ライフサイエンスコーパス: RAPTOR

1 ing the activity of let-363 (TOR) or daf-15 (RAPTOR).

2 a rapamycin-sensitive complex that involves Raptor.

3 king out rictor or Sin1 but not by silencing raptor.

4 to 43% in two decades of this once-abundant raptor.

5 cross-linking and interaction of 4E-BP1 with Raptor.

6 sult of enhanced interaction of p70S6K1 with raptor.

7 ween the two substrates for interaction with raptor.

8 phorylation site, RPGT908T, for ICK in human Raptor.

9 ines correlate well with theory generated by RAPTOR.

10 iation between mTOR and the mTORC1 co-factor Raptor.

11 b1, AMP-activated protein kinase (AMPK), and raptor.

12 in vitro is unaffected by the elimination of raptor.

13 curs through mTOR itself rather than through raptor.

14 an amino acid-dependent manner with mTOR and raptor.

15 enetic reduction of the mTOR-binding protein Raptor.

16 ey component of the mTOR complex 1 (mTORC1), Raptor.

17 mbly and signaling by folding both mLST8 and Raptor.

18 ORC1 inhibitor rapamycin or by knocking down raptor.

19 assay) and mTOR pathway protein expression (raptor, 4e-bp-1, and p70S6K proteins) along with enhance

20 Mass spectrometric analysis of cross-linked Raptor-4E-BP1 led to the identification of several cross

21 3% (median 19%) improvement as compared with RAPTOR (a well-known threading method) and even a mean 1

22 r stress, ABA-activated SnRK2s phosphorylate Raptor, a component of the TOR complex, triggering TOR c

23 When Raptor, a critical scaffold protein for mammalian target

24 addition, we found that MARK4 phosphorylates Raptor, a key component of mTORC1, and this phosphorylat

25 owth factor-induced nuclear translocation of Raptor, a regulatory scaffolding component in mTORC1, an

26 ed serine phosphorylation of RAPTOR in a new Raptor (AA) mouse model, in which AMPK phospho-serine si

27 Loss of Raptor abrogated T cell priming and T helper 2 (Th2) cel

28 Knockdown of rictor but not raptor abrogated UVB-induced mitophagy responses.

29 uent signaling to AMPK substrates, including Raptor, acetyl coenzyme A carboxylase, and PGC-1alpha, i

30 ic acetyl-CoA levels, which led to decreased Raptor acetylation and reduced lysosomal localization of

31 fects on autophagy are mediated by decreased raptor acetylation causing mTORC1 inhibition, rather tha

32 tutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we dis

33 Our findings indicate that the Raptor alpha-solenoid directly detects the nucleotide st

34 Ablation of Raptor also significantly extends survival of mice in mo

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

36 Conversely, targeted mutation of Raptor, an essential component of mTORC1, increased miRN

37 of the Hippo pathway, phosphorylate S606 of Raptor, an essential component of mTORC1, to attenuate m

38 ctive mutant displays higher affinity toward Raptor, an essential scaffolding component of mTORC1 tha

39 neage-specific deletion of the gene encoding RAPTOR, an essential signaling adaptor for rapamycin-sen

40 d mice with adipocyte-specific deficiency of raptor, an mTORC1 constituent.

41 we used live imaging of the mTORC1 component RAPTOR and a cell permeant fluorescent analogue of di-le

42 PK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phospho

43 n the DDB1-CUL4 ubiquitin ligase complex and raptor and counteracts DDB1-CUL4-mediated raptor ubiquit

44 tly by phosphorylation of the mTORC1 subunit Raptor and indirectly by phosphorylation of the regulato

45 TOR and its primary interactors, RAPTOR and LST8, have been remarkably evolutionarily sta

46 In the nucleus, CDK9 binds to RAPTOR and mLST8, forming CTORC1, to promote transcripti

47 as evidenced by decreased phosphorylation of raptor and mTOR and the downstream targets S6 kinase and

48 We find that the mTORC1 components raptor and mTOR are both present in nucleoli, where they

49 S100B calcium-binding protein, mTOR proteins RAPTOR and P70S6, the AMP-kinase catalytic subunit AMPKA

50 ese effects were accompanied by decreases in raptor and PRAS40 and an increase in RagC associated wit

51 159/T2164 phosphorylation modulates the mTOR-raptor and raptor-PRAS40 interactions and augments mTORC

52 In contrast, mTORC1 regulators Raptor and Rheb are dispensable for NKT17 differentiatio

53 We used an inducible Raptor and Rictor knockout mouse embryonic fibroblast (M

54 Raptor and Rictor serve as specific functional component

55 SP9X can co-immunoprecipitate mTOR with both Raptor and Rictor, components of mTOR complexes 1 and 2

56 ted by complex specific cofactors, including Raptor and Rictor, respectively.

57 This work used short hairpin RNA against Raptor and Rictor, unique components of mTORC1 and mTORC

58 tein, creating a unique mTOR complex lacking Raptor and Rictor.

59 l diameter was significantly reduced in both Raptor and Tsc1 conditional knockout mice, albeit with v

60 urine liver requires AMPK regulation of both RAPTOR and TSC2 to fully inhibit mTORC1, and this regula

61 a core subunit Raptor, whereas mTORC2 lacks Raptor and, instead, has Rictor and SIN1 as distinct ess

62 ds to regulatory-associated protein of mTOR (Raptor) and causes it to translocate to the nucleus upon

63 t of rapamycin (mTOR) complexes mTORC1 (mTOR-Raptor) and mTORC2 (mTOR-Rictor) in PAVSMC proliferation

64 ng rapamycin or stable inhibition of mTORC1 (Raptor) and mTORC2 (Rictor), attenuated migration and in

65 ion of key mTOR pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPAR

66 The signaling adaptor p62 binds raptor, and integral component of the mTORC1 pathway.

67 A significant downregulation of p-mTOR, p-Raptor, and p-S6RP was observed, which was restored to n

68 ed association of mTOR with RagB/RagC, Rheb, raptor, and PRAS40.

69 genous substrates acetyl CoA carboxylase and Raptor, and provokes mitochondrial biogenesis.

70 mTOR, Raptor, and Rictor protein levels were also significantl

71 rug insensitive, higher levels of mTOR-bound raptor are detected than in cells where rapamycin stimul

72 ous Caenorhabditis elegans RHEB-1 and DAF-15/Raptor are expressed ubiquitously and localize to lysoso

73 LET-363/TOR and DAF-15/Raptor are required for development beyond the third lar

74 LCs lacking Raptor are smaller and display reduced expression of Lan

75 pamycin (mTOR) pathway by phosphorylation of raptor as a transient cell's compensatory mechanism to p

76 Here, we identify raptor as an interacting partner of p62.

77 ifferentiation as expected, the knockdown of raptor, as well as Rheb, enhances differentiation.

78 (mTOR) functions in two distinct complexes: Raptor-associated mTORC1 and Rictor-associated mTORC2.

79 Although Raptor-associated mTORC1 is a known key upstream regulat

80 y blocking mTORC1 via the phosphorylation of Raptor at S792 through activated AMPKalpha (T172).

81 Conversely, a phosphomimetic RAPTOR augmented S6K1 activity.

82 he subunits of these complexes are mLST8 and Raptor, beta-propeller proteins that stabilize the mTOR

83 Mutations that disrupted Rag-Raptor binding inhibited mTORC1 lysosomal localization a

84 Raptor binding to Rag, although necessary, is not suffic

85 Despite amino acid-independent raptor binding to Rag, mTORC1 is inhibited by amino acid

86 The RagC variants increased raptor binding while rendering mTORC1 signaling resistan

87 Raptor-bound mTOR (mTORC1) governs cap-dependent mRNA tr

88 NA)-induced downregulation of Rheb, mTOR, or raptor, but also by siRNA for rictor.

89 ese loci requires the mTORC1 kinase adaptor, Raptor, but not Xbp1.

90 malian target of rapamycin complex 1 subunit Raptor by aldosterone induces abnormal pulmonary artery

91 [sulfosuccinimidyl] suberate, we showed that Raptor can be cross-linked with 4E-BP1.

92 (mTORC1) signaling by conditionally deleting Raptor causes severe defects in iNKT-cell development at

93 ers of NFATc1 and NFATc2 in T cells, such as Raptor, CHEK1, CREB1, RUNX1, SATB1, Ikaros, and Helios.

94 tects the nucleotide state of RagA while the Raptor "claw" threads between the GTPase domains to dete

95 tion of MID1, lead to disruption of the mTOR/Raptor complex and down-regulated mTORC1 signaling.

96 al evidence that ICK interacts with the mTOR/Raptor complex in cells and phosphorylates Raptor in vit

97 SIRT1 physically interacts with the mTOR-Raptor complex, and a single amino acid substitution in

98 city of Delhi-India, which hosts the largest raptor concentration of the world.

99 Raptor conditional knockout mice showed decreased extrac

100 The Raptor containing mTOR complex 1 (mTORC1) has been well

101 ion (amino acid residues 56-72) we call RCR (Raptor cross-linking region).

102 Compared with Raptor(+/+) mice, Raptor(D/D) knock-in mice exhibited smaller livers and h

103 blasts or in 293 cells by down-regulation of raptor decreased the levels of the transcription factor

104 Furthermore, Raptor deficiency and rapamycin treatment lead to aberra

105 with rapamycin recapitulated the effects of RAPTOR deficiency, and both strategies led to the ablati

106 They convincingly demonstrate that Raptor deficiency, with consequent mTORC1 inhibition, bl

107 ly in WT, but Tm colonization in both WT and Raptor deficient mice.

108 cells and IL-25 were induced in both WT and Raptor deficient organoids.

109 of a transgenic BCR or a BclxL transgene on Raptor-deficient B cells failed to rescue B cell develop

110 Neurospheres derived from raptor-deficient brains are smaller, and differentiation

111 deficit in the rate of protein synthesis in Raptor-deficient chondrocytes.

112 Indeed, Raptor-deficient iNKT cells are mostly blocked at thymic

113 In young mice Raptor-deficient LCs show an increased tendency to leave

114 ter turnover rate and increased apoptosis of Raptor-deficient LCs, which might additionally affect th

115 Furthermore, Raptor-deficient mice exhibited a block in B cell lineag

116 proliferation were significantly reduced in Raptor-deficient mice.

117 d genes remains inappropriately expressed in Raptor-deficient mice.

118 Raptor-deficient pre-B cells exhibited significant decre

119 Rapamycin or raptor deletion ameliorates the aberrant TFH cell expans

120 (betaraKO) and inducible (MIP-betaraKO(f/f)) raptor deletion.

121 Furthermore, the mTORC1 component Raptor directly interacts with PI(3,5)P(2).

122 Abrogation of the PKA site within RAPTOR disrupted betaAR/mTORC1 activation of S6K1 withou

123 r Thr-908 both in vitro and in vivo and when Raptor exists in protein complexes with or without mTOR.

124 ion systems were used to specifically target Raptor(fl/fl) (mTORC1), either in all tissues upon poly(

125 commitment was confirmed in adult Mx1-cre(+)Raptor(fl/fl) mice upon cre-recombinase induction.

126 the early stages of development in Vav-cre(+)Raptor(fl/fl) mice, revealed that these mice do not surv

127 aling was blocked, by crossing Raptor loxed (Raptor(flox/flox)) mice with CX3CR1(CreER) mice, which e

128 ts proteome, it does induce loss of mTOR and raptor from them.

129 elper 2 (Th2) cell differentiation, although Raptor function is less important for continuous prolife

130 GDI2 by rictor is not related to the Sin1 or raptor function that excludes a role of mTORC2 or mTORC1

131 Disruption of the Raptor gene impairs chromosomal synapsis and prevents th

132 pression in Fib-MCs in experiments utilizing raptor gene silencing and overexpression of dominant-inh

133 ile downregulation of mTORC1 activity, using Raptor genetic mouse model or mTORC1 inhibitor treatment

134 ve genomic analysis and comparisons with non-raptor genomes identify common molecular signatures that

135 Overall, raptor genomes show genomic signatures associated with t

136 at the balance of free and mTORC1-associated Raptor governs hepatic lipid accumulation, and uncover t

137 ion of either mTOR or the associated protein Raptor greatly diminishes embryonic skeletal growth asso

138 nd angiogenesis in vivo, whereas the loss of Raptor had only a modest effect on endothelial cells (EC

139 horylation in cells, comparable depletion of raptor has no effect; moreover, the ability of mTOR to p

140 lowing: (i) LARP1 associates with mTORC1 via RAPTOR; (ii) LARP1 interacts with TOP mRNAs in an mTORC1

141 In addition, loss of Raptor impairs iNKT-cell proliferation and production of

142 Depletion of mTOR and Rictor, but not Raptor, impairs actin polymerization, leading-edge estab

143 arget of rapamycin (mTOR) or rictor, but not raptor, implicating mTORC2 as the target of rapamycin fo

144 rect AMPK-mediated serine phosphorylation of RAPTOR in a new Raptor (AA) mouse model, in which AMPK p

145 ue-specific deletion of the mTORC1 regulator Raptor in alpha cells (alphaRaptorKO), we showed that mT

146 disruption of the mTOR coactivating protein Raptor in developing mouse B cells resulted in a develop

147 ffect mimicked by shRNA knockdown of mTOR or raptor in ECs.

148 sgenic mice, PRAS40(T246A) remained bound to raptor in keratinocytes even after treatment with TPA, c

149 EAT repeats of Tor2 that are engaged by Kog1/Raptor in mammalian TORC1, explaining the mutual exclusi

150 Raptor in mTOR complex 1 is believed to recruit 4E-BP1,

151 Also, we show that loss of Raptor in oligodendrocytes results in differential dysmy

152 Loss of mTORC1 signaling by removal of Raptor in tendons caused severe tendon defects postnatal

153 Conditional ablation of Raptor in the male germline causes infertility due to me

154 The role of raptor in the mechanical load-induced regulation of mTOR

155 mTORC1 in mice by deleting the gene encoding raptor in the progenitors of the developing CNS.

156 , conditional depletion of endogenous DAF-15/Raptor in the soma revealed that TORC1 is required at ea

157 R/Raptor complex in cells and phosphorylates Raptor in vitro.

158 the TBK1 dependent phosphorylation sites on Raptor in vitro.

159 n the regulatory associated protein of mTOR (Raptor) in microglia, whose mTORC1 signaling was blocked

160 nent, regulatory-associated protein of mTOR (Raptor), in mouse HSCs and its loss causes a nonlethal p

161 In contrast, the loss of Raptor increased the phosphorylation of AKT despite inhi

162 rget of rapamycin complex 1 (mTORC1) subunit Raptor induces cell growth and is a downstream target of

163 Silencing raptor (inhibits mTORC1) or rictor (inhibits mTORC2) mar

164 Silencing raptor (inhibits mTORC1) or rictor (inhibits mTORC2) mar

165 TORC1 before complete disruption of the mTOR-raptor interaction, whereas mTORC2 stoichiometry is unaf

166 To date, all known functions of Raptor involve its scaffolding mTOR kinase with substrat

167 Furthermore, Raptor is required for HSC regeneration, and plays large

168 , our study reveals that enterocyte specific Raptor is required for initiating a type 2 immune respon

169 n (in particular residues from 89 to 180) of Raptor is the major site of interaction with 4E-BP1.

170 athway, in that mTORC1 (with adaptor protein Raptor) is the main complex mediating the maturation and

171 mplex 1 (mTORC1), defined by the presence of Raptor, is an evolutionarily conserved and nutrient-sens

172 h was also observed in rictor mutants, while raptor knockdown did not phenocopy the TSC mutant phenot

173 this signaling pathway with mTOR inhibitors, raptor knockdown or p70S6K inhibitors elevated PD-L1 lev

174 STRAP is also attenuated by rapamycin and by raptor knockdown.

175 In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the rol

176 Moreover, residual iNKT cells in Raptor knockout mice are impaired in their rapid cytokin

177 eated skeletal muscle specific and inducible raptor knockout mice to eliminate signaling by mTORC1, a

178 fference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, alt

179 tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on

180 Adipocyte-specific Raptor KO mice experienced exacerbated alcohol-induced s

181 4/80(high)) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading

182 ipocyte-specific mTOR KO, adipocyte-specific Raptor KO, and adipocyte-specific tuberous sclerosis com

183 specific deletion of the essential component raptor leads to a profound loss of T(reg)-cell suppressi

184 1 activity in DCs by conditional deletion of Raptor leads to a progressive loss of LCs in the skin of

185 Increased RAPTOR levels correlated with decreased filaggrin expres

186 Free Raptor levels in liver decline with age and in obesity;

187 with age and in obesity; restoration of free Raptor levels reduces liver triglyceride content, throug

188 se mTORC1 signaling was blocked, by crossing Raptor loxed (Raptor(flox/flox)) mice with CX3CR1(CreER)

189 ulatory associated protein of mTOR-mediated (RAPTOR-mediated) suppression, and altered kinase kinetic

190 Compared with Raptor(+/+) mice, Raptor(D/D) knock-in mice exhibited sm

191 In a study involving three species of raptor migrating from Europe to Sub-Saharan Africa, Klaa

192 tently, knockdown of rictor or mTOR, but not raptor, mimicked PP242 in decreasing FLIP(S) levels and

193 nd survival through forming 2 complexes with raptor (mTOR complex 1; mTORC1) or rictor (mTOR complex

194 inhibited phosphorylation of ribosomal S6, a raptor/mTOR complex 1 (mTORC1) target, without a compens

195 We silenced raptor (mTORC1 inhibition), rictor (mTORC2 inhibition) o

196 The essential role of Raptor (mTORC1) in erythrocyte and B lineage commitment

197 We show that Raptor (mTORC1) is a positive regulator of developmental

198 omplexes are functionally dependent on their raptor (mTORC1) or rictor (mTORC2) subunits.

199 d unaltered ability to express CCR9, whereas Raptor (mTORC1)-deficient Treg were unable to upregulate

200 ammalian target of rapamycin in complex with raptor (mTORC1).

201 Activation of Raptor-mTORC1 integrated T cell receptor and CD28 costim

202 Here we describe that Raptor-mTORC1-dependent metabolic reprogramming is a cen

203 Our studies identify a Raptor-mTORC1-dependent pathway linking signal-dependent

204 Using mice with T-cell-specific ablation of Raptor/mTORC1 or Rictor/mTORC2, we revealed that both mT

205 Mechanistically, raptor/mTORC1 signalling in T(reg) cells promotes choles

206 e peptides revealed that the most N-terminal Raptor N-terminal conserved domain (in particular residu

207 In support of the idea that the Raptor N-terminal conserved domain and the 4E-BP1 centra

208 e we report that mTORC1-independent ('free') Raptor negatively regulates hepatic Akt activity and lip

209 d not inhibit the association of mTORC1 with Raptor nor did it affect AMP-activated protein kinase ac

210 Mechanistically, NLK phosphorylates Raptor on S863 to disrupt its interaction with the Rag G

211 ically, PKA directly phosphorylated mTOR and RAPTOR on unique serine residues, an effect that was ind

212 st the presence of two structured regions of Raptor: one in the N-terminal region and the other in th

213 acological or genetic inhibition of mTOR and Raptor or expression of a hypophosphorylated mutant vers

214 ither through adipocyte-specific deletion of Raptor or pharmacologic rapamycin treatment, were refrac

215 Genetic suppression of RAPTOR or RHEB ablated P-S6 and restored sensitivity to

216 Using mouse models of Raptor or Rictor gene targeting, we discovered that Rict

217 sed mice with conditional deletion of either Raptor or Rictor genes to determine potential contributi

218 Knockdown of mTOR, Raptor or Rictor in lal(-/-) MDSCs suppressed their stim

219 myelination, we conditionally ablated either Raptor or Rictor in the oligodendrocyte lineage, in vivo

220 1 and S6K phosphorylation is maintained when raptor or rictor is depleted, suggesting that either mTO

221 1 (mTORC1) and mTORC2, by binding to either Raptor or Rictor, respectively.

222 iting mTOR, depleting its regulatory subunit raptor, or inducing hypoxia all trigger reactivation.

223 4E axis, secondary to aberrant assembly of a raptor-p62-TRAF6 complex.

224 mammalian target of rapamycin (mTOR) through Raptor phosphorylation (Serine 792).

225 ivity, suggesting that inhibitory effects of raptor phosphorylation are circumvented.

226 However, Raptor phosphorylation by AMPK was independent of p53 an

227 In liver cells, raptor phosphorylation is essential for both AMPK and hy

228 s, context-specific signals are required for raptor phosphorylation-induced mTORC1 inhibition.

229 tivated AMPK inhibited mTORC1 solely through Raptor phosphorylation.

230 localize to lysosomes due to CDK1-dependent RAPTOR phosphorylation.

231 hosphorylation modulates the mTOR-raptor and raptor-PRAS40 interactions and augments mTORC1-associate

232 and this phosphorylation may interfere with Raptor-Rag interaction.

233 monstrate that ectopic expression of TOR and Raptor (regulatory-associated protein of mTOR), a protei

234 or the Regulatory Associated Protein of TOR (RAPTOR) regulatory subunit.

235 ering RNA (siRNA), we find that knockdown of raptor relieves autophagy and the eIF4E effector pathway

236 lines, but not silencing the mTORC1 cofactor Raptor (RPTOR).

237 The phosphomimetic Raptor-S606D knock-in mutant led to a reduction in cell

238 Cells with Nlk deletion or knock-in of the Raptor S863 phosphorylation mutants are defective in the

239 tified in vitro, we found that TBK1 promotes Raptor Ser877 phosphorylation in cells both basally and

240 The levels of Raptor Ser877 phosphorylation were inversely correlated

241 hat TBK1 limits mTORC1 activity by promoting Raptor Ser877 phosphorylation.

242 The brains deficient for raptor show a microcephaly starting at E17.5 that is the

243 ovided a basis for investigating aldosterone-Raptor signaling in human PASMCs.

244 We hypothesized that aldosterone-Raptor signaling induces abnormal pulmonary artery smoot

245 systemic administration of the 4-1BB aptamer-raptor siRNA to mice downregulated mTORC1 activity in th

246 d with rapamycin, but not with 4-1BB aptamer-raptor siRNA, failed to reject a subsequent tumor challe

247 In PASMCs transfected with Raptor-small interfering RNA or treated with spironolact

248 polyethylene glycol that was formulated with Raptor-small interfering RNA plus spironolactone in vivo

249 present separately in 5 additional fowl and raptor species, all of which are native to areas of Asia

250 istochemistry to evaluate this claim in five raptor species: the common buzzard (Buteo buteo), the ho

251 location to the lysosomal surface, where its Raptor subunit interacts with the Rag guanosine triphosp

252 hows the details of RagA/RagC binding to the RAPTOR subunit of mTORC1 and explains why only the RagA(

253 d in part by the Rag GTPases, which bind the raptor subunit of mTORC1 in an amino acid-stimulated man

254 It contains the atypical kinase mTOR and the RAPTOR subunit that binds to the Tor signalling sequence

255 Intramolecular cross-links of Raptor suggest the presence of two structured regions of

256 Although expression of the Raptor T908A mutant did not affect the mTORC1 integrity,

257 In conclusion, we found that raptor talon evolution has been strongly influenced by r

258 In this study we investigate whether raptor talons have evolved primarily in response to adap

259 osteronism expressed increased levels of the Raptor target, p70S6K, which provided a basis for invest

260 Expression of a mutant Raptor that could not be phosphorylated at Ser877 led to

261 rthermore, we show that the scaffold protein raptor, that typically recruits mTOR substrates, is not

262 ry associated protein of the MTOR complex 1 (RAPTOR), the serine/threonine kinase V-Akt murine thymom

263 Depletion of Raptor, the defining subunit of mTORC1, by small interfe

264 ze and questions: movements of an endangered raptor, the snail kite (Rostrhamus sociabilis plumbeus),

265 ctivity of mTORC1 through phosphorylation of Raptor Thr-908 and thus implicate a potential signaling

266 ICK is able to phosphorylate Raptor Thr-908 both in vitro and in vivo and when Raptor

267 a phospho-specific antibody, we showed that Raptor Thr-908 is a novel in vivo phosphorylation site.

268 and movement of the key TORC1 component Kog1/Raptor to a single body near the edge of the vacuole.

269 rone (10(-9) to 10(-7) M) increased Akt/mTOR/Raptor to activate p70S6K and increase proliferation, vi

270 ated an siRNA targeting the mTORC1 component raptor to an aptamer that binds 4-1BB, a costimulatory m

271 tabilizes the interaction between PRAS40 and Raptor to inactive mTORC1-mediated hyper-glycolytic meta

272 we investigated whether and how ICK targets Raptor to regulate the activity of mTORC1.

273 ing component in mTORC1, and localization of Raptor to the nucleus results in nuclear mTORC1 activity

274 he use of rapid protein threading predictor (RAPTOR) to generate tertiary structures of closely relat

275 n one of the mTOR effector complex proteins, Raptor, to elucidate the role of mTORC1 in leukemia.

276 Here, we inactivate the core component, Raptor, to show that mTORC1 function is critical for mal

277 mutants lacking LST8, expression of TOR and RAPTOR, together with their upstream activator Rheb, was

278 genetic knockout of the major mTOR cofactors raptor (TOR complex 1 [TORC1]) and rictor (TORC2), we no

279 knockout of the major mTOR complex cofactors raptor (TORC1) and rictor (TORC2), we now show that TORC

280 We also present crystal structures of RAPTOR-TOS motif complexes that define the determinants

281 and are no longer able to recruit RACK1 and Raptor, two TRAPP-interactive signaling proteins, sensit

282 nd raptor and counteracts DDB1-CUL4-mediated raptor ubiquitination.

283 In keratinocyte cell cultures RAPTOR upregulation or AKT1 short hairpin RNA knockdown

284 atches propagate direct (high and low threat raptor vocalizations) or indirect (high and low threat c

285 ro Optimal inhibition of pulmonary arteriole Raptor was achieved by treatment with Staramine-monometh

286 the effect AMPK activation if either mTOR or Raptor was suppressed, indicating that the inhibitory ef

287 When S6K1 is co-expressed with raptor we show that S6K1 is translocated from the nucleu

288 sing mice with T cell-restricted deletion of Raptor, we show that mTORC1 is selectively required for

289 On 4E-BP1, we found that cross-links with Raptor were clustered in the central region (amino acid

290 PK phospho-serine sites Ser722 and Ser792 of RAPTOR were mutated to alanine.

291 mTOR by enhancing PRAS40's association with RAPTOR, whereas AICAR blocked the cell cycle through pro

292 plex 1 (mTORC1) is defined by a core subunit Raptor, whereas mTORC2 lacks Raptor and, instead, has Ri

293 Epidermis-specific loss of Raptor, which encodes an essential component of mTORC1,

294 ) family members with the TORC1 subunit Kog1/Raptor, which in turn allow the TORC1 proximal kinase Sc

295 including mammalian target of rapamycin and raptor, which resulted in a stimulation of endothelial a

296 Combining RAPTOR with IM-MS and collision-induced dissociation (CI

297 termine the structure of the supercomplex of Raptor with Rag-Ragulator at a resolution of 3.2 angstro

298 sparrowhawk (Accipiter nisus), a monogamous raptor with reversed sexual size dimorphism.

299 1 activation by impairing the interaction of Raptor with Rheb.

300 ependent acetylation of the mTORC1 component raptor, with consequent activation of mTORC1.