ライフサイエンスコーパス: mTORC1

1 is an essential regulator of mTOR complex 1 (mTORC1).

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

3 y mechanistic target of rapamycin complex 1 (mTORC1).

4 and mammalian target of rapamycin complex 1 (mTORC1).

5 ly influences T cell differentiation through mTORC1.

6 drugs to incomplete/nondurable inhibition of mTORC1.

7 vel of protein phosphorylation downstream of mTORC1.

8 d renders PI3K for IRS-1, thereby activating mTORC1.

9 alleviated the dependence of HH signaling on mTORC1.

10 the 3.4 angstrom structure of activated RHEB-mTORC1.

11 l proteolysis to exit lysosomes and activate mTORC1.

12 When combined with DNA damage, inhibition of mTORC1/2 blocked transcriptional induction more strongly

13 Only mTORC1/2 inhibition reversed cancer cell resistance to D

14 Inhibition of mTORC1 or mTORC1/2 within ovaries was achieved during chemotherapy

15 1 or mTORC2 but was blocked by inhibition of mTORC1/2.

16 combination with trastuzumab, AZD2014 (dual mTORC1/2i), AZD5363 (AKTi) and selumetinib (AZD6244/ARRY

17 -cell apoptosis, size and autophagy, whereas mTORC1/4E-BP2-eIF4E pathway regulates beta-cell prolifer

18 pamycin (aka mammalian target of rapamycin) (mTORC1), a master metabolic sensor.

19 the mammalian target of rapamycin complex 1 (mTORC1), a signaling pathway that regulates synaptic pro

20 mTORC1-activated S6K1 phosphorylates SRPK2 at Ser494, wh

21 a substrate for OGDH, which in turn leads to mTORC1 activation and a subsequent reduction in autophag

22 Thus, lysosomal cholesterol drives mTORC1 activation and growth signaling through the SLC38

23 t AMPK activation by low energy, it enforces mTORC1 activation and overrides a physiological response

24 Moreover, SLC38A9 enables mTORC1 activation by cholesterol independently from its

25 nsmembrane protein, SLC38A9, is required for mTORC1 activation by cholesterol through conserved chole

26 Amino acids or glucose facilitates mTORC1 activation by inducing RagA GTPase recruitment of

27 stress-induced AMPK activation, it enforced mTORC1 activation despite the presence of activated AMPK

28 el mechanism by which CAMK2gamma antagonizes mTORC1 activation during hepatocarcinogenesis.

29 Thus, mTORC1 activation is required for fueling B cells prior

30 Our data provide a mechanism by which mTORC1 activation may be finely regulated in a tissue-sp

31 pertrophy, but the detailed mechanism of how mTORC1 activation occurs under pathological conditions i

32 nstrate that the leucine sensor function for mTORC1 activation of LRS can be decoupled from its catal

33 In human sarcoidosis patients, mTORC1 activation, macrophage proliferation and glycolys

34 or TSC2 causes reduced pigmentation through mTORC1 activation, which results in hyperactivation of g

35 he lysosomal v-ATPase to negatively regulate mTORC1 activation.

36 2 (TSC2(-/-) cells), which show constitutive MTORC1 activation.

37 to the cell periphery, thereby facilitating mTORC1 activation.

38 translocation to the cell periphery promotes mTORC1 activation.

39 sed mammalian target of rapamycin complex 1 (mTORC1) activation, which has been linked to inhibition

40 These data unveil TBK1 as a direct mTORC1 activator and suggest unanticipated roles for mTO

41 e alphaherpesvirus-specific Us3 kinase as an mTORC1 activator that subverts the host cell energy-sens

42 We conclude that mTORC1 actively suppresses autophagy and maintains endos

43 suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistance to sunitinib i

44 After 2 days of arginine deprivation, mTORC1 activity declined paralleling a selective down-re

45 Enhanced mTORC1 activity drives characteristic phenotypes of sene

46 allow myelination to start, while remaining mTORC1 activity drives myelin growth.

47 Here, we demonstrate that mTORC1 activity in HSV-1-infected cells is largely insen

48 ly, we identified TBK1 as a key regulator of mTORC1 activity in Trex1(-/-) cells.

49 An ensuing decline in mTORC1 activity is crucial to allow myelination to start

50 utophagy and raises ER cholesterol even when mTORC1 activity is high, suppresses SREBP-2 activation.

51 rab5, ER cholesterol fails to increase when mTORC1 activity is low, and SREBP-2 is activated.

52 Furthermore, when mTORC1 activity is low, cholesterol is delivered to lyso

53 Interventions that enhance or diminish mTORC1 activity or other nodes in this pathway in melano

54 ether our data suggest a model in which high mTORC1 activity promotes proliferation of immature SCs a

55 ion to this developmental role, excessive SC mTORC1 activity stimulates myelin growth, even overgrowt

56 Furthermore, resistance of mTORC1 activity to low-energy-induced stress, while not

57 luster perinuclearly, accompanied by reduced mTORC1 activity under nutrient-rich conditions.

58 We found mTORC1 activity was unaffected in the initial G1 block.

59 protein synthesis that is independent of Akt/mTORC1 activity.

60 latory effect on BORC that is independent of mTORC1 activity.

61 ppears to function through the regulation of mTORC1 activity.

62 ced mammalian target of rapamycin complex 1 (mTORC1) activity, although the underlying mechanism is u

63 e mechanistic target of rapamycin complex 1 (mTORC1) activity, one of the major kinases in cells that

64 Using it, we find that, independently of mTORC1, amino acid scarcity induces protein scavenging a

65 Importantly, phosphorylation of LARP1 by mTORC1 and Akt/S6K1 dissociates it from 5'UTRs and relie

66 target of rapamycin) pathway at the level of mTORC1 and also regulates the transcription factor Myrf,

67 Taken together, these data unveil a role for mTORC1 and autophagy in the pathogenesis of skeletal dis

68 ) tumor suppressors results in activation of mTORC1 and development of the tumor syndrome TSC.

69 of cocaine seeking, which may be mediated by mTORC1 and ERK1/2 signaling.

70 by a high-protein diet in adulthood, through mTORC1 and GCN-2 activity.

71 ism that requires the permissive activity of mTORC1 and GSK3beta, demonstrating the importance of the

72 s study, we found that burn injury activated mTORC1 and hypoxia-inducible factor (HIF)-1alpha, which

73 The mTORC1 and IFN-gamma production defects were partially r

74 This was concurrent with reduced activity of mTORC1 and its downstream mRNA translation initiation fa

75 us hydrogen sulfide but normal inhibition of mTORC1 and maintenance of ApoB100 during asparaginase ex

76 te tumor growth, suggesting a combination of mTORC1 and MAPK inhibitors may be of therapeutic value i

77 ntly active tumor driver that activates both mTORC1 and MAPK to promote tumor growth, suggesting a co

78 We report here that mTORC1 and mTORC2 are activated in response to exogenous

79 We show that mTORC1 and mTORC2 are both required to enact DNA damage

80 Thus, both mTORC1 and mTORC2 kinase activity is tightly controlled

81 Cre;KD-mTOR (Homozygous) mice showed reduced mTORC1 and mTORC2 signaling along with transcripts and p

82 orylation of specific functional readouts of mTORC1 and mTORC2 signaling in multiple maternal and fet

83 folate is positively correlated to placental mTORC1 and mTORC2 signalling activity in human pregnancy

84 Here, we show that mTORC1 and mTORC2 specifically and synergistically regul

85 ate that, as part of two distinct complexes, mTORC1 and mTORC2, mTOR is the major regulator of growth

86 rapamycin (mTOR), existing in two complexes, mTORC1 and mTORC2.

87 gstrom cryo-electron microscopy structure of mTORC1 and the 3.4 angstrom structure of activated RHEB-

88 tify the mTORC1/FoxA2 axis as a link between mTORC1 and transcriptional regulation of key genes respo

89 tionally distinct complexes, mTOR complex 1 (mTORC1) and 2 (mTORC2), whose activities and substrate s

90 of mammalian target of rapamycin complex 1 (mTORC1) and activation of Akt, ultimately leading to inc

91 Mammalian target of rapamycin complex 1 (mTORC1) and cell senescence are intimately linked to eac

92 -component kinase complexes, mTOR complex 1 (mTORC1) and mTORC2.

93 -poor conditions the pro-anabolic effects of mTORC1 are functionally opposed to growth.

94 eveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also iden

95 se data suggest that an AKT-independent PI3K/mTORC1 axis operates in these cells.

96 inhibition of S6K1, a downstream effector of mTORC1, blocked within-session extinction, indicating a

97 ishes that the Us3 kinase not only activated mTORC1 but also enabled sustained mTORC1 signaling durin

98 ation of mTORC1 is specific to activation of mTORC1 by amino acid stimulation, rather than by growth

99 Activation of mTORC1 by arginine requires SLC38A9, a poorly understood

100 Constitutive activation of mTORC1 by depletion of tuberous sclerosis complex 2 (TSC

101 is actually known regarding the functions of mTORC1 compared to mTORC2 in this regard or the respecti

102 itors, such as rapamycin, incompletely block mTORC1 compared with mTOR kinase inhibitors (TORKi).

103 adipocyte-specific deficiency of raptor, an mTORC1 constituent.

104 e mechanistic target of rapamycin complex 1 (mTORC1) controls cell growth and metabolism in response

105 e mechanistic target of rapamycin complex 1 (mTORC1) decreases in DENV-infected cells and is inversel

106 maintains macrophage quiescence and prevents mTORC1-dependent granulomatous disease with clinical imp

107 al that aPC protects from IRI by restricting mTORC1-dependent inflammasome activation and that mimick

108 stically, this metabolic rewiring stems from mTORC1-dependent regulation of S-adenosylmethionine deca

109 wever, simultaneous mutation of three of the mTORC1-dependent sites results in significantly reduced

110 onstrate that TBK1 activates mTOR complex 1 (mTORC1) directly.

111 ctivator and suggest unanticipated roles for mTORC1 downstream of TBK1 in control of innate immunity,

112 Through genetic reconstitution of mTORC1 downstream targets, we identify mTORC1/S6K pathwa

113 Thereby, RagA alters mTORC1-driven growth in times of nutrient abundance or s

114 SRPK2 is a potential therapeutic target for mTORC1-driven metabolic disorders.

115 N2 but is not required for downregulation of mTORC1 during asparaginase.

116 ch was associated with failure to inactivate mTORC1 during fasting.

117 Mechanistically, mTORC1 engaged glucose metabolism and initiated a transc

118 A Tsc2/mTORC1 expression signature identified in Tsc2-deficient

119 h the unique mTORC2 component SIN1 to favour mTORC1 formation.

120 Additionally, our data identify the mTORC1/FoxA2 axis as a link between mTORC1 and transcrip

121 ate the core component, Raptor, to show that mTORC1 function is critical for male meiosis and the ina

122 Together, these results demonstrate that mTORC1 has an essential role in the meiotic progression

123 Mammalian target of rapamycin complex 1 (mTORC1) has an essential role in dendritic mRNA translat

124 Finally, we discuss how GABABR activation of mTORC1 helps resolve key discrepancies between rapid-act

125 ndent of conventional AMPK signalling or the mTORC1-HIF-1alpha axis, but contributed to the activatio

126 sults provide evidence of involvement of the mTORC1-HIF-1alpha pathway in burn-induced metabolic dera

127 uction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (

128 mTORC1 hyperactivation leads to podocyte hypertrophy, bu

129 and anaplastic dedifferentiation, as well as mTORC1 hyperactivation with reduced Akt phosphorylation.

130 The subsequent reconstitution of SC mTORC1 hyperactivity in adult animals resulted in focal

131 Surprisingly, the resulting mTORC1 hyperactivity led to markedly delayed onset of bo

132 human disease of TSC1/TSC2 inactivation and mTORC1 hyperactivity.

133 lthood, depending on the level and timing of mTORC1 hyperactivity.

134 mTORC1 hyperphosphorylates the protein UV radiation resi

135 f glucagon secretion and identify a role for mTORC1 in controlling alpha cell-mass maintenance.

136 is study also demonstrates a central role of mTORC1 in controlling insulin processing by regulating c

137 amino acid or glucose deprivation to inhibit mTORC1 in cultured human cells.

138 nutrient-sensing dependence through RagA and mTORC1 in hematopoietic progenitors, which dynamically d

139 , our results reveal a potential function of mTORC1 in nutrient-dependent regulation of glucagon secr

140 -dependent inactivation of mTORC1 signaling, mTORC1 inactivation is independent of AMPK activation du

141 ses the translation of downstream targets of mTORC1, including collapsin response mediator protein-2

142 positioning through Ragulator-dependent, but mTORC1-independent, modulation of BORC.

143 Inhibition of mTORC1 induced apoptosis and completely resolved granulo

144 cinoma, and melanoma triggered RagD-mediated mTORC1 induction, resulting in cell hyperproliferation a

145 ent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels

146 t, was increased by asparaginase, suggesting mTORC1 inhibition during asparaginase exposure is not dr

147 -activated protein kinase (AMPK) activation, mTORC1 inhibition, and autophagy induction.

148 esults demonstrate that PIM3 is induced upon mTORC1 inhibition, with potential implications for the e

149 nsor function of LRS can be a new target for mTORC1 inhibition.

150 lination could be rescued by pharmacological mTORC1 inhibition.

151 implicated in coordinating this response to mTORC1 inhibition.

152 sely, samples from a clinical trial with the mTORC1 inhibitor everolimus exhibit a predominant decrea

153 ex (PFC), and that infusion of the selective mTORC1 inhibitor rapamycin into the medial PFC (mPFC) bl

154 Similar effects are seen using mTORC1 inhibitor rapamycin or by knocking down raptor.

155 Abnormalities were blocked by the mTORC1 inhibitor sirolimus.

156 In mice, an mTORC1 inhibitor suppressed medulloblastoma driven by a

157 The mammalian target of rapamycin complex 1 (mTORC1) inhibitor rapamycin slows progression of these d

158 th potential implications for the effects of mTORC1 inhibitors in TSC, cancers, and the many other di

159 There is significant excitement around using mTORC1 inhibitors to treat cancer and neurological disea

160 by mammalian target of rapamycin complex 1 (mTORC1) inhibitors.

161 mTORC1 is a signal integrator and master regulator of ce

162 mTORC1 is activated by the small GTPase RHEB (Ras homolo

163 licative exhaustion, or oncogene activation, mTORC1 is constitutively active and resistant to serum a

164 decreased tendon thickness, indicating that mTORC1 is necessary for postnatal tendon development.

165 This regulation of mTORC1 is specific to activation of mTORC1 by amino acid

166 mTOR complex I (mTORC1) is a central growth regulator that senses amino

167 e mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of cell growth that respo

168 Mechanistic target of rapamycin complex 1 (MTORC1) is a critical negative regulator of general auto

169 e mechanistic target of rapamycin complex 1 (mTORC1) is a protein kinase complex that localizes to ly

170 re, we demonstrated that the mTOR complex 1 (mTORC1) is essential for this sustained VLDL-TAG secreti

171 The mTORC1 kinase is a master growth regulator that senses m

172 The mammalian target of rapamycin complex 1 (mTORC1) kinase promotes cell growth by activating biosyn

173 Conversely, constitutively active mTORC1 led to DZ enrichment but loss of competitiveness

174 r effects and signaling feedback sequelae of mTORC1 loss of function in epithelial tissue.

175 In mice with mTORC1 loss of function, we found that Rho kinase (ROCK)

176 melanosomal biogenesis and autophagy-control mTORC1 lysosomal recruitment and activity by directly re

177 We hypothesized that MTORC1 may specifically regulate autophagic clearance of

178 re controversial and its regulatory roles in mTORC1-mediated translation remain unclear.

179 and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon plus insulin on A

180 approach to disable nonredundant subunits of mTORC1, mTORC2, or both, we showed that mice lacking mTO

181 both, we showed that mice lacking mTORC1 or mTORC1/mTORC2 but not mTORC2 alone develop a Fanconi-lik

182 Additionally, inhibition of mTORC1 or GSK3beta promotes neuronal survival following

183 ge was not impaired by rapalog inhibition of mTORC1 or independent inhibition of mTORC1 or mTORC2 but

184 Inhibition of mTORC1 or mTORC1/2 within ovaries was achieved during ch

185 mTORC2, or both, we showed that mice lacking mTORC1 or mTORC1/mTORC2 but not mTORC2 alone develop a F

186 ition of mTORC1 or independent inhibition of mTORC1 or mTORC2 but was blocked by inhibition of mTORC1

187 can be significantly restored by inhibiting mTORC1 or p70S6 kinase (p70S6K), downstream kinases whos

188 monstrate that deregulation of the PI3K-AKT/ mTORC1/ p70S6K pathways, an event frequently observed in

189 ch uncovered evidence that TBK1 supports AKT/mTORC1 pathway activation and function through direct mo

190 ly dependent on TBK1-mediated support of AKT/mTORC1 pathway activation for survival.

191 single dose of GLYX-13 rapidly activates the mTORC1 pathway in the prefrontal cortex (PFC), and that

192 tudies show they inhibit the activity of the mTORC1 pathway.

193 synthetase (LRS) is a leucine sensor of the mTORC1 pathway.

194 ing mammalian target of rapamycin complex 1 (mTORC1) pathway was activated in Cpt2M(-/-) hearts; howe

195 ibition, or depletion of Protrudin or FYCO1, mTORC1-positive lysosomes cluster perinuclearly, accompa

196 Upon overexpression of Protrudin and FYCO1, mTORC1-positive lysosomes translocate to the cell periph

197 stream targets, such as GSK3beta, FOXO1, and mTORC1, prior to NMDA-induced injury.

198 Moreover, mTORC1 promoted metabolic reprogramming via CDK4 toward

199 Additionally, mTORC1 promoted TAG secretion by regulating phosphocholi

200 Here, we demonstrate that mTORC1 promotes lipid biogenesis via SRPK2, a key regula

201 e mechanistic target of rapamycin complex 1 (mTORC1) protein kinase is a master growth regulator that

202 form for the presentation of active Rags for mTORC1 recruitment, and might suggest an unconventional

203 o and in vivo The constitutive activation of mTORC1 reduced hepatic lipogenic gene expression and pro

204 Our data demonstrate that mTORC1-regulated autophagy is necessary and sufficient f

205 mTORC1/S6K pathway as the mechanism by which mTORC1 regulates beta-cell apoptosis, size and autophagy

206 results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of

207 mTOR complex 1 (mTORC1) regulates cell growth and metabolism in response

208 t mechanistic target of rapamycin complex 1 (mTORC1) regulates polyamine dynamics, a metabolic route

209 Although many details of mTORC1 regulation are well understood, a systems-level,

210 for the NPRL2, distinct from its function in mTORC1 regulation.

211 ealing a stimulus-selective role for TBK1 in mTORC1 regulation.

212 TOR- and SESN-dependent nutrient sensing and mTORC1 regulation.

213 ng mice with tissue-specific deletion of the mTORC1 regulator Raptor in alpha cells (alphaRaptorKO),

214 Thus, the dynamic response of mTORC1 requires intersubunit communication by the Rag GT

215 This growth enhancement depends on mTORC1's canonical function in controlling translation r

216 on of mTORC1 downstream targets, we identify mTORC1/S6K pathway as the mechanism by which mTORC1 regu

217 Phosphorylation of EPRS at Ser999 by mTORC1-S6K1 induces its release from the aminoacyl tRNA

218 Further results demonstrated that mTORC1-S6K1 signaling controls transcription of CHK1 via

219 glutamyl-prolyl-tRNA synthetase (EPRS) as an mTORC1-S6K1 target that contributes to adiposity and age

220 These findings help explain how mTORC1 selects its substrates, how its kinase activity i

221 s out of lysosomes, including leucine, which mTORC1 senses through the cytosolic Sestrin proteins.

222 , mechanistic target of rapamycin complex 1 (mTORC1) signal transduction was unleashed, and this coin

223 ation of TFH cells in mice via alteration of mTORC1 signaling and inhibition of Bcl6 expression.

224 Therefore, the interplay between mTORC1 signaling and metabolic reprogramming underlies M

225 Here, we show that enhanced mTORC1 signaling arrests bone growth in lysosomal storag

226 ciated genes together with activation of AKT-mTORC1 signaling as a consequence of BRD4 stabilization.

227 In contrast, negative regulation of mTORC1 signaling by DNA damage is abrogated in many canc

228 Loss of mTORC1 signaling by removal of Raptor in tendons caused

229 tors, including the Raf/Mek/Erk and PI3K/Akt/mTORC1 signaling cascades, and also the WNT/beta-catenin

230 d T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.

231 the hepatic transcriptome and mediating GCN2-mTORC1 signaling during asparaginase.

232 activated mTORC1 but also enabled sustained mTORC1 signaling during simulated energy insufficiency t

233 Increased mTORC1 signaling from TSC1/TSC2 inactivation is found in

234 Pharmacological approaches targeting AMPK/mTORC1 signaling greatly ameliorated muscle function in

235 Moreover, inhibition of mTORC1 signaling in alphaRaptorKO mice and in WT animals

236 that, under stressful conditions, maintained mTORC1 signaling in cancer cells promotes survival by su

237 Here we examine the role of mTORC1 signaling in postnatal tendon development using m

238 fructose acutely and transiently suppressed mTORC1 signaling in vitro and in vivo The constitutive a

239 alpha cells (alphaRaptorKO), we showed that mTORC1 signaling is dispensable for alpha cell developme

240 est that maintaining physiological levels of mTORC1 signaling is essential for postnatal tendon devel

241 In mouse models of LSD, normalization of mTORC1 signaling or stimulation of the Beclin 1-Vps34-UV

242 these phenotypes restore sensitivity to the mTORC1 signaling pathway and cause death, indicating tha

243 We establish a role for the nutrient-sensing mTORC1 signaling pathway within AGRP neurons in the dete

244 was impaired under starved conditions, while mTORC1 signaling remained active.

245 mage is abrogated in many cancer cells, thus mTORC1 signaling remains active under microenvironmental

246 Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically relevant

247 , the HRI-eIF2alphaP-ATF4 pathway suppresses mTORC1 signaling specifically in the erythroid lineage.

248 Here we report that mTORC1 signaling suppresses endogenous DNA damage and re

249 mental stages, physiologically high PI3K-Akt-mTORC1 signaling suppresses expression of Krox20 (Egr2),

250 These data prove the necessity of intact MTORC1 signaling to regulate two synergistic processes r

251 vely, our findings provide insights into how mTORC1 signaling within AGRP neurons surveys energy avai

252 how that mTOR S2159 phosphorylation promotes mTORC1 signaling, IRF3 nuclear translocation, and IFN-be

253 ly stimulates TSC2-dependent inactivation of mTORC1 signaling, mTORC1 inactivation is independent of

254 the antiapoptotic protein MCL-1 and inducing mTORC1 signaling, thus evoking little cytotoxicity.

255 red a decline in MCL-1 levels, and inhibited mTORC1 signaling.

256 cogene PIM3 as being repressed downstream of mTORC1 signaling.

257 glycogen storage are repressed by ATXN2 via mTORC1 signaling.

258 inks methionine and one-carbon metabolism to mTORC1 signaling.

259 ther disease settings influenced by aberrant mTORC1 signaling.

260 nd Atf4(-/-) mice by inhibiting both HRI and mTORC1 signaling.

261 vity, which was due in part to activation of mTORC1 signaling.

262 s mechanistic target of rapamycin complex 1 (mTORC1) signaling and anabolic metabolism.

263 and mammalian target of rapamycin complex 1 (mTORC1) signaling.

264 of mammalian target of rapamycin complex 1 (mTORC1) signaling.

265 SZT2 deficiency resulted in constitutive mTORC1 signalling in cells under nutrient-deprived condi

266 s not prevent hyperproliferation or elevated mTORC1 signalling in Ndfip1-deficient Treg cells.

267 utionarily conserved GATOR complex regulates mTORC1 signalling through Rag GTPases, and GATOR1 displa

268 a lysosome-associated negative regulator of mTORC1 signalling, which, like GATOR1, is mutated in hum

269 Deregulation of mTOR complex 1 (mTORC1) signalling increases the risk for metabolic dise

270 Pharmacologic inhibition of mTORC1 significantly increased red blood cell counts and

271 ons of GLYX-13, indicating a requirement for mTORC1 similar to ketamine.

272 These results thus reveal a novel role of mTORC1-SRPK2 signaling in post-transcriptional regulatio

273 enzymes are among the downstream targets of mTORC1-SRPK2 signaling.

274 e that accumulates in cells with hyperactive mTORC1, such as kidney cells with mutations in the tumor

275 and mammalian target of rapamycin complex 1 (mTORC1) suppressed the ability of glucagon plus insulin

276 Depleting 4EBP1, an mTORC1 target that inhibits translation, alleviated the

277 biosynthetically demanding process in which mTORC1, the gatekeeper of anabolism, occupies a privileg

278 ed cells, TBK1 associates with and activates mTORC1 through site-specific mTOR phosphorylation (on S2

279 asticity to myelinate and remodel myelin via mTORC1 throughout life.

280 amino acid metabolite homocysteine activates mTORC1 to inhibit autophagy and form abnormal proteins i

281 e complex regulatory landscape controlled by mTORC1 to integrate and translate growth signals into an

282 has been proposed to function downstream of mTORC1 to regulate the translation of 5'TOP mRNAs such a

283 Upstream of Atf4, BMP2 activates mTORC1 to stimulate protein synthesis, resulting in an e

284 ation by inducing RagA GTPase recruitment of mTORC1 to the lysosomal outer surface, enabling activati

285 ses (GTPases) to promote the localization of mTORC1 to the lysosomal surface, its site of activation.

286 Rag GTPases to promote the translocation of mTORC1 to the lysosomal surface, its site of activation.

287 nslation-regulation pathways, eIF2alphaP and mTORC1, to circumvent ineffective erythropoiesis, highli

288 veal a metabolic vulnerability downstream of mTORC1 triggered by anabolic imbalance.

289 in dissecting the relative contributions of mTORC1 versus mTORC2 in cancer, their role in tumor-asso

290 lar nutrient levels, which are transduced to mTORC1 via the Rag GTPases and the Ragulator complex.

291 However, if mTORC1 was hyperactivated after myelination onset, radia

292 for mammalian target of rapamycin complex 1 (mTORC1), was acutely deleted in intestinal epithelium vi

293 e of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylati

294 tes mammalian target of rapamycin complex 1 (mTORC1) when GTP loaded.

295 on mammalian target of rapamycin complex 1 (mTORC1), which appeared to have both positive and negati

296 e mechanistic target of rapamycin complex 1 (mTORC1), which promotes the anabolic program that suppor

297 mTOR exists in two complexes: mTORC1, which stimulates protein, lipid, and ribosome bi

298 Inhibition of mTORC1 with rapamycin induces PIM3 transcript and protei

299 downstream branches of the pathway, in that mTORC1 (with adaptor protein Raptor) is the main complex

300 th the PI3K/Akt/mTOR pathway at the level of mTORC1, working together to drive the growth of the myel