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 ORC1 inhibitor rapamycin or by knocking down raptor.

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

4 sult of enhanced interaction of p70S6K1 with raptor.

5 ween the two substrates for interaction with raptor.

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

7 ines correlate well with theory generated by RAPTOR.

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

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

10 in vitro is unaffected by the elimination of raptor.

11 curs through mTOR itself rather than through raptor.

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

13 ag heterodimer that is further stabilized by raptor.

14 a rapamycin-sensitive complex that involves Raptor.

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

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

17 toward the substrate 4EBP1, with a multisite raptor 6A mutant more strongly defective that single-sit

18 3% (median 19%) improvement as compared with RAPTOR (a well-known threading method) and even a mean 1

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

20 When Raptor, a critical scaffold protein for mammalian target

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

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

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

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

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

26 interference to inhibit expression of mTOR, raptor (also known as 4932417H02Rik) or FKBP12 (also kno

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

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

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

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

31 tion, we have studied the phosphorylation of raptor, an mTOR-interacting partner.

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

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

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

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

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

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

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

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

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

41 159/T2164 phosphorylation modulates the mTOR-raptor and raptor-PRAS40 interactions and augments mTORC

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

43 itical mediator of the myogenic functions of raptor and Rheb.

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

45 Raptor and Rictor serve as specific functional component

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

47 ined by the presence of the adaptor proteins raptor and rictor, respectively.

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

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

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

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

52 ylation of specific sites of mTOR inhibitors raptor and tuberous sclerosis complex 2 (TSC2).

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

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

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

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

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

58 lation of a component of mTORC1, the protein raptor, and demonstrate that mitotic raptor phosphorylat

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

60 e, it has been shown that knockdown of mTOR, Raptor, and mLST8, but not Rictor and mSin1, suppresses

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

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

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

64 We found that increased expression of mTOR, Raptor, and Rictor mRNA was noted with advanced stages o

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

66 mTORC1 immunoprecipitated by the use of anti-raptor antibody from mammalian cells starved for nutrien

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

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

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

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

71 duce activation of mTORC1 (mTOR complexed to raptor) as indicated by increased p70S6K and 4E-BP1 phos

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

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

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

75 Importantly, the site-directed mutation of raptor at one phosphorylation site, Ser(863), reduced mT

76 Conversely, a phosphomimetic RAPTOR augmented S6K1 activity.

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

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

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

80 At the molecular level, Raptor binds the SAIN (Shc and IRS-1 NPXY binding) domai

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

82 so both enhanced the binding of 4E-BP[5A] to raptor but only insulin stimulated S6K1 and 4E-BP phosph

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

84 sses were lowered by Torin1 treatment and by raptor, but not rictor, depletion, suggesting that mTORC

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

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

87 Phosphorylation-deficient mutants of raptor cause cells to delay in G(2)/M, whereas depletion

88 lls to delay in G(2)/M, whereas depletion of raptor causes cells to accumulate in G(1).

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

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

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

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

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

94 Raptor conditional knockout mice showed decreased extrac

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

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

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

98 Furthermore, Raptor deficiency and rapamycin treatment lead to aberra

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

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

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

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

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

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

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

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

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

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

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

110 proliferation were significantly reduced in Raptor-deficient mice.

111 Raptor-deficient pre-B cells exhibited significant decre

112 Rapamycin or raptor deletion ameliorates the aberrant TFH cell expans

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

114 fected cells, and this activity is lost upon raptor depletion.

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

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

117 C1 containing phosphorylation site-defective raptor exhibits reduced in vitro kinase activity toward

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

119 demonstrate that mitotic phosphorylation of raptor facilitates cell cycle transit through G(2)/M.

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

121 ntified that curcumin was able to dissociate raptor from mTOR, leading to inhibition of mTORC1 activi

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

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

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

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

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

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

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

129 lation and Na+ current, whereas knockdown of raptor had no effect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 In contrast, when mTOR assembled with raptor in the rapamycin-inhibited complex (mTORC1), it d

147 rein we demonstrate that mTOR phosphorylates raptor in vitro and in vivo.

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

149 ffering by the substrate specificity factors raptor (in mTORC1) and rictor (in mTORC2).

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

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

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

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

154 mponent rictor, but not the mTORC1 component raptor, inhibited rapamycin-induced Akt phosphorylation

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

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

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

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

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

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

161 The phosphorylation of raptor is stimulated by insulin and inhibited by rapamyc

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

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

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

165 cking the SAIN domain does not interact with Raptor, is not phosphorylated at Ser-636/639, and favora

166 on of mTORC1 activity by either rapamycin or Raptor knockdown cannot resensitize these cells to serum

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

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

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

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

171 1 activity in DCs by conditional deletion of Raptor leads to a progressive loss of LCs in the skin of

172 Increased RAPTOR levels correlated with decreased filaggrin expres

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

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

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

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

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

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

179 Everolimus is an oral agent targeting raptor mTOR (mTORC1).

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

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

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

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

184 Here, we evaluated the role of the mTOR/raptor (mTORC1) signaling in proliferative conditions in

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

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

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

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

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

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

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

192 data suggest that mTORC1 activation leads to raptor multisite phosphorylation and that raptor Ser(863

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

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

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

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

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

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

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

200 Rictor, but not Raptor or mTOR alone, promotes SGK1 ubiquitination.

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

202 se proteins in myogenesis, overexpression of raptor or Rheb inhibits C2C12 differentiation.

203 er, the enhanced differentiation elicited by raptor or Rheb knockdown is accompanied by increased Akt

204 e enhancement in differentiation elicited by raptor or Rheb knockdown, suggesting that IRS1 is a crit

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

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

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

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

209 1 and S6K phosphorylation is maintained when raptor or rictor is depleted, suggesting that either mTO

210 Knockdown of mTOR, but not Raptor or Rictor, reduced p-ULK1 at Ser(757) and enhance

211 on of mTORC1 or mTORC2 by down-regulation of raptor or rictor, respectively, inhibited the activities

212 1 (mTORC1) and mTORC2, by binding to either Raptor or Rictor, respectively.

213 RNA-mediated silencing of mTORC1/2 subunits Raptor or Rictor.

214 ucose were not associated with a decrease in raptor or TSC2 phosphorylation.

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

216 4E axis, secondary to aberrant assembly of a raptor-p62-TRAF6 complex.

217 In conclusion, the Rheb-mTOR/raptor pathway negatively regulates myogenic differentia

218 ochemical switch that modulates hierarchical raptor phosphorylation (e.g. on Ser(859) and Ser(855)).

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

220 protein raptor, and demonstrate that mitotic raptor phosphorylation alters mTORC1 function during mit

221 kinase pathways involved in mitosis-specific raptor phosphorylation and altered mTORC1 activity.

222 zole-4-carboxamide riboside [AICAR]) induces raptor phosphorylation and inhibits mTORC1 in both mouse

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

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

225 en together, these data suggest that complex raptor phosphorylation functions as a biochemical rheost

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

227 re, our findings indicate that mTOR-mediated raptor phosphorylation plays an important role on activa

228 We have identified six raptor phosphorylation sites that lie in two centrally l

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

230 tivated AMPK inhibited mTORC1 solely through Raptor phosphorylation.

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

232 In addition, mitotic raptor promotes translation by internal ribosome entry s

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

234 The loss of raptor (regulatory associated protein of mTOR, complex 1

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

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

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

238 t and other major components including mTOR, raptor, rictor, 70-kDa ribosomal S6 kinase, and 4E-bindi

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

240 study we have investigated the functions of raptor, S6K1, and Rheb in the differentiation of C2C12 m

241 OR complex 1 signaling components, including raptor, S6K1, and Rheb, had been suggested in muscle mai

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

243 ant more strongly defective that single-site raptor S863A.

244 ) phosphorylation is absolutely required for raptor Ser(859) and Ser(855) phosphorylation.

245 overexpression increases phosphorylation on raptor Ser(863) as well as on the five other identified

246 to raptor multisite phosphorylation and that raptor Ser(863) phosphorylation functions as a master bi

247 Strikingly, raptor Ser(863) phosphorylation is absolutely required f

248 focus primarily although not exclusively on raptor Ser(863) phosphorylation.

249 signaling, and cellular energy) also promote raptor Ser(863) phosphorylation.

250 romotes mTORC1-associated phosphorylation of raptor Ser(863) via the canonical PI3K/TSC/Rheb pathway

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

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

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

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

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

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

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

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

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

260 C1 signaling by rapamycin or by knockdown of raptor stimulates lipolysis primarily via activation of

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

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

263 terlocking interactions between the mTOR and raptor subunits.

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

265 eracted selectively with rictor but not with raptor, suggesting selective recruitment of SGK1 to mTOR

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

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

268 mTORC1 cascade by rapamycin or by the use of raptor-targeted shRNA failed to decrease PGE(2)-mediated

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

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

271 K)-mediated phosphorylation of serine 792 of raptor, the specificity subunit of mTORC1, increases in

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

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

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

275 dition, NVP-BEZ235 inhibited both rictor and raptor, thus abrogating the rictor-induced Akt phosphory

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

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

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

279 rior to exercise also reduced the ability of raptor to associate with mTORC1 during post-exercise rec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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