ライフサイエンスコーパス: mTORC1

1 the mammalian target of rapamycin complex 1 (mTORC1).

2 e mechanistic target of rapamycin complex 1 (mTORC1).

3 ediated by mammalian target of rapamycin C1 (mTORC1).

4 e mechanistic target of rapamycin complex 1 (mTORC1).

5 the mammalian target of rapamycin complex 1 (mTORC1).

6 with rapamycin, the allosteric inhibitor of mTORC1.

7 ponent raptor, with consequent activation of mTORC1.

8 8 MAPK as an anti-aging target downstream of mTORC1.

9 echanisms at play in metformin inhibition of mTORC1.

10 dinated by the cellular energetics regulator mTORC1.

11 s drove IFN-gamma production by NK cells via mTORC1.

12 ich activates AMPK, leading to inhibition of mTORC1.

13 f the Rag GTPase heterodimers complexed with mTORC1.

14 similar separation to the pair in activated mTORC1.

15 gene which encodes an upstream suppressor of mTORC1.

16 RTKs, c-KIT, and SFK members independent of mTORC1/2 activation.

17 For these reasons, we investigated activated mTORC1/2 and EPH receptor-mediated signaling in sporadic

18 Drug treatment co-targeting mTORC1/2 and IGF1R/insulin receptor attenuated pAkt T308

19 The DEPTOR-mTORC1/2 axis has been shown to play an important, but a

20 Transcriptomics after mTORC1/2 inhibition confirmed decreased ERBB3/ERBB4 whil

21 mTORC1/2 inhibition downregulates NRG1-ERBB3, while upre

22 These data suggest that mTORC1/2 inhibition, regulated by amino acid levels, is

23 fficacy of combination therapy with the dual mTORC1/2 inhibitor AZD2014 and the multi-kinase inhibito

24 t model of schwannoma, we evaluated the dual mTORC1/2 inhibitor AZD2014 and the tyrosine kinase inhib

25 mTORC1/2 inhibitor treatment decreased NRG1 expression a

26 This effect of mTORC1/2 inhibitors on protein synthesis and RRM2 levels

27 exogenous NRG1 stimulated ERBB3, EPHA2, and mTORC1/2 signaling, suggesting pathway crosstalk.

28 as been hypothesized that ketamine activates mTORC1-4E-BP signalling in pyramidal excitatory cells of

29 Accordingly, interfering with the mTORC1/4E-BP/eIF4E axis inhibited the growth potential e

30 leads to hyperactivation of mTOR Complex 1 (mTORC1), a master regulator of cell growth and metabolis

31 of mTOR, resulting in impaired activation of mTORC1, a central regulator of autophagy.

32 tural and functional decline is regulated by mTORC1, a sensor of nutrients and growth factors, which

33 es sex- and age-specific gene changes in the mTORC1-activated lung mesenchyme and establishes the imp

34 We demonstrate that inhibition of mTORC1 activates TFEB, which increases expression of lys

35 therapeutic benefit in cancer by preventing mTORC1 activation and simultaneously blocking lysosomal

36 ploit the PLD-PA pathway and thereby sustain mTORC1 activation at the lysosome in the absence of amin

37 While mTORC1 activation at the lysosome is well characterized,

38 C1 activation in response to leucine whereas mTORC1 activation by growth factors or eccentric contrac

39 essential component of mTORC1, to attenuate mTORC1 activation by impairing the interaction of Raptor

40 definitive role of PRAS40 phosphorylation in mTORC1 activation downstream of PDGFRbeta in mesangial c

41 ylates TSC2 via its kinase domain to mediate mTORC1 activation in CD8(+) T cells.

42 l in which MK2/3 regulate IL-6 and IL-13 via mTORC1 activation in ILC2s.

43 PHD1(KO) muscles show impaired mTORC1 activation in response to leucine whereas mTORC1

44 ociated with enhanced TGFbeta expression and mTORC1 activation in the kidney cortex and glomeruli of

45 Mechanistically, mTORC1 activation increases protein synthesis of MKK6 an

46 Here, we address the question of whether mTORC1 activation or suppression is beneficial for skele

47 e identified how TGFbeta receptor I achieves mTORC1 activation through PDGFRbeta-mediated Akt/PRAS40

48 troversial role of PI3K-Akt in CD8(+) T cell mTORC1 activation, a link between Akt-mTORC1 signaling a

49 eatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited autophagy, and increased he

50 7 to LAMTOR1 prevents Ragulator assembly and mTORC1 activation, promoting autophagy.

51 Consistent with increased mTORC1 activation, targeted neurons were enlarged and bo

52 and p70S6K, known effectors and readouts of mTORC1 activation.

53 he surface of lysosomes leading to decreased mTORC1 activation.

54 ng that TARS2 is necessary for Thr-dependent mTORC1 activation.

55 , and also serve as functional platforms for mTORC1 activation.

56 , limits the lysosomal surface available for mTORC1 activation.

57 BCKAs increased protein translation and mTORC1 activation.

58 e amino acid and growth factor signaling for mTORC1 activation.

59 multiple pathways and iron is essential for mTORC1 activation.

60 ponent of the Ragulator complex required for mTORC1 activation.

61 ired the lysosome and lysosomal function for mTORC1 activation.

62 nd Ras-transformed tumor cells via sustained mTORC1 activation.

63 und that LIN28B overexpression increased Akt-mTORC1 activity and allowed supporting cells that were u

64 2Ac-PRAS40 axis as a new layer in regulating mTORC1 activity and downstream glycolytic alterations du

65 Specifically, CDC42u stimulated mTORC1 activity and thereby induced neuroprogenitor form

66 slation is maintained during mitosis despite mTORC1 activity being repressed.

67 Inhibition of mTORC1 activity can rescue the defect in notochord vacuo

68 mTORC1 activity in cells lacking TARS2 is resistant to T

69 of Raptor to the nucleus results in nuclear mTORC1 activity in the absence of growth factor stimulat

70 hen demonstrate that decanoic acid decreases mTORC1 activity in the absence of insulin and under high

71 rom its lysosomal activation, which controls mTORC1 activity in the nuclear compartment.

72 robe the regulation of growth factor-induced mTORC1 activity in the nucleus.

73 MTORC1 activity is critical for tissue regeneration in m

74 The ability of PHD1 to promote mTORC1 activity is independent of its hydroxylation acti

75 ion on osteoclastogenesis are independent of mTORC1 activity or global transcriptional and translatio

76 How limitations in nutrients suppress mTORC1 activity remains poorly understood.

77 e show that growth factor-stimulated nuclear mTORC1 activity requires nuclear Akt activity.

78 RIPK1 loss results in a high basal mTORC1 activity that drives defective lysosomes in cells

79 t studies have demonstrated how AAs regulate mTORC1 activity through Rags.

80 show that RPE cells with constitutively high mTORC1 activity were reprogramed to be hyperactive in gl

81 describe upstream regulators of mTORC1 activity which promote paligenosis, a process whe

82 se pharmacologically in beta-cells increased mTORC1 activity, suggesting involvement of the V-ATPase

83 ium, we show that decanoic acid can decrease mTORC1 activity, under conditions of constant glucose an

84 nal layer of complexity in the regulation of mTORC1 activity.

85 ype and associated lethality, and normalized mTORC1 activity.

86 genesis are due to their opposing effects on mTORC1 activity.

87 sed lysosome mass with aging leads to higher mTORC1 activity.

88 ersed the siPDGFRbeta-mediated inhibition of mTORC1 activity; however, co-expression of the phospho-d

89 miRNA let-7g, suppressed Akt-mTOR complex 1 (mTORC1) activity and renders young, immature supporting

90 showed that CDC42 stimulates mTOR complex 1 (mTORC1) activity and thereby up-regulates transcription

91 phagy pathway, or in upstream signalling via mTORC1 and AMPK.

92 Ddit4(-/-) cells never suppress mTORC1 and bypass the IFRD1 checkpoint on proliferation.

93 is and resynthesis, leading to inhibition of mTORC1 and cancer cell growth arrest.

94 ults establish Peli1 as a novel regulator of mTORC1 and downstream mTORC1-mediated actions on T cell

95 ation and protein function, is controlled by mTORC1 and EIF-4E Binding Proteins (EIF4EBPs).

96 which markedly increases association between mTORC1 and its lysosome-borne activators, leading to mTO

97 le fusion and replenishment, suggesting that mTORC1 and mTORC2 differentially modulate postsynaptic r

98 ly, DEPTOR depletion not only activated both mTORC1 and mTORC2 signals to promote cell proliferation

99 promotes tumorigenesis via the activation of mTORC1 and mTORC2 signals.

100 ZIKV infection results in activation of both mTORC1 and mTORC2 to promote virus replication.

101 rapamycin (mTOR) functions as two complexes (mTORC1 and mTORC2), regulating cell growth and metabolis

102 , the mTOR kinase operates in two complexes, mTORC1 and mTORC2, suggesting that mTOR's role in synapt

103 replication requires the activation of both mTORC1 and mTORC2, which negatively regulates autophagy

104 mTORC1 and mTORC2-specific serum/glucocorticoid-regulate

105 structural plasticity required activation of mTORC1 and new protein synthesis.

106 which shows a strong binding preference for mTORC1 and supports its activation, while the Ub-Rheb is

107 referentially inactivate pRB, upregulate the mTORC1 and WNT signaling pathways, and exhibit nuclear l

108 e mechanistic target of rapamycin complex 1 (mTORC1) and cell growth-regulating processes.

109 inct multiprotein complexes, mTOR Complex 1 (mTORC1) and Complex 2 (mTORC2).

110 s mechanistic target of rapamycin complex 1 (mTORC1) and mechanistic target of rapamycin complex 2 (m

111 IKV infection activates both mTOR complex 1 (mTORC1) and mTORC2.

112 aptor, a regulatory scaffolding component in mTORC1, and localization of Raptor to the nucleus result

113 RAS40), an intrinsic inhibitory component of mTORC1, and prevented activation of mTORC1 in the absenc

114 ion of both RAPTOR and TSC2 to fully inhibit mTORC1, and this regulation is critical for both the tra

115 We conclude that mTORC1 appears to regulate cell growth, perhaps in part

116 ng cholesterol storage, implicating aberrant mTORC1 as a pathogenic driver downstream of cholesterol

117 hed in brain (Rheb), which in turn activates mTORC1 at the lysosome.

118 n together, these results suggest a model of mTORC1-ATF4 hyperactivation and impaired lysosomal acidi

119 P-S6K) are downstream effectors regulated by mTORC1 but converge to regulate two independent pathways

120 The TSCC negatively regulates mTORC1 by acting as a GTPase-activating protein (GAP) to

121 Depletion of Raptor, the defining subunit of mTORC1, by small interfering RNA (siRNA) negatively affe

122 the mammalian target of rapamycin complex 1 (mTORC1) caused early drusen-like pathologies, as well as

123 nd provide genomic bases for the efficacy of mTORC1, CDK4/6, and PARP inhibitors in metastatic breast

124 enhancing EP300-dependent acetylation of the mTORC1 component raptor, with consequent activation of m

125 mTORC1 controls various neuronal functions(12), particul

126 Mechanistic target of rapamycin complex 1 (mTORC1) controls cell growth and proliferation by sensin

127 r phospholipase D (PLD), which promotes both mTORC1-dependent cell proliferation and sphingosine-1-ph

128 8B promotes supporting cell plasticity in an mTORC1-dependent manner.

129 type III (Dio3) locus are up-regulated in an mTORC1-dependent manner.

130 e we find that p27 controls autophagy via an mTORC1-dependent mechanism in amino acid-deprived cells.

131 hord vacuole and lysosome biogenesis through mTORC1-dependent repression of TFEB nuclear translocatio

132 nal region that confers the interaction with mTORC1 did not.

133 so reveals new therapeutic opportunities for mTORC1-driven diseases.

134 signaling reverses age-dependent changes of mTORC1-driven lung phenotype, but WNT activation alone i

135 portance of the WNT signaling pathway in the mTORC1-driven lung phenotype.

136 e neuromuscular junction as a focal point of mTORC1-driven muscle aging.

137 wn to block proliferation and progression in mTORC1-driven tumorigenesis but the picture of the relev

138 These findings reveal that mTORC1 drives aging by augmenting a prominent stress res

139 ese findings shed light on the regulation of mTORC1 during energetic stress and unveil a point of cro

140 to inform the future study of autophagy and mTORC1 during mitosis.

141 re, we detail a molecular network regulating mTORC1 during paligenosis in both mouse pancreatic acina

142 rotein 1 (LARP1), an RNA-binding protein and mTORC1 effector that has been shown to repress TOP mRNA

143 Interestingly, mTORC1 enhances REGgamma activity in HCC, forming a posi

144 e the serine biosynthesis pathway to support mTORC1 growth signaling.

145 ese data not only support a primary role for mTORC1 hyperactivation in epilepsy following homozygous

146 ol accumulation within lysosomes, leading to mTORC1 hyperactivation, disrupted mitochondrial function

147 main driver of the kidney abnormalities and mTORC1 hyperactivity in a mouse model of Birt-Hogg-Dube

148 redisposition to sarcopenia correlating with mTORC1 hyperactivity.

149 nd its lysosome-borne activators, leading to mTORC1 hyperactivity.

150 and renders amino acid-induced activation of mTORC1 in aT reg cells.

151 like deposits was dependent on activation of mTORC1 in cones.

152 These data revealed a crucial role of DAPK1-mTORC1 in mediating CD8(+) trafficking and antitumor fun

153 In summary, in vivo iNKT cells activated mTORC1 in NK cells to produce IFN-gamma, which worsened

154 Mice with activated mTORC1 in PRs also displayed other early disease feature

155 ver an unconventional pathway that activates mTORC1 in response to variations in threonine (Thr) leve

156 onent of mTORC1, and prevented activation of mTORC1 in the absence of any effect on Smad 2/3 phosphor

157 t the role of systemic vs. local blockade of mTORC1 in the antidepressant effects of ketamine, provid

158 hat the N-terminal region of AKAP8L binds to mTORC1 in the cytoplasm.

159 ved upon loss of TSC1 and hyperactivation of mTORC1 in the liver.

160 The functional consequences of hyperactive mTORC1 in the RPE are unclear.

161 e postsynaptic inhibition of evoked release, mTORC1 inactivation enhanced spontaneous vesicle fusion

162 Consistently, mTORC1 inhibition ameliorates mitochondrial dysfunction

163 MTORC1 inhibition and autophagy activity are directly li

164 , which is mirrored by a sustained effect on mTORC1 inhibition and autophagy.

165 of cellular energy sensing and AMPK-mediated mTORC1 inhibition are not fully delineated.

166 Here, we discover that RIPK1 promotes mTORC1 inhibition during energetic stress.

167 Genetic and pharmacologic mTORC1 inhibition restores lysosomal proteolysis without

168 Therefore, glutamine depletion or mTORC1 inhibition stimulates release from Rab11a compart

169 Mechanistically, iron chelation-induced mTORC1 inhibition was not related to ROS induction, copp

170 We demonstrate that chronic mTORC1 inhibition with rapamycin is overwhelmingly, but

171 mTORC1 inhibition with rapamycin significantly improved

172 ated by decreased raptor acetylation causing mTORC1 inhibition, rather than by altered acetylation of

173 shortage AMPK-dependent sensing, leading to mTORC1 inhibition.

174 rtially contribute to iron chelation-induced mTORC1 inhibition.

175 The mTORC1 inhibitor rapamycin also reduced IL-6 and IL-13 p

176 me PHGDH was required for sensitivity to the mTORC1 inhibitor rapamycin in breast-cancer-derived lung

177 Pretreating cells with mTORC1 inhibitor rapamycin restored BCKA's effect on ins

178 Finally, using the mTORC1 inhibitor rapamycin, we demonstrate that LIN28B p

179 patients were pretreated with rapamycin, an mTORC1 inhibitor, prior to receiving ketamine.

180 ent signaling by conditional deletion of the mTORC1 inhibitor, TSC2, in alpha-cells (alphaTSC2(KO)).

181 Peli1 is mediated through regulation of the mTORC1-inhibitory proteins, TSC1 and TSC2.

182 e mechanistic target of rapamycin complex 1 (mTORC1) integrates growth, nutrient and energy status cu

183 Here, we identified a novel mTORC1-interacting protein called protein kinase A ancho

184 However, how the mTORC1 interacts with Rheb on the lysosome remains elusi

185 In response to nutrients, mTORC1 is activated on lysosomes by Rag and Rheb guanosi

186 mTORC1 is an important regulator of muscle mass but how

187 Our results show that mTORC1 is differentially regulated by amino acids throug

188 Indeed, mTORC1 is inactive during mitosis, reflecting its failur

189 ncta, is repressed during mitosis, even when mTORC1 is inhibited.

190 genetic, muscle fiber-specific activation of mTORC1 is sufficient to induce molecular signatures of s

191 e mechanistic target of rapamycin complex 1 (mTORC1) is a key metabolic hub that controls the cellula

192 ever, the regulation of these processes, and mTORC1 itself, is different during mitosis, and this has

193 ial transcription of these loci requires the mTORC1 kinase adaptor, Raptor, but not Xbp1.

194 n their lumen and metabolic signaling by the mTORC1 kinase on their limiting membranes.

195 6R)-HNK in rodents require activation of the mTORC1 kinase(10,11).

196 y these as a metric that accurately predicts mTORC1/LARP1 regulation called a TOPscore.

197 als amino acid (AA) availability to modulate mTORC1 localization and activity.

198 its degradation instigates robust lysosomal mTORC1 localization and its activation without the Ragul

199 l mechanistic target of rapamycin complex 1 (mTORC1) localization through the Rag GTPases is a critic

200 d signaling through the Rag GTPases promotes mTORC1 lysosomal localization and subsequent activation.

201 netic inhibition of endogenous PLD prevented mTORC1 lysosomal translocation.

202 I and MLIII downregulate the protein complex mTORC1 (mammalian target of rapamycin complex 1) signali

203 s a novel regulator of mTORC1 and downstream mTORC1-mediated actions on T cell metabolism and antitum

204 to accumulation of phosphorylated PRAS40 and mTORC1-mediated activation of HIF1alpha.

205 action between PRAS40 and Raptor to inactive mTORC1-mediated hyper-glycolytic metabolism.

206 EB oligomers display increased resistance to mTORC1-mediated inactivation and are more stable under p

207 Importantly, loss of AKAP8L decreased mTORC1-mediated processes such as translation, cell grow

208 cd4 expression in hippocampus via decreasing mTORC1-mediated proteasomes degradation pathway, which r

209 mTORC1 mediates ribosome biogenesis, protein translation

210 While mTORC1 normally represses autophagy via phosphorylation

211 The mammalian Target of Rapamycin complex 1 (mTORC1) nutrient-sensing pathway is a central regulator

212 ink their translation to the mTOR Complex 1 (mTORC1) nutrient-sensing signaling pathway.

213 e mechanistic target of rapamycin complex 1 (mTORC1) occur on the lysosome surface, increased lysosom

214 oked EPSCs (eEPSCs), however, the effects of mTORC1 on eEPSCs were postsynaptic and the effects of mT

215 s no longer dependent on acute activation of mTORC1 or de novo protein synthesis.

216 tic transmission, we genetically inactivated mTORC1 or mTORC2 in cultured mouse glutamatergic hippoca

217 S1), which in turn inhibits the PI3K-PKB/Akt-mTORC1 pathway and promotes TFEB/TFE3 nuclear translocat

218 d in heterotopias and hyperactivation of the mTorC1 pathway in pallial regions, which are homologous

219 olecular interplays between the AMPK and the mTORC1 pathway in the hepatic benefits of metformin are

220 bolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered

221 nt for LAMTOR4 and LAMTOR5 in regulating the mTORC1 pathway under fed and starved conditions.

222 complexes and the intimate interplay of the mTORC1 pathway with lysosomal function, validating the a

223 rough monitoring of the supply of nutrients (mTORC1 pathway) or of energy supply in cells (AMPK pathw

224 reveals a direct link between the Hippo and mTORC1 pathways to fine-tune organ growth.

225 and mammalian target of rapamycin complex 1 (mTORC1) pathways are the two predominant growth-control

226 Exactly how mTORC1 promotes cell growth remains unclear.

227 mTORC1 promotes skeletal muscle hypertrophy, but also dr

228 Mammalian target of rapamycin complex 1 (mTORC1) promotes cell growth and proliferation in respon

229 The kinase mTOR complex 1 (mTORC1) promotes cellular growth and is frequently dysre

230 paligenosis because persistent p53 prevents mTORC1 reactivation and cell proliferation.

231 ucing full-length AKAP8L into cells restored mTORC1-regulated processes, whereas reintroduction of AK

232 structural plasticity, normally provided by mTORC1 regulation of protein synthesis, is absent in FX.

233 le of nutrient signaling via mTOR complex 1 (mTORC1) regulation that controls glucagon secretion and

234 While leucine (Leu) is a critical mTORC1 regulator under AA-starved conditions, how Leu re

235 tor subunit LAMTOR4, revealed the known core mTORC1 regulatory signaling complexes and the intimate i

236 etabolic stress, and 4E-BP1 disinhibition on mTORC1 repression may be neuroprotective; however, wheth

237 Inhibition of mTORC1 rescues the lysosomal defects and vulnerability t

238 However, whether mTORC1 responds to diverse stimuli by differentially pho

239 In conclusion, PHD1 ensures an optimal mTORC1 response to leucine after episodes of metabolic s

240 ition reduced constitutive activation of the mTORC1/ribosomal protein S6 pathway and downregulated co

241 mTOR complex 1 (mTORC1) senses amino acids to control cell growth, metab

242 mTOR complex 1 (mTORC1) senses nutrients to mediate anabolic processes w

243 T cell mTORC1 activation, a link between Akt-mTORC1 signaling and CD8(+) trafficking has been demonst

244 ally, pyruvate uptake through Mct2 supported mTORC1 signaling by fueling serine biosynthesis-derived

245 lysosomes and nature of aberrant cholesterol-mTORC1 signaling contribution to organelle pathogenesis

246 Thus, cholesterol-mTORC1 signaling controls organelle homeostasis and is a

247 Sustained mTORC1 signaling during development prevented CpG methyl

248 Here, we determined whether mTORC1 signaling is also a target for decanoic acid, a k

249 Thus, nutrient mTORC1 signaling is an essential component of TCR-initia

250 We showed that activation of mTORC1 signaling is sufficient to induce chronic hypergl

251 in lysosomal surface availability can impact mTORC1 signaling output.

252 phosphatidic acid (PA) pathway, required for mTORC1 signaling through mechanisms that are not fully u

253 We observed decreased mTORC1 signaling which increased neuronal death, whereas

254 ens for identifying regulatory mechanisms of mTORC1 signaling, a key growth control pathway that sens

255 ses RagA and RagB impairs amino acid-induced mTORC1 signaling, causing defective amino acid anabolism

256 tion of lipolysis by ABHD5 potently inhibits mTORC1 signaling, leading to a significant downregulatio

257 d that iron chelators consistently inhibited mTORC1 signaling, which was blocked by pretreatment with

258 ponse to low energy levels and mediates AMPK-mTORC1 signaling.

259 ion and suppressing S6K1 phosphorylation and mTORC1 signaling.

260 luded elevated ribogenesis and activation of mTORC1 signaling.

261 reduce lysosome abundance, which suppresses mTORC1 signaling.

262 t this effect was found to be independent of mTORC1 signaling.

263 a new therapeutic approach to down-regulate mTORC1 signaling.

264 trols (n = 42) showed significantly enriched mTORC1 signaling.

265 iRNA is a downstream effector of hyperactive mTORC1 signaling.

266 e mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway, potentially leading to a rang

267 lysis and dedicated experiments, we identify mTORC1 signalling as a major regulation network during e

268 Conversely, p27(-/-) cells exhibit elevated mTORC1 signalling as well as impaired lysosomal activity

269 and a significant inhibition of elevation in mTORC1 signalling induced by Nf2 or Lats1 and Lats2 loss

270 Loss of Myog dysregulates mTORC1 signalling, resulting in an 'alerted' state of Mu

271 e mechanistic target of rapamycin complex 1 (mTORC1) signalling complex in response to nutrient avail

272 t/mechanistic Target of Rapamycin Complex 1 (mTORC1) signalling or depleting the key metabolic substr

273 ntrols the activation of a metabolic kinase, mTORC1, stimulated by both the TCR signal and growth fac

274 that enables differential phosphorylation of mTORC1 substrates, the dysregulation of which leads to k

275 orylation of TFEB-unlike other substrates of mTORC1, such as S6K and 4E-BP1- is strictly dependent on

276 gy via the impact of its metabolite AcCoA on mTORC1, suggesting that AcCoA and EP300 play pivotal rol

277 several pH-dependent proteins, including the mTORC1 suppressor Tsc2 and the longevity regulator Sirt1

278 morphogenesis and spine development through mTORC1/TFEB pathway.

279 these results reveal a mode of regulation of mTORC1 that is distinct from its lysosomal activation, w

280 Identifying the changes downstream of mTORC1 that lead to advanced pathologies in mouse might

281 e mechanistic target of rapamycin complex 1 (mTORC1) that promotes T cell growth.

282 In contrast, glutamine activates mTORC1 through a Rag GTPase-independent mechanism that r

283 Like glutamine, asparagine signals to mTORC1 through Arf1 in the absence of the Rag GTPases.

284 transcriptome scale and show how it connects mTORC1 to a tunable and dynamic program of gene expressi

285 DDIT4 initially suppresses mTORC1 to induce autodegradation of differentiated cell

286 We thus conclude that B cells utilize mTORC1 to prepare for subsequent plasma cell function, b

287 dification, which facilitates the binding of mTORC1 to Rheb on the lysosome and is another crosstalk

288 Tsc2 induction inhibits mTORC1 to suppress cellular metabolism and prevent acido

289 The Rag GTPases (Rags) recruit mTORC1 to the lysosomal membrane in response to nutrient

290 hat exogenously supplied PA vesicles deliver mTORC1 to the lysosome in the absence of amino acids, Ra

291 te S606 of Raptor, an essential component of mTORC1, to attenuate mTORC1 activation by impairing the

292 s is achieved in large part by a switch from mTORC1- to cyclin-dependent kinase 1 (CDK1)-mediated reg

293 which functions through the mTOR complex 1 (mTORC1)-transcription factor EB (TFEB) axis in the host

294 h factors trigger PA production required for mTORC1 translocation and activation at the lysosome.

295 sis and autophagy(4,5), is phosphorylated by mTORC1 via a substrate-specific mechanism that is mediat

296 ndings indicate that iron chelation inhibits mTORC1 via multiple pathways and iron is essential for m

297 mino acids induce lysosomal translocation of mTORC1 via the Rag GTPases.

298 dent activation of AMPK classically inhibits mTORC1 via TSC/RHEB, but several lines of evidence sugge

299 nterestingly, ABHD5-dependent suppression of mTORC1 was abrogated by pharmacological inhibition of DG

300 Transcriptionally, AMPK and mTORC1 were both important for regulation of anabolic me