TLR4-activated Rictor(-/-) DC display augmented allogeneic T cell stimu

85 ng Dectin-1 (C-type lectin family member) on Rictor(-/-) DC.

86 an increase in SIRT1-MTORC2 interaction and RICTOR deacetylation.

87 model of breast cancer, genetic ablation of Rictor decreased cell survival and phosphorylation at S4

88 Rictor deficiency caused a partial block of thymocyte de

89 The effect of Rictor deficiency is selective for the T cell lineage, a

90 ed storage of fatty acids that resembles the rictor deficiency phenotype.

91 Strikingly, Rictor deficiency selectively abolished the NKT17 lineag

92 nt in rictor or Sin1 compared with parent or rictor-deficient cells with re-expression of ectopic ric

93 hat phosphorylation of FoxO1 was impaired in rictor-deficient cells, resulting in elevated nuclear Fo

94 d AKT (Myr-AKT) rescued vascular assembly in Rictor-deficient endothelial cells, whereas PKCalpha res

95 ra generated from a mixture of wild-type and Rictor-deficient hematopoietic stem cells demonstrated t

96 a defective Akt signaling axis, because both rictor-deficient MEFs and rictor knockdown dendritic cel

97 the hyperinflammatory phenotype exhibited by rictor-deficient MEFs.

98 Upon LPS stimulation, both rictor-deficient mouse embryonic fibroblasts (MEFs) and

99 that the morphological deficits observed in rictor-deficient neurons are mediated by PKCs.

100 ate of proliferation, and differentiation of Rictor-deficient pre-T cells.

101 e significantly attenuated on the surface of rictor-deficient thymocytes.

102 g, likely through suppressing GSK3-dependent rictor degradation.

103 However, Rictor deletion had little effect on the function of nor

104 was significantly decreased upon EC-specific Rictor deletion in mice.

105 Here we show that Rictor deletion prevents leukemogenesis and HSC depletio

106 our proteomics study we identified that the rictor-dependent deficiency in cell migration is caused

107 In this study, we examined the role of Rictor-dependent regulation of HIF-2alpha through eIF4E-

108 enerative response, characterized by an mTOR/Rictor-dependent T helper 2 pathway that guides interleu

109 d by Torin1 treatment and by raptor, but not rictor, depletion, suggesting that mTORC1 is involved in

110 ning protein, mammalian target of rapamycin, Rictor, Dock2, and GM130 as novel B-Raf interaction part

111 Posttranslational regulation of rictor (e.g. via degradation) and its underlying mechani

112 ted mutants within the acetylation region of Rictor exhibit reduced insulin-like growth factor 1 (IGF

113 However, the mechanisms regulating Rictor expression in these tumors is not clearly underst

114 adjudin-induced BTB disruption, illustrating rictor expression is positively correlated with the stat

115 We have previously demonstrated that rictor expression is substantially downregulated in term

116 ve overexpression of HuR is able to maintain Rictor expression under conditions of AKT or HSF1 loss.

117 In invasive breast cancer specimens, Rictor expression was upregulated significantly compared

118 h continued mTORC2 activity is able to drive Rictor expression.

119 kinase S6-Kinase (S6K) through modulation of Rictor expression.

120 mTORC2 signaling in their beta-cells (RIPCre;Rictor(fl/fl)) also showed reduced Pdx-1.

121 STAT3 and NFKBIA, for activated pathways and RICTOR for mitochondrial genes.

122 The cells expressing the rictor G934E mutant remain deficient in the mTORC2 signa

123 Using mouse models of Raptor or Rictor gene targeting, we discovered that Rictor ablatio

124 g because of the conditional deletion of the Rictor gene, iNKT cell numbers were reduced in the thymu

125 hed in cells with targeted disruption of the Rictor gene, whose protein product is a key element of m

126 ith conditional deletion of either Raptor or Rictor genes to determine potential contribution of the

127 binding partner Sin1, a single amino acid of rictor Gly-934 controls its interaction with Sin1 and as

128 A substitution of the rictor Gly-934 residue to a charged amino acid prevents

129 Overexpression of Rictor has been demonstrated to result in increased mech

130 islets, whereas mTORC2 (with adaptor protein Rictor) impacts islet mass and architecture.

131 However, the role of Rictor in B cells still remains elusive.

132 We replicated these findings by silencing Rictor in breast cancer cell lines, but not silencing th

133 Loss of rictor in fat cells prevents insulin-stimulated phosphor

134 Knockdown of mTOR, Raptor or Rictor in lal(-/-) MDSCs suppressed their stimulation on

135 mice lacking the essential mTORC2 component rictor in liver (Lrictor(KO)) are unable to respond norm

136 Selective deletion of Rictor in macrophages prevents M2 differentiation and cl

137 onally deleting the essential mTORC2 subunit Rictor in mature adipocytes decreases ChREBPbeta express

138 genes mTOR, Rptor, Rictor, or both Rptor and Rictor in mouse ISCs, progenitors, and differentiated in

139 obligatory component of mTORC2, the role of Rictor in T cells is well established.

140 ines that are devoid of the mTORC2 component rictor in the entire central nervous system or in Purkin

141 te-specific genetic deletion of Rptor and/or Rictor in the mouse, that CNS myelination is mainly depe

142 n, we conditionally ablated either Raptor or Rictor in the oligodendrocyte lineage, in vivo.

143 We found that conditional deletion of Rictor in the postnatal murine forebrain greatly reduced

144 kinase-independent function and mechanism of Rictor in the regulation of neutrophil chemotaxis.

145 data demonstrated that targeted mutation of Rictor in the thymocytes drastically reduced the thymic

146 bited mTORC2 activity and disassociated mTOR/rictor in vitro.

147 Further, local knockout of Rictor in VTA decreases DA soma size and reduces rewardi

148 e specificity factors raptor (in mTORC1) and rictor (in mTORC2).

149 plexes mTORC1 (mTOR-Raptor) and mTORC2 (mTOR-Rictor) in PAVSMC proliferation and survival in PAH and

150 ith rapamycin-insensitive companion of mTOR (Rictor) in these processes.

151 Overexpression of rictor, in contrast with knockdown, suppressed Fcepsilon

152 p300-mediated acetylation of Rictor increases mTORC2 activity toward Akt, whereas sit

153 IgE (FcepsilonRI) is negatively regulated by rictor independently of mTOR.

154 conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while l

155 Silencing raptor (inhibits mTORC1) or rictor (inhibits mTORC2) markedly decreased basal folate

156 Silencing raptor (inhibits mTORC1) or rictor (inhibits mTORC2) markedly decreased basal System

157 n does not interfere with the binding of the rictor-interacting protein Protor.

158 ccludin, ZO-1) at the BTB, illustrating that rictor is a crucial BTB regulator.

159 se to NVP-BEZ235 treatment and revealed that Rictor is a key downstream target of FoxOs in NVP-BEZ235

160 n together, these data provide evidence that rictor is a multifunctional signaling regulator that can

161 Rictor is a regulatory component of the mammalian target

162 stem cells demonstrated that the function of Rictor is cell intrinsic.

163 Hence, rictor is degraded through an FBXW7-mediated ubiquitinat

164 In mice in which the mTORC2 component Rictor is deleted in liver [Rictor-knockout (RKO) mice],

165 phosphorylation is maintained when raptor or rictor is depleted, suggesting that either mTOR complex

166 eport here that the mTORC2 obligate cofactor Rictor is enriched in HER2-amplified samples, correlatin

167 Our studies establish that Rictor is essential for the generation of type II IFN-de

168 Rictor is involved in B cell development, especially the

169 We found that a suppression of RhoGDI2 by rictor is not related to the Sin1 or raptor function tha

170 In this report, we demonstrate that Rictor is regulated at the level of mRNA translation via

171 a molecular circuit of T-bet, PTEN, AKT, and RICTOR is regulated by miR-BART20-5p, miR-494-3p, and mi

172 Although Rictor is required for the stability and activity of mTO

173 Thus, although a full length of rictor is required to interact with its binding partner

174 Avo3/Rictor is unique to TORC2, but interacts with the same H

175 ced degranulation, whereas downregulation of rictor itself resulted in an increased sensitivity ( app

176 Rictor KD also abolishes the ability of chemoattractants

177 Rictor knockdown by RNAi was also found to impede Sertol

178 IO2 through the mTORC2 pathway as defined in rictor knockdown cells.

179 Rictor knockdown decreased FLIP(S) stability, whereas en

180 cient mouse embryonic fibroblasts (MEFs) and rictor knockdown dendritic cells exhibited a hyperinflam

181 axis, because both rictor-deficient MEFs and rictor knockdown dendritic cells exhibited attenuated Ak

182 TORKinib treatment and rictor knockdown did not alter Mcl-1 mRNA levels but rat

183 However, both Torin 1 treatment and Rictor knockdown led to reduced COX-2 expression and pho

184 Inhibition of mTORC2 activity by Rictor knockdown not only dramatically decreases PKCbeta

185 ndependent calcium signal, was unaffected by rictor knockdown.

186 f Cbl abrogated FLIP(S) reduction induced by rictor knockdown.

187 f Akt or mTOR kinase activity, as well as by rictor knockdown.

188 was reduced in cells treated with INK128 or rictor knockdown.

189 cued Mcl-1 reduction induced by TORKinibs or rictor knockdown.

190 This study used B cell-specfic Rictor knockout (KO) mice to investigate how Rictor regu

191 cerbate insulin resistance in adipose tissue Rictor knockout mice, implicating adipose tissue DNL as

192 We used an inducible Raptor and Rictor knockout mouse embryonic fibroblast (MEF) system

193 mTORC2 component Rictor is deleted in liver [Rictor-knockout (RKO) mice], we used genomic and phospho

194 actin (F-actin) is drastically increased in Rictor KO B cells after BCR stimulation through dysregul

195 of actin polymerization with latrunculin in Rictor KO B cells rescues the defects of BCR signaling a

196 , are reduced and enhanced, respectively, in Rictor KO B cells.

197 with a decreased humoral immune response in Rictor KO mice.

198 Second, FoxO1 elevates the expression of Rictor, leading to increased mTORC2 activity that conseq

199 Finally, enforced activation of Akt enhanced rictor levels and increased mTORC2 activity as evidenced

200 nhibited rictor ubiquitination and increased rictor levels, whereas enforced expression of FBXW7 decr

201 We examined the role of Rictor/mammalian target of rapamycin complex 2 (mTORC2),

202 YAP was also shown to be required for Rictor-mediated GBM growth and survival.

203 ated bone marrow-derived DC from conditional Rictor(-/-) mice exhibit lower coinhibitory B7-H1 molecu

204 Using novel CD11c-specific Rictor(-/-) mice, we confirm the alloreactive Th1 and Th

205 at increased expression of mTOR, Raptor, and Rictor mRNA was noted with advanced stages of CRC, sugge

206 oRNAs Let-7 and miR-16 targeted the Mtor and Rictor mRNAs.

207 exes with raptor (mTOR complex 1; mTORC1) or rictor (mTOR complex 2; mTORC2).

208 Additionally, Rictor (mTOR complex [mTORC]2)-deficient Treg showed una

209 osphorylated on Ser 2448, suggesting mTORC2 (rictor+mTOR) as the dominant form.

210 nduced phosphorylation of AKT at Ser-473 was RICTOR-mTOR-dependent, whereas ILK and PAK1/2 were dispe

211 The Rictor/mTOR complex (also known as mTORC2) plays a criti

212 elination when mTORC2 is functional, whereas Rictor (mTORC2) ablation has a modest positive effect on

213 onally dependent on their raptor (mTORC1) or rictor (mTORC2) subunits.

214 We observed that mTOR, in conjunction with rictor (mTORC2), phosphorylated SGK1 and stimulated ENaC

215 As Rictor/mTORC2 (mammalian target of rapamycin complex 2)

216 Our data suggest that Rictor/mTORC2 controls an amino acid-sensitive checkpoin

217 Instead, we found that Rictor/mTORC2 has an essential role in T cell amino acid

218 Mechanistically, Rictor/mTORC2 promotes ChREBPbeta expression in part by

219 Taken together, our findings establish that Rictor/mTORC2 signaling drives Akt-dependent tumor progr

220 et, without a compensatory activation of the rictor/mTORC2 target Akt (S475).

221 ed cell cycle arrest was mediated in part by Rictor/mTORC2, providing evidence that this nutrient rec

222 T-cell-specific ablation of Raptor/mTORC1 or Rictor/mTORC2, we revealed that both mTORC1 and, to a le

223 Our results showed that RICTOR/MTORC2-AKT can integrate convergent hormonal and

224 Through additional Rptor, Rictor, and Rptor/Rictor mutant mouse models, we identify mechanistic targ

225 creased synaptic growth was also observed in rictor mutants, while raptor knockdown did not phenocopy

226 e in a putative CDC4 phospho-degron motif of rictor; mutation of this site impaired the interaction b

227 increased SGK1 protein levels as detected in Rictor null cells.

228 Rictor null mice exhibited mild hyperglycemia and glucos

229 Reconstitution of Rictor-null cells with myristoylated AKT (Myr-AKT) rescu

230 Furthermore, rictor-null fat cells are unable to suppress lipolysis i

231 However, the role of Rictor on B cell receptor (BCR) signaling as well as the

232 Finally, knockdown of rictor or mSin1 attenuated the expression of Hif1alpha,

233 Consistently, knockdown of rictor or mTOR, but not raptor, mimicked PP242 in decrea

234 Mice with beta-cell-specific deletions of Rictor or Pten were studied to determine the effects of

235 by knocking down rictor and by knocking out rictor or Sin1 but not by silencing raptor.

236 1 levels were detected in cells deficient in rictor or Sin1 compared with parent or rictor-deficient

237 s show that transient or stable knockdown of Rictor or Sin1 results in defects in activation of eleme

238 We disrupted the genes mTOR, Rptor, Rictor, or both Rptor and Rictor in mouse ISCs, progenit

239 Suppression of mTORC2 signaling with siRNA rictor, or inhibition of mTORC1 signaling with rapamycin

240 ificantly, T-bet inhibited the PTEN-AKT-mTOR/RICTOR pathway through induction of PTEN and suppression

241 Rictor phosphorylation by p70S6K1 was specifically enhan

242 overexpression of Rheb to activate TORC1 and Rictor plus Sin1 to augment TORC2 in naive CD4 T cells f

243 that in mammalian cells the analogous single rictor point mutation (G934E) prevents the binding of ri

244 This suggests that Rictor positively regulates the early events of BCR sign

245 mTOR, Raptor, and Rictor protein levels were also significantly elevated i

246 L28170 reduced cytokine-induced increases in Rictor protein, which is the most important component of

247 ORC2), which contains the regulatory protein Rictor (rapamycin-insensitive companion of mTOR), was di

248 Mechanistically, the loss of Rictor reduced the phosphorylation of AKT, protein kinas

249 Knockdown of mTOR, but not Raptor or Rictor, reduced p-ULK1 at Ser(757) and enhanced chemothe

250 g cell metablism to BCR activation, in which Rictor regulates BCR signaling via actin reorganization.

251 Rictor knockout (KO) mice to investigate how Rictor regulates BCR signaling.

252 Here we show that rictor regulates cell migration by controlling a potent

253 How rictor regulates cell migration is poorly characterized.

254 ) and mTORC2, by binding to either Raptor or Rictor, respectively.

255 lex specific cofactors, including Raptor and Rictor, respectively.

256 mTORC1-S6K1 pathway, which in turn inhibits rictor, resulting in decreased mTORC2 signaling in Purki

257 Ablation of mTORC2 function by deletion of Rictor results in a modest reduction of LCs in skin drai

258 ed NKT17 generation, but concomitant loss of Rictor reversed the NKT17 dysregulation.

259 s of function of the essential TORC2 subunit Rictor (RICT-1) in Caenorhabditis elegans results in slo

260 rly chemotaxis studies in Dictyostelium, the rictor's ortholog has been identified as a regulator of

261 Raptor and Rictor serve as specific functional components of TORC1

262 C2 activity, achieved via knock down (KD) of Rictor, severely inhibits neutrophil polarization and di

263 vate HSF1 and demonstrate continued HSF1/HuR/Rictor signaling in the context of AKT knockdown.

264 ts suggest that multiple-site acetylation of Rictor signals for increased activation of mTORC2, provi

265 Silencing Rictor significantly decreased cyst volume and expressio

266 The decreased cyst size in the Rictor silenced cells was reversed by introduction of a

267 aling mediated by suppression of mTORC2 with Rictor similarly increased cardiomyocyte apoptosis and t

268 sembled by mTOR and its essential components rictor, Sin1 and mLST8.

269 co-expression its four essential components (rictor, SIN1, mTOR, mLST8).

270 provide evidence for critical functions for Rictor/Sin1 complexes in type I IFN signaling and the ge

271 charged amino acid prevents formation of the rictor/Sin1 heterodimer.

272 ersed growth inhibition induced by siRNA for rictor, siRNA TSC1, reexpression of TSC2, or simvastatin

273 ereas enforced expression of FBXW7 decreased rictor stability and levels.

274 creased rictor ubiquitination, and increased rictor stability.

275 S) stability, whereas enforced expression of rictor stabilized FLIP(S).

276 al mTORC1/mTORC2 inhibitor Torin, or through rictor-targeted shRNA, resulted in a significant attenua

277 s or post-translational modifications within Rictor that are responsible for regulating mTORC2.

278 monstrate the role of mTORC2 on cyst growth, Rictor, the functional component of mTORC2, was silenced

279 Rictor, the key component of mTORC2 that is known to reg

280 knockdown decreased the protein abundance of RICTOR, the key component of the mTORC2 complex, without

281 gans has linked a specific point mutation of rictor to an elevated storage of fatty acids that resemb

282 Remarkably, returning Mtor and Rictor to normal levels by deleting one allele of Mtor a

283 c and Cdc42 serve as downstream effectors of Rictor to regulate actin assembly and organization in ne

284 int mutation (G934E) prevents the binding of rictor to Sin1 and the assembly of mTORC2, but this muta

285 cofactors raptor (TOR complex 1 [TORC1]) and rictor (TORC2), we now show that TORC1 supports flavivir

286 or mTOR complex cofactors raptor (TORC1) and rictor (TORC2), we now show that TORC1 supports WNV grow

287 ectly bind the 3' untranslated region of the Rictor transcript and enhance translational efficiency.

288 echanism by which mTORC2 activity stimulates Rictor translational efficiency via an AKT/HSF1/HuR sign

289 regulates transcription of the gene encoding Rictor, triggering a cascade of phosphorylation of Akt a

290 sion of a dominant-negative mutant inhibited rictor ubiquitination and increased rictor levels, where

291 mical inhibition of the proteasome increased rictor ubiquitination and levels.

292 eraction between rictor and FBXW7, decreased rictor ubiquitination, and increased rictor stability.

293 rk used short hairpin RNA against Raptor and Rictor, unique components of mTORC1 and mTORC2, respecti

294 y in Gpat1(-/-) hepatocytes was ablated when rictor was knocked down.

295 Rictor was more abundantly expressed in Dicer(-/-) T cel

296 eleting one allele of Mtor and one allele of Rictor was sufficient to reduce Akt S473 phosphorylation

297 gulators, including NFE2L2, ATF4, Srebf1 and Rictor were identified as potential key upstream regulat

298 The mTOR components Mtor and Rictor were posttranscriptionally deregulated, and the m

299 e is the S phase translational regulation of RICTOR, which is associated with cell cycle-dependent ac

300 Survival of B lymphocytes depended on Rictor, which was vital for normal induction of prosurvi