ライフサイエンスコーパス: mTOR

1 mTOR activation is essential and sufficient to cause pol

2 mTOR activation was increased in the interfollicular spa

3 mTOR complex 1 (mTORC1) senses amino acids to control ce

4 mTOR inhibition increased LT protein expression for all

5 mTOR inhibitors, at therapeutic levels, directly activat

6 mTOR-inhibitor treatment with sirolimus for >=3 months i

7 ion channel that regulates PI3K-AKT, ERK1/2, mTOR signaling, muscle differentiation, myoblast fusion,

8 ombined correction of endothelial Smad1/5/8, mTOR, and VEGFR2 pathways opposes HHT pathogenesis.

9 Aberrant mTOR signaling occurs frequently in cancers, so mTOR has

10 nd phosphorylation state, and found abnormal mTOR expression in both complexes in SZ DLPFC.

11 n initiation factors 4E and 4G and activates mTOR-independent translation of the mRNA encoding the tu

12 with sphingolipid (S1P) signaling, activates mTOR and allows translation of Tfap2c.

13 tumor-promoting effects by mainly activating mTOR pathway in Glioma.

14 In addition, mTOR-deficient microglia did not effectively engulf inju

15 omponents and its deletion promotes PI3K-AKT-mTOR signaling in NPCs of mouse cortex and cerebral orga

16 the LRRC8 complex regulates insulin-PI3K-AKT-mTOR signaling in skeletal muscle to influence skeletal

17 ession in Lrrc8a KO myotubes boosts PI3K-AKT-mTOR signaling to supra-normal levels and fully rescues

18 ng; focal adhesion, MAPK signaling, PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signaling, TGF-b

19 he antagonistic miRNA let-7g, suppressed Akt-mTOR complex 1 (mTORC1) activity and renders young, imma

20 idence that proteins associated with the AKT-mTOR signaling cascade are downregulated in SZ DLPFC.

21 The AKT-mTOR signaling cascade has been implicated in SZ by gene

22 in-inhibitory neurons in mPFC, activates Akt/mTOR signaling, and increases levels of synaptic protein

23 reduction of IL-1A and IL-2, as well as Akt/mTOR phosphorylation.

24 led to activation of Ras, inhibition of Akt/mTOR pathways, and increased expression of autophagy mar

25 ke receptor 2 as the initiating event of Akt/mTOR-dependent induction of MDSC.

26 of phosphatidylinositide-3-kinase (PI3K)/AKT/mTOR pathway is frequently detected in MCC, making it an

27 active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in early human embryos, and in both prim

28 involved in lymphocyte development, PI3K-AKT/mTOR (6%), and loss-of-function mutations in TP53 (12%)

29 is strongly relies on overactivated PI3K/Akt/mTOR and VEGFR2 pathways in endothelial cells (ECs).

30 m that sustains the activity of the PI3K/AKT/mTOR pathway and glycolysis in B-cell lymphomas.

31 mental metastasis by activating the PI3K/AKT/mTOR pathway and its downstream effectors HIF-1alpha and

32 Dysregulation of the PI3K/Akt/mTOR pathway has become a point of convergence in autism

33 ion linked to ROS-mitochondrial and PI3K/Akt/mTOR signaling pathways.

34 The Akt/mTOR pathway played a critical role in the AML-EV-induce

35 and then correspondingly inactivated the AKT/mTOR signaling pathway.

36 ic phenotype concomitant with decreased Akt1/mTOR signaling.

37 e synthetic phenotype and downregulated Akt1/mTOR signaling.

38 o be a major mechanism through which altered mTOR signaling leads to neurological disease.

39 Although mTOR signaling is known as a broad regulator of cell gro

40 Ras homolog enriched in brain, an mTOR activator, rescued the effect of Slc7a5 knockdown o

41 Together, our results identify an mTOR-responsive neuronal autophagy pathway, wherein RILP

42 In contrast, MPs activate translation in an mTOR-independent manner due, at least in part, to protea

43 s, and they suggest that a combination of an mTOR inhibitor and platinum-based chemotherapy might be

44 antations, exposure of wild-type HSPCs to an mTOR(ECKO) microenvironment was sufficient to recapitula

45 in LDLR resulted from iNOS inhibition via an mTOR complex 1-dependent mechanism.

46 as small-molecule inhibitors of Aurora A and mTOR, are currently being evaluated in early phase clini

47 AKT and mTOR are serine/threonine kinases which play important r

48 bunit PI3K-P85alpha, which increased AKT and mTOR phosphorylation, enhancing cell survival.

49 We found a reduction in AKT and mTOR protein expression and/or phosphorylation state in

50 Both AKT and mTOR require phosphorylation at specific sites for their

51 Insulin, AMPK, and mTOR signalling activity was similar in control and IUGR

52 puromycin incorporation in SUnSET assay) and mTOR pathway protein expression (raptor, 4e-bp-1, and p7

53 th simultaneous enhancement of autophagy and mTOR pathway.

54 of endolysosomal, autophagic, catabolic, and mTOR-related proteins.

55 utathione normalize GAPDH-Rheb complexes and mTOR activity in S47 cells.

56 pression of ERBB2 protein and both ERBB2 and mTOR target phosphosite levels in cases associated with

57 btype is susceptible to combination FGFR and mTOR inhibition, with implications for targeted therapy.

58 s the intake and utilization of glucose, and mTOR, a kinase downstream of PI3K that stimulates transc

59 rotein interaction between hexokinase II and mTOR.

60 switches 5' AMP-activated protein kinase and mTOR, and also numerous metabolic enzymes and their resp

61 he late endosomal/lysosomal adaptor MAPK and mTOR activator (LAMTOR) complex as an important regulato

62 a A kinase inhibitor alisertib (MLN8237) and mTOR inhibitor vistusertib (AZD2014).

63 ually potent dual inhibitor of PI3Kalpha and mTOR kinases.

64 Rapalogs and mTOR kinase inhibitors (TORKi) have recently been applie

65 ted to downregulation of SIRT1 signaling and mTOR was not implicated.

66 regulation of eIF4 and p70S6K signaling, and mTOR signaling pathways.

67 rial hyperpolarization, oxidative stress and mTOR signalling underwrite the known function of T cell

68 y by inhibiting beta-catenin translation and mTOR activity and thereby reduces HCC cell survival.

69 identified an activation of anti-angiogenic mTOR effectors.

70 IL-6 stimulation augmented mTOR activation in iMCD patients, which was abrogated wi

71 Basal mTOR activation was reduced by 50% in HF-fed mdKO mice,

72 RASGRP1 overexpression enhances baseline mTOR-S6 signaling in the bone marrow, but not in vitro c

73 nctional studies revealed increased baseline mTOR pathway activation in peripheral monocytes and T ce

74 effects via activation of AMPA receptor/BDNF/mTOR signaling in mice, which subsequently increase syna

75 work has shown that concomitant belatacept + mTOR inhibitor therapy is effective for maintenance immu

76 proteasome in regulating cross talk between mTOR signaling and glycolysis in liver cancer progressio

77 ether NET-1 upregulation induced by blocking mTOR might be a useful adjunct to (131)I-mIBG therapy.

78 ls in culture, ZIKV infection activates both mTOR complex 1 (mTORC1) and mTORC2.

79 hemical analyses revealed dysregulated brain mTOR and GSK3beta signaling, consistent with observed le

80 m study to determine the impact of the broad mTOR inhibitor, everolimus, on residual HIV burden, tran

81 are responsible for autophagy impairment but mTOR is involved minimally.

82 oproliferative syndrome, a disease driven by mTOR hyperactivation that responds to sirolimus treatmen

83 eplication, it is subsequently suppressed by mTOR.

84 These results implicated an NKT cell/mTOR/IFN-gamma axis in immunosuppression following endot

85 nd selective brain-penetrant ATP-competitive mTOR inhibitor.

86 In contrast, mTOR inhibition (e.g., temsirolimus) blocked cisplatin-i

87 vation of signaling pathways including CREB, mTOR, and Src-FAK.

88 Slc7a5 knockdown also decreased mTOR pathway activity.

89 nt, in vitro WB analysis indicated decreased mTOR signalling and enhanced NET-1 expression in both ce

90 ematopoietic aging, we conditionally deleted mTOR in ECs (mTOR(ECKO)) of young mice and observed that

91 dence to support the hypothesis of disrupted mTOR signaling in SZ, and we have addressed this by char

92 eutralizing antibody partially downregulated mTOR pathway activation but showed no effect on viabilit

93 aging, we conditionally deleted mTOR in ECs (mTOR(ECKO)) of young mice and observed that their HSPCs

94 ve oxygen species (ROS) levels are elevated, mTOR and IRF/IFN-beta signaling pathways are enhanced, l

95 tumor activity, advocating particularly for mTOR inhibitor use in this subgroup of patients.

96 We further show a critical role for mTOR in expression and localization of myelin basic prot

97 study evaluated IS withdrawal directly from mTOR-I therapy in LTRs and achieved > 50% operational to

98 Transcriptional profiling of HSPCs from mTOR(ECKO) mice revealed that their transcriptome resemb

99 e demonstrate that Slc7a5 is required for GC mTOR pathway activity, maturation and survival, which ma

100 r-S6 ribosomal protein (pS6RP) revealed high mTOR activity in PECs of the FSGS lesions of these mice.

101 However, the mechanisms behind how mTOR is involved in striatal physiology and its relative

102 We identified mTOR to be redundant for sustaining T-bet expression in

103 These results identify mTOR signaling as an important regulator of striatal fun

104 rdioprotection and a concomitant decrease in mTOR activity.

105 we demonstrate aging leads to a decrease in mTOR signaling within BMECs that potentially underlies t

106 Mutations in mTOR pathway genes are linked to a variety of neurodevel

107 n Ag-expCD4(+) T cells but that reduction in mTOR activity may not directly underpin Ag-expTh1 cell l

108 mutated or altered in metastases, including mTOR, CDK/RB, cAMP/PKA, WNT, HKMT, and focal adhesion.

109 containing the S47 variant display increased mTOR activity and oxidative metabolism, as well as large

110 ted 3 anti-IL-6 nonresponders with increased mTOR activation who responded to mTOR inhibition with si

111 ccumulation, which correlated with increased mTOR activation.

112 re, we show that GBM-initiating cells induce mTOR signalling in the microglia but not bone marrow-der

113 We observed that cisplatin induced mTOR and S6K1 phosphorylation, increased the number and

114 , supporting a damaging role for IOP-induced mTOR activation in perturbing metabolism and promoting g

115 tion upregulates LAT1 expression and induces mTOR activation in IL-17(+) gammadelta and T(H)17 cells.

116 Inhibiting mTOR activity with rapamycin rescued the generation of F

117 or anti-angiogenic agents, EGFR inhibitors, mTOR inhibitors, CTLA-4 inhibitors, or PD-1/PD-L1 inhibi

118 Alum inhibits mTOR activation and alters metabolic reprogramming by sh

119 AMPK inhibits mTOR, and the mTOR inhibitor rapamycin also decreases Na

120 Interestingly, mTOR inhibition induced a new pattern of cyclin C promot

121 We further investigated mTOR complex-specific subunit composition and phosphoryl

122 was phenocopied by inhibition of the kinase mTOR, by induction of ER stress, or by glucose deprivati

123 mport of amino acids is required to maintain mTOR activity.

124 tes, which plays a central role in mediating mTOR inactivation and inhibition of glycolysis.

125 More importantly, microglial mTOR-deficient mice displayed increased neuronal loss an

126 We found that activation of microglial mTOR is antiepileptogenic.

127 To determine the role of microglial mTOR signaling in excitatory injury and epileptogenesis,

128 These findings suggest that microglial mTOR plays a protective role in mitigating neuronal loss

129 erhaps because inhibition of hepatic mTORC2 (mTOR Complex 2) specifically reduces the lifespan of mal

130 The new mTOR inhibitor 7 showed good brain exposure and signific

131 ctor, the rapamycin-insensitive complex-2 of mTOR (mTORC2), and genes involved in axon growth, wherea

132 Abrogation of mTOR or AKT activation rescued the biological consequenc

133 In the near absence of mTOR, CDK1 activates eIF4E-dependent translation in MPs

134 IRGM and GABARAPs countered the action of mTOR as a negative regulator of TFEB.

135 Aberrant activation of mTOR expression and signaling in c-Cbl-deficient MPs res

136 triggered by Pten loss via the activation of mTOR signaling.

137 ompensated hypertrophy through activation of mTOR while Gfat1 deficiency shows cardioprotection and a

138 art failure through persistent activation of mTOR.

139 constitutively active RagB, an activator of mTOR.

140 and promoting kidney cysts in conditions of mTOR hyperactivity.

141 better understanding of the contribution of mTOR to T-cell fate decisions will ultimately aid in the

142 least in part, to proteasomal degradation of mTOR by the E3 ubiquitin ligase c-Cbl.

143 Further, the degree of mTOR activation in iMCD was comparable to autoimmune lym

144 generated mice with restrictive deletion of mTOR in microglia.

145 Disruption of mTOR signaling can result in neurological abnormalities.

146 nd simultaneously caused the dissociation of mTOR from the surface of lysosomes leading to decreased

147 Median duration of mTOR inhibition at last examination was 106 months (rang

148 nificant association between the duration of mTOR inhibitor therapy and psoas muscle area on multiple

149 physiological homeostasis, dysregulation of mTOR signalling has been implicated in metabolic disorde

150 However, the effect of mTOR inhibitors in preclinical models of acquired epilep

151 This may explain why the net effect of mTOR inhibitors is paradoxical in the acquired models of

152 autophagy (by 3-MA) reversed the effects of mTOR inhibition, leading to increased levels of ZIKV pro

153 igation of the cell type-specific effects of mTOR signaling in the CNS.

154 TSC2 deficiency leads to hyperactivation of mTOR Complex 1 (mTORC1), a master regulator of cell grow

155 The impact of mTOR inhibitors and/or cisplatin on MEC stemness was exa

156 cent studies demonstrating the importance of mTOR signaling in lung fibrosis.

157 mming depends on Akt kinases, independent of mTOR complex 1 and is efficiently inhibited by 2-deoxy-d

158 Independent of mTOR signaling, rapalogs induce cytoxicity by dysregulat

159 VEGFA that is mechanistically independent of mTOR, but requires an autophagic regulator, paternally e

160 tes, is dependent on CDK1 but independent of mTOR.

161 IB3 was mediated by LRRFIP1 independently of mTOR and disrupted its interaction with the spliceosome,

162 gate the effect of therapeutic inhibition of mTOR (mechanistic target of rapamycin) on resistance of

163 Inhibition of mTOR (mechanistic Target Of Rapamycin) signaling by rapa

164 s demonstrate that therapeutic inhibition of mTOR ablates cytotoxic-resistant CSCs, and they suggest

165 iNKT cells in Cd1d-/- mice or inhibition of mTOR by rapamycin reduced immunosuppression and suscepti

166 e whether endothelial-specific inhibition of mTOR can influence hematopoietic aging, we conditionally

167 cantly correlated with greater inhibition of mTOR gene pathway transcriptional activity.

168 Inhibition of mTOR kinase by Torin1 or rapamycin results in reduction

169 Loss or inhibition of mTOR reduced expression of profilin2 and ARPC3, actin po

170 Rapamycin-induced inhibition of mTOR robustly prevented glaucomatous neurodegeneration,

171 gs reveal that pharmacological inhibition of mTOR using Rapamycin has deleterious effects on hematopo

172 We further demonstrate that inhibition of mTOR was sufficient to promote Mefv expression and pyrin

173 Importantly, inhibition of mTOR, or Rheb, rescues HSC defects in Sel1L knockout mic

174 D translation is unaffected by inhibition of mTOR, unless RHA was down-regulated by siRNA.

175 nt cells are refractory to the inhibition of mTOR-dependent signaling by Torin1.

176 rotein kinase (AMPK)-dependent inhibition of mTOR; this in turn reduces the sensitivity of NSCLC cell

177 lation and reduced lysosomal localization of mTOR, resulting in impaired activation of mTORC1, a cent

178 In neuronal cell-based models of mTOR hyperactivity, 7 corrected the mTOR pathway activit

179 and nintedanib blocked the overactivation of mTOR and VEGFR2, respectively.

180 his new insight into the pharmacodynamics of mTOR inhibitors in regulation of neuronal autophagy may

181 s the culture of NK cells in the presence of mTOR inhibitors, such as rapamycin or torin1, had minima

182 study reveals a novel layer of regulation of mTOR by p53, and raises the possibility that this varian

183 is a critical and non-redundant regulator of mTOR activity in brain.

184 responses 1 (REDD1), a negative regulator of mTOR/protein kinase B, is poorly understood.

185 omplicated pregnancies) indicating a role of mTOR in regulating placental transport of these amino ac

186 provide an updated overview of the roles of mTOR in T-cell development, homeostasis, activation, and

187 Moreover, we summarize the emerging roles of mTOR in T-cell exhaustion and transdifferentiation.

188 These results reveal critical roles of mTOR signaling and autophagy in ZIKV infection and point

189 timately aid in the therapeutic targeting of mTOR in human disease.

190 We propose a clinical trial of mTOR inhibitors as a means to shrink large ganglioneurom

191 Our findings could better guide the use of mTOR inhibitors in preventing acquired epilepsy.

192 g, has demonstrated the therapeutic value of mTOR inhibitors for central nervous system (CNS) indicat

193 endent of the effect of IL-15 or TGF-beta on mTOR, as the culture of NK cells in the presence of mTOR

194 reports on the effects of iron chelation on mTOR complexes are inconsistent or controversial.

195 o test therapeutic hypotheses that depend on mTOR hyperactivity in the CNS.

196 rs, including IL-1beta, and was dependent on mTOR and hypoxia-inducible factor (HIF)1alpha.

197 r, rescued the effect of Slc7a5 knockdown on mTOR pathway activity and dendrite arbors.

198 T cells rely on mTOR activity for their development and to establish the

199 a RANKL inhibitor, antiangiogenic agents, or mTOR inhibitors.

200 rapamycin (mTOR) protein kinase deletion or mTOR inhibition.

201 LAMTOR1 silencing or mTOR inhibition restores autophagy and induces apoptosis

202 ing ribophagy induced by oxidative stress or mTOR inhibition to show that 28S and 18S rRNAs undergo a

203 d elevation in the expression levels of p21, mTOR/pS6, interleukin 6, and tumor necrosis factor alpha

204 As an integrator of molecular pathways, mTOR (mammalian target of rapamycin) has been associated

205 canonical RAF/MAPK/ERK/RSK and PI3K/AKT/PDK/mTOR/S6K pathways are identified.

206 PI3K/mTOR pathway inhibitors (PI3K/mTORi) showed supra-additi

207 PIM and PI3K/mTOR pathways are often dysregulated in prostate cancer,

208 Dual inhibition of CHK1 and PI3K/mTOR pathways yields potent synthetic lethality by causi

209 nctions supporting proper RhoGTPase and PI3K/mTOR signaling.

210 defects as compared to normal controls, PI3K/mTOR hyperactivation interfered with primary cilia assem

211 ned the effect of several inhibitors of PI3k/mTOR signaling (e.g., temsirolimus, BKM120, AZD8055, PF4

212 investigated the novel multikinase PIM/PI3K/mTOR inhibitor, AUM302, versus a combination of the PIM

213 rvival, and tumor growth by suppressing PI3K/mTOR/Akt activities in mouse models generated from MCC c

214 of the PIM inhibitor, AZD-1208, and the PI3K/mTOR inhibitor BEZ235 (Dactolisib) to determine their im

215 mphocyte count one year before Pneumocystis, mTOR inhibitors used as maintenance immunosuppressive dr

216 ith increased mammalian target of rapamycin (mTOR) activity and also with decreased production of tum

217 eg have low mechanistic target of rapamycin (mTOR) activity and would be less dependent on this kinas

218 cesses, and mechanistic target of rapamycin (mTOR) and cytokine pathways are up-regulated in high-tit

219 ays involving mammalian target of rapamycin (mTOR) and lysophosphatidylcholine acyltransferase (LPCAT

220 endent on the mammalian target of rapamycin (mTOR) for proliferation and the lipid peroxidase GPX4 fo

221 The mammalian target of rapamycin (mTOR) functions as two complexes (mTORC1 and mTORC2), re

222 tophagy and mechanistic target of rapamycin (mTOR) in alcohol-induced adipose and liver pathogenesis,

223 ore and after mammalian target of rapamycin (mTOR) inhibition.

224 owth, whereas mammalian target of rapamycin (mTOR) inhibitors like sirolimus have anticancer effects.

225 mechanistic (mammalian) target of rapamycin (mTOR) kinase is important for cell survival and prolifer

226 trol of the mechanistic target of rapamycin (mTOR) pathway and independent of alterations in MAPK and

227 The mechanistic target of rapamycin (mTOR) pathway is hyperactivated in cancer and neurologic

228 STATEMENT The mammalian target of rapamycin (mTOR) pathway is strongly implicated in epilepsy.

229 ar to that of mammalian target of rapamycin (mTOR) protein kinase deletion or mTOR inhibition.

230 ctivating the mammalian target of rapamycin (mTOR) signaling and blocking ER stress.

231 d propose the mammalian target of rapamycin (mTOR) signaling pathway as a candidate mechanism.

232 The mammalian Target of Rapamycin (mTOR) signaling pathway is active in human oRG cells.

233 y mediated by mammalian target of rapamycin (mTOR) signaling that directly contributes to enhanced NK

234 eractivated mechanistic target of rapamycin (mTOR) signaling, has demonstrated the therapeutic value

235 deletion of mechanistic target of rapamycin (mTOR) to demonstrate that mTOR regulates expression of s

236 intersect at mammalian target of rapamycin (mTOR), a critical node for cell proliferation and surviv

237 kinase (AMPK)-mammalian target of rapamycin (mTOR)-S6 kinase-dependent manner in LXA4-treated KSHV-in

238 The mechanistic target of rapamycin (mTOR)-signaling pathway plays a key role in nutrient sen

239 ecruitment of mammalian target of rapamycin (mTOR).

240 R-alpha), and mammalian target of rapamycin (mTOR).

241 cardiomyocyte growth accompanied by reduced mTOR (mammalian target of rapamycin) activity and malada

242 We observed reduced mTOR signalling and proliferation in human parietal epit

243 irectly affects myocyte growth by regulating mTOR activation.

244 2-associated kinase (ACK) in down-regulating mTOR expression and promoting neuronal differentiation.

245 K38A or S637A mutant phenocopies or rescues mTOR activation and senescence in PGAM5(-/-) cells, resp

246 R signaling occurs frequently in cancers, so mTOR has become an attractive target for cancer therapy.

247 cific Atg5 knockout (KO), adipocyte-specific mTOR KO, adipocyte-specific Raptor KO, and adipocyte-spe

248 ed steatosis, but neither adipocyte-specific mTOR nor adipocyte-specific tuberous sclerosis complex 1

249 ng may be useful as predictors of successful mTOR-I therapy withdrawal.

250 These findings support mTOR activation as a novel therapeutic target for iMCD,

251 p53-4KR retained the ability to suppress mTOR function but this activity was abolished in p53-5KR

252 exhibited significantly higher and sustained mTOR activity than effector T-bet- (non-Th1) Ag-expT cel

253 ive study, patients with TSC who were taking mTOR inhibitors and who underwent at least two abdominal

254 Inhibition of the downstream AKT target, mTOR, in zebrafish with ganglioneuroma effectively reduc

255 It is commonly believed that mTOR inhibitors (mTORi) should not be used in high-immun

256 rget of rapamycin (mTOR) to demonstrate that mTOR regulates expression of specific cytoskeletal targe

257 Here, we present evidence that mTOR promotes the initiation of myelination through regu

258 In the present study, we found that mTOR is strongly activated in microglia following excita

259 Mechanistically, we show that mTOR and its positive regulator Rheb display increased a

260 We show that mTOR expression by Treg is critical for their differenti

261 Thus, our work shows that mTOR is crucial for Treg differentiation, migration, and

262 Collectively, our data suggest that mTOR activity is linked to T-bet in Ag-expCD4(+) T cells

263 The mTOR activity is robustly enhanced in mutant outer radia

264 The mTOR pathway integrates a diverse set of environmental c

265 The mTOR pathway, an important regulator of cell survival/pr

266 The mTOR signaling cascade is tightly regulated and central

267 AMPK inhibits mTOR, and the mTOR inhibitor rapamycin also decreases NaCT expression.

268 een molecules involved in cell death and the mTOR pathway to regulate the pyrin inflammasome, which c

269 ion, highlighting the cross-talk between the mTOR pathway and regulation of the pyrin inflammasome.

270 me biogenesis machinery and regulated by the mTOR pathway.

271 Out of these compounds, the mTOR inhibitor AZD2014, was the most potent against chor

272 odels of mTOR hyperactivity, 7 corrected the mTOR pathway activity and the resulting neuronal overgro

273 tigation of the morpholine ring engaging the mTOR solvent exposed region led to the discovery of PQR6

274 , from a small-molecule screen, identify the mTOR inhibitors OSI-027, AZD2014 and AZD8055.

275 n1 (0 to 200 nmol/L) was used to inhibit the mTOR pathway at various time points.

276 This remodeling involves activation of the mTOR (mammalian target of rapamycin) signaling pathway,

277 (Ser235/236), a marker for activation of the mTOR and ERK signaling pathways.

278 ice was suppressed upon the treatment of the mTOR inhibitor.

279 These cells had increased activation of the mTOR pathway, as assessed by phosphorylated ribosomal pr

280 eatment with everolimus, an inhibitor of the mTOR pathway, reduces the number of large lysosomes, dec

281 ral studies have shown the importance of the mTOR signaling pathway in chordoma and suggest it as a p

282 ypothesized that transient inhibition of the mTOR-signaling pathway could lead cardiomyocytes to a qu

283 Rictor, the unique subunit of mTORC2, or the mTOR kinase itself also inhibits the viral processes, th

284 acids including leucine, which regulates the mTOR signaling pathway.

285 Co-targeting the mTOR and EPH receptor pathways with these or similar com

286 of mRNAs that link their translation to the mTOR Complex 1 (mTORC1) nutrient-sensing signaling pathw

287 In this study we questioned whether the mTOR inhibitor rapamycin (sirolimus) could attenuate the

288 ated monogenic disorders associated with the mTOR signaling pathway.

289 Even though mTOR/protein kinase B signaling is important for adipoge

290 at mediates translational repression through mTOR-dependent signaling and that ALS-linked FUS mutants

291 Thus, mTOR signaling can regulate the architecture of the deve

292 h increased mTOR activation who responded to mTOR inhibition with sirolimus.

293 genes that impact cell growth in response to mTOR pathway inhibition.

294 es and that this association is sensitive to mTOR (mammalian target of rapamycin) kinase activity.

295 Rac1 in mediating a PI3K-independent MET-to-mTOR pathway and suggest alternative or combined strateg

296 ilar clinical outcomes may be obtained using mTOR inhibitors compared to mycophenolate.

297 to and control the transcription of various mTOR and metabolism-related genes within effector CD4(+)

298 roblast growth factor 19 (FGF19), acting via mTOR/ERK signaling and TFEB phosphorylation, feedback in

299 cells triggers pro-inflammatory stimuli via mTOR activation.

300 t expression in activated Th1 cells, whereas mTOR was necessary but not sufficient for maintaining IF