ライフサイエンスコーパス: mTOR

1 mTOR and the lysosomal protein LAMP2 were highly co-loca

2 mTOR complex 1 (mTORC1) regulates cell growth and metabo

3 mTOR complex I (mTORC1) is a central growth regulator th

4 mTOR exists in two complexes: mTORC1, which stimulates p

5 mTOR folate sensing may have broad biological significan

6 mTOR has been almost exclusively examined in adult roden

7 mTOR has important roles in regulation of both innate an

8 mTOR kinase acts in two functionally distinct complexes,

9 mTOR primarily functions as a catalytic subunit in two s

10 paLink-1 associated with FKBP12, an abundant mTOR-interacting protein, enabling accumulation of RapaL

11 providing critical amino acids that activate mTOR and enable the metabolic transition of activated T

12 accumulation of BCAAs and FAs that activate mTOR signaling and stimulate apoptosis, respectively.

13 te 40 kDa (PRAS 40), which in turn activated mTOR.

14 Here, we demonstrate that TBK1 activates mTOR complex 1 (mTORC1) directly.

15 In addition, mTOR co-localised with Eukaryotic translation initiation

16 ed in CNI-treated patients but recover after mTOR-i conversion, reducing SCC relapses.

17 One-year after mTOR-i conversion, a significant increase in FOXP3 + Tre

18 AKT-mTOR-mediated attenuation of IRE1 activity is important

19 mparative analysis revealed an activated AKT-mTOR pathway in tumors.

20 ith EGFR signaling, including downstream AKT-mTOR pathways, MAPK pathway, as well as redox enzymes we

21 osphorylation of Akt and mTOR, impairing Akt-mTOR signaling and this may result in an increased risk

22 utinib and reciprocal activation of PI3K-AKT-mTOR and integrin-beta1 signalling.

23 n of B-cell receptor signalling and PI3K-AKT-mTOR axis leads to release of MCL cells from TME, revers

24 we show that although inhibition of PI3K-AKT-mTOR signaling markedly decreased glycolysis and restrai

25 e B-mechanistic Target of Rapamycin (PKB/AKT-mTOR) signaling controls the dynamics of IRE1 deactivati

26 We suggest that AKT-mTOR activity is part of a 'timing mechanism' to deactiv

27 by resveratrol via its inhibition of the Akt-mTOR pathway.

28 Grade Index, immune, proliferation, and AKT/mTOR GSs.

29 lts from low TCR signal strength and low Akt/mTOR signaling.

30 in miRNAs involved in the regulation of AKT/mTOR or in those involved in epithelial to mesenchymal t

31 hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer.

32 K pathway, which converges with the PI3K/Akt/mTOR (mechanistic target of rapamycin) pathway at the le

33 were associated with suppression of PI3K/Akt/mTOR activation and STAT3 phosphorylation upon CX-4945 t

34 y signaling pathways, including the PI3K/Akt/mTOR and MAPK pathways, and with other receptors, includ

35 ally, IL-15 robustly stimulated the PI3K/Akt/mTOR and MEK/ERK pathways in CD56bright compared with CD

36 binding promoted activation of the PI3K/Akt/mTOR axis and FoxO1 nuclear exclusion in DCs, leading to

37 Molecular alterations involving the PI3K/AKT/mTOR pathway (including mutation, copy number, protein,

38 n through a mechanism involving the PI3K/AKT/mTOR pathway and matrix metalloproteinase-9.

39 Myrf, as well as converges with the PI3K/Akt/mTOR pathway at the level of mTORC1, working together to

40 but only an inhibitor targeting the PI3K/Akt/mTOR pathway blocked proliferation induced by IL-15 as w

41 The PI3K/Akt/mTOR pathway mediates signals from multiple receptors in

42 Activation of the PI3K/AKT/mTOR pathway occurs frequently in breast cancer that is

43 that occur in genes regulating the PI3K/Akt/mTOR pathway-a key pathway in neuronal growth and migrat

44 lating PIK3IP1, a suppressor of the PI3K/Akt/mTOR pathway.

45 ion between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a RasPIK3IP1PI3K signaling network.

46 growth in part by inhibiting prosurvival AKT/mTOR pathways and stimulating proapoptotic survivin and

47 gressive model of ADPKD, decreased renal Akt/mTOR activity, cell proliferation, cyst growth, and inte

48 LPA-stimulated Akt/mTOR signaling is critical for LPA-mediated macrophage d

49 The Akt/mTOR pathway is a key driver of murine CD4(+) T cell dif

50 MARCKS acted upstream of the AKT/mTOR pathway, activating HIF-target genes, notably vascu

51 bellar granule cells and activating the AKT1-mTOR pathway, we increased the caliber of normally unmye

52 Allosteric mTOR inhibitors, such as rapamycin, incompletely block m

53 is was associated with significantly altered mTOR, but not Akt or HIF-1alpha, activation and only min

54 ructural plasticity by recruitment of AMPAR, mTOR and BDNF signaling in both mouse mesencephalic and

55 yl-CoA/tryptophan degradations and EIF2/AMPK/mTOR signaling.

56 We describe an mTOR-driven mouse model that displays hepatosteatosis pr

57 nefit to be gained by early conversion to an mTOR inhibitor-based maintenance regime.

58 clear co-localization between CSNK-2beta and mTOR.

59 ial interactions of IGFBP-1, CSNK-2beta, and mTOR as a prerequisite for protein-protein interaction.

60 ld interfere with phosphorylation of Akt and mTOR, impairing Akt-mTOR signaling and this may result i

61 induced resistance to combinations of AR and mTOR inhibitors by inducing cap-independent translation.

62 emonstrate that while combinations of AR and mTOR inhibitors were effective in suppressing tumor grow

63 s characterized by activation of T cells and mTOR signaling, whereas advanced PVR is characterized by

64 In this context, B cell-specific genes and mTOR signaling were associated with an effective vaccina

65 ng multiple pathways including hedgehog, and mTOR pathways and angiogenesis.

66 MALAT1, suggesting that SRSF1 induction and mTOR activation are essential for MALAT1-induced transfo

67 mutants for pkd1 and noted cystic kidney and mTOR activation in pkd1a mutants, suggesting a conserved

68 Three AD subtypes showed high p38 and mTOR pathway activation.

69 ate JNK and beta-catenin phosphorylation and mTOR pathway activation, and inhibit apoptosis, thereby

70 ic islets, fasting conditions reduce PKA and mTOR activity and induce Sox2 and Ngn3 expression and in

71 eractions were in the perinuclear region and mTOR and CSNK-2beta interactions were also predominantly

72 p-PLCr1/2), hedgehog (Gli1, Ptch1, SMO), and mTOR (pS6K1) signaling pathways to determine the mechani

73 d relapsed on or after endocrine therapy and mTOR inhibitors, were recruited from 200 trial centres i

74 inhibiting both AR-induced transcription and mTOR-induced cap-dependent translation, pre-treatment wi

75 ferred with donor-specific MHC I antibodies, mTOR inhibition significantly reduced vascular injury, E

76 ng from the universal biomarkers, as well as mTOR signaling from the male bipolar biomarkers.

77 cterized by exploitable dependencies on BCR, mTOR, or MEK signaling and associated with mutations, ge

78 Because mTOR signaling is required for initiation of messenger R

79 e sensing by mTOR in PHT cells involves both mTOR Complex 1 and 2 and requires the proton-coupled fol

80 e sensing by mTOR in PHT cells involves both mTOR Complex 1 and 2 and requires the proton-coupled fol

81 inuclear rather than nuclear as indicated by mTOR and CSNK-2beta co-localization.

82 inhibited upon its serine phosphorylation by mTOR The overall mechanisms by which TFEB activity in th

83 Folate sensing by mTOR in PHT cells involves both mTOR Complex 1 and 2 and

84 Folate sensing by mTOR in PHT cells involves both mTOR Complex 1 and 2 and

85 id not change the phosphorylation of ULK1 by mTOR and AMPK.

86 Thus, in response to cellular mTOR activity, LARP1 serves as a phosphorylation-sensiti

87 acts in two functionally distinct complexes, mTOR complex 1 (mTORC1) and 2 (mTORC2), whose activities

88 y distinct multi-component kinase complexes, mTOR complex 1 (mTORC1) and mTORC2.

89 inding domain of TACI, or B-cell-conditional mTOR deficiency interrupts TACI signaling via NF-kappaB

90 Finally, we found that constitutive mTOR activation lowered a behavioral measure of the juve

91 ng either one or two copies of a kinase-dead mTOR mutant (KD-mTOR) transgene exclusively in beta-cell

92 llular signal-regulated kinase 1/2-dependent mTOR inhibition, thereby promoting pSTAT1 nuclear transl

93 tein synthesis to autophagy, and deregulated mTOR signaling is implicated in the progression of cance

94 of PI3K or AKT minimally affects downstream mTOR activity in glioma.

95 phages and those isolated from genome edited mTOR S2159A knock-in mice, we show that mTOR S2159 phosp

96 ssociated signaling pathways, including ERK, mTOR, and Akt signaling, via PTPN13-mediated phosphoryla

97 Our study re-establishes mTOR as a central target in glioma and traces the failur

98 growth that avoid the resistance to existing mTOR inhibitors resulting from cancer-associated MTOR mu

99 o decades has established a central role for mTOR in regulating many fundamental cell processes, from

100 We identified two genes (mTOR, PIK3R1) and several variants previously described

101 On one hand, mTOR inhibition blunts the induction of cyclin-dependent

102 uscle and melanocyte-lineage markers, harbor mTOR-activating mutations in tuberous sclerosis complex

103 Inhibition of hepatic mTOR in Am mice increased hepatic lipid deposition and H

104 Activation of hepatic mTOR in AT mice decreased lipid accumulation attenuated

105 substantial fraction of cancers showed high mTOR pathway activity without an associated canonical ge

106 e and adaptive immunity, but whether and how mTOR modulates humoral immune responses have yet to be f

107 immune activation and the immunosuppressive mTOR inhibitor rapamycin.

108 uced levels of which have been implicated in mTOR-independent autophagy, and we found that IMPase act

109 The involvement of PCFT in mTOR folate sensing is not dependent on its function as

110 as little as a two- to fourfold reduction in mTOR activity preserves ovarian function and normal birt

111 ressor AMPKalpha1/2-LKB1, and a reduction in mTOR signaling.

112 Taken together, these studies indicate mTOR inhibition suppresses ERM phosphorylation in endoth

113 Inhibition of PLCgamma/PKC-induced mTOR activation impairs IL-7-mediated B cell development

114 es a protein whose main action is to inhibit mTOR under stress conditions whilst several in vitro stu

115 Notably, Leishmania actively inhibited mTOR-regulated autophagy even at later stages of infecti

116 Here, we investigated mTOR in juvenile zebra finch songbirds.

117 ing mGluR-LTD, through a mechanism involving mTOR and ribosomal protein S6 activation.

118 two copies of a kinase-dead mTOR mutant (KD-mTOR) transgene exclusively in beta-cells.

119 high-fat diet, mice carrying one copy of KD-mTOR mutant transgene developed glucose intolerance and

120 Islets from RIPCre;KD-mTOR (Homozygous) mice showed reduced mTORC1 and mTORC2

121 with two copies of the transgene [RIPCre;KD-mTOR (Homozygous)] develop glucose intolerance due to a

122 It contains the atypical kinase mTOR and the RAPTOR subunit that binds to the Tor signal

123 enic stimulation and signals from the kinase mTOR.

124 elation between phosphorylated P70S6 kinase (mTOR downstream target), VEGF and SK1 protein expression

125 ellular senescence, activation of PI3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfun

126 dentify combinatorial inhibition of the MAPK/mTOR pathway as a potential therapeutic strategy for CRA

127 modification(s) in response to combined MEK/mTOR inhibition in PTEN-loss contexts and identified JAK

128 f two distinct complexes, mTORC1 and mTORC2, mTOR is the major regulator of growth (mass accumulation

129 Nevertheless, mTOR inhibition promotes growth of cells reliant on eati

130 Our findings highlight a novel mTOR-dependent regulatory network for nutrient transport

131 osomal outer surface, enabling activation of mTOR by the Ras homolog Rheb.

132 he magnitude of the EC-induced activation of mTOR signaling was significantly blunted in muscles from

133 equired for an insulin-induced activation of mTOR signaling.

134 early B lymphopoiesis through activation of mTOR via PLCgamma/DAG/PKC signaling, not via Akt/Rheb si

135 inhibition blocks IL-7-induced activation of mTOR, but not Stat5.

136 iched in brain (Rheb), a direct activator of mTOR, and its inhibitor, the GTPase-activating protein t

137 d that miR-124-3p suppressed the activity of mTOR signaling mainly through inhibiting the expression

138 eting PDE4B, thus inhibiting the activity of mTOR signaling.

139 n was exerted by suppressing the activity of mTOR signaling.

140 lume is exerted through a large community of mTOR-related genes.

141 expression of RICTOR, a pivotal component of mTOR complex 2 (mTORC2), to further enhance AKT activity

142 We find that targeted deletion of mTOR in the VTA had no significant effects on soma size

143 Deregulation of mTOR complex 1 (mTORC1) signalling increases the risk fo

144 MIA-induced transcriptional dysregulation of mTOR and EIF4E-dependent signaling.

145 Dysregulation of mTOR signalling is associated with a variety of human di

146 and reduces the anti-proliferative effect of mTOR kinase inhibitors.

147 ibition as a strategy to improve efficacy of mTOR inhibitors in the clinic.

148 Direct evidence of mTOR activation by ketamine was revealed by its inductio

149 discovered that these distinct functions of mTOR are mediated by separate downstream branches of the

150 and that under such conditions the impact of mTOR signaling on protein scavenging rate is minimal.

151 The induction of mTOR by oleic acid was dependent upon the enzymes respon

152 ass effect associated with the inhibition of mTOR and is associated with everolimus therapy for breas

153 s the reactivation of AKT post-inhibition of mTOR in PDAC cells.

154 y reduces tumor growth through inhibition of mTOR pathway.

155 Pharmacological inhibition of mTOR resulted in a proportional decrease in NK cell reac

156 Pharmacological inhibition of mTOR signaling resulted in phosphorylation of H2AX conco

157 deficiency in PHT cells caused inhibition of mTOR signalling and decreased the activity of key amino

158 Inhibition of mTOR strongly reduced the lysosomal efflux of most essen

159 ffects of rapamycin, a specific inhibitor of mTOR, on B cell and CD4 T cell responses during acute in

160 efficacy of endocrine therapy; inhibitors of mTOR and inhibitors of the cyclin-dependent kinases CDK4

161 Rheb and increased in the co-localisation of mTOR and Rheb post exercise in both FED and CON.

162 lopment and remodeling through modulation of mTOR signaling.

163 Moreover, while numbers of mTOR-deficient lung CD11b(+) DCs were not changed, they

164 establish autophagy, a downstream pathway of mTOR, as a new therapeutic target for PKD.

165 nomic pathway and involves the regulation of mTOR signaling since inhibition of this pathway restored

166 rous sclerosis complex (TSC), a regulator of mTOR activity.

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

168 To understand the functional relevance of mTOR enzymatic activity in beta-cell development and glu

169 included elucidation of the pivotal roles of mTOR signaling in the regulation of cellular metabolism

170 al, prompting further mechanistic studies of mTOR-based therapy.

171 ata demonstrate that cellular trafficking of mTOR occurs in human muscle in response to an anabolic s

172 exercise resulted in rapid translocation of mTOR/LAMP2 towards the cell membrane.

173 view recent advances in our understanding of mTOR function, regulation, and importance in mammalian p

174 tential, thus enhancing our understanding of mTOR targeting failure.

175 mpact of exogenously supplied fatty acids on mTOR in KRas-driven cancer cells, which are programmed t

176 Similarly, on mTOR blockade, hMSCs also enhanced their immunoregulator

177 and tumor immunity, and provide an update on mTOR inhibitors.

178 within the growth-hormone, insulin/IGF-1 or mTOR signalling pathways.

179 Chemical inhibition of AKT or mTOR rescued MaSCs from Cbl/Cbl-b DKO-induced depletion.

180 Inhibition of SRSF1 expression or mTOR activity abolishes the oncogenic properties of MALA

181 estored only by reducing eIF4E expression or mTOR activity and also blocking MNK1 phosphorylation of

182 ion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re) Mtor(fl/fl) ) did not affect acute all

183 ant patients with SCC on CNI (KT-CNI-SCC) or mTOR-i (KT-mTORi-SCC), 25 nontransplants developing SCC

184 tern blot analysis of pathway checkpoints, p-mTOR (p=0.03) and PI3K-alpha (P = 0.04) were downregulat

185 A significant downregulation of p-mTOR, p-Raptor, and p-S6RP was observed, which was resto

186 role of immunometabolism and, in particular, mTOR alterations in the pathophysiology of sepsis-induce

187 on of mammalian target of rapamycin (phospho-mTOR).

188 levels of homocysteine had no effect on PHT mTOR signalling, suggesting that mTOR senses low folate

189 adhesion kinase activation upstream of PI3K-mTOR, and induces transcriptional changes that include u

190 omotes glioma proliferation through the PI3K-mTOR pathway.

191 study is to determine the efficacy of a PI3K/mTOR dual inhibitor, LY3023414, on established EAC in an

192 ome 9q loss, resulting in increased AKT/PI3K/mTOR signaling.

193 CRAF fusions activate both the MAPK and PI3K/mTOR signaling pathways, we identify combinatorial inhib

194 Treatment with dual PI3K/mTOR inhibitor gedatolisib resulted in near eradication

195 ing Kit(V558Delta/+) mice with the dual PI3K/mTOR inhibitor voxtalisib, the pan-PI3K inhibitor pilara

196 Overall, PI3K/mTOR inhibition potently decreased ALL burden in vivo; a

197 3-kinase/mammalian target of rapamycin (PI3K/mTOR) signaling are being investigated in multiple clini

198 3 kinase/mammalian target of rapamycin (PI3K/mTOR) signaling pathways.

199 onitor drug-induced perturbation of the PI3K/mTOR pathway in sarcomas.

200 s with related functions, including the PI3K/mTOR pathway, altered in 60% of lines; BRCA DNA repair,

201 anges that occur with inhibition of the PI3K/mTOR pathway.

202 utically to target tumours resistant to PI3K/mTOR inhibition.

203 tion or growth factor starvation, where PI3K/mTOR signalling is decreased, matrix-attached human mamm

204 co-loading of 17-AAG (Hsp90) and rapamycin (mTOR) (g-EAR).

205 rotein kinase mammalian target of rapamycin (mTOR) (or mechanistic target of rapamycin), leading to d

206 activation, mechanistic target of rapamycin (mTOR) activation, loss of glutamate and potassium buffer

207 egulated by mechanistic target of rapamycin (mTOR) and casein kinase (CSNK)-2.

208 naling by the mammalian target of rapamycin (mTOR) contributes to the devastating features of cancer

209 The mechanistic target of rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism

210 hibition of mechanistic target of rapamycin (mTOR) effectively slows cyst expansions in animal models

211 Mechanistic target of rapamycin (mTOR) enhances immunity in addition to orchestrating met

212 The mechanistic target of rapamycin (mTOR) has a key role in the integration of various physi

213 ay by which mechanistic target of rapamycin (mTOR) influences reprogramming.

214 d efficacy of mammalian target of rapamycin (mTOR) inhibition in combination with liposomal doxorubic

215 The mammalian target of rapamycin (mTOR) is a crucial signaling node that integrates enviro

216 and AKT to mechanistic target of rapamycin (mTOR) is prominently dysregulated in high-grade glial br

217 bition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine upta

218 the effect of mammalian target of rapamycin (mTOR) manipulation in MSCs was studied in vivo in a mous

219 1 (4ebp1), a mammalian target of rapamycin (mTOR) pathway component that inhibits protein translatio

220 or of the Akt/mammalian target of rapamycin (mTOR) pathway downstream of multiple TLRs.

221 he PI3K/Akt/mechanistic target of rapamycin (mTOR) pathway is also known to regulate myelin thickness

222 ase B (AKT)/mechanistic target of rapamycin (mTOR) pathway is one of the most commonly dysregulated s

223 ctivating the mammalian target of rapamycin (mTOR) pathway.

224 n-induced Akt/mammalian target of rapamycin (mTOR) signaling and ADPKD cell proliferation in vitro Ho

225 Mechanistic target of rapamycin (mTOR) signaling is necessary to generate a mechanically

226 cilitation of mammalian target of rapamycin (mTOR) signaling pathway and inhibition of glycogen synth

227 NF-kappaB and mammalian target of rapamycin (mTOR) signaling strongly increased.

228 Further, the mammalian target of rapamycin (mTOR) signaling was implicated as being involved in the

229 receptor and mammalian target of rapamycin (mTOR) signaling, respectively.

230 tion of the mechanistic target of rapamycin (mTOR) using rapamycin prevented the increase in cellular

231 e mammalian/mechanistic target of rapamycin (mTOR) with clinically available small-molecule inhibitor

232 of insulin, mechanistic target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), and autophag

233 ining S6K1 or mammalian target of rapamycin (mTOR), and appears to represent an incomplete preinitiat

234 f PI3K/Akt, mechanistic target of rapamycin (mTOR), and MEK/ERK pathways in the regulation of RPE pha

235 tein kinase mechanistic target of rapamycin (mTOR), existing in two complexes, mTORC1 and mTORC2.

236 gulation of mechanistic target of rapamycin (mTOR), proinflammatory, and anti-apoptotic signaling pat

237 6 (TRAF6) and mammalian target of rapamycin (mTOR), respectively.

238 ivating the mechanistic target of rapamycin (mTOR).

239 (PKB/Akt) and mammalian target of rapamycin (mTOR).

240 vity of the mechanistic target of rapamycin (mTOR).

241 kappaB) and mechanistic target of rapamycin (mTOR).

242 diated by the mammalian target of rapamycin (mTOR)/sphingosine-kinase-1 (SK1) pathway.

243 al function in controlling translation rate: mTOR inhibition slows translation, thereby matching prot

244 ynthesis, suppress ER stress, and reactivate mTOR signaling.

245 s) through which mechanical stimuli regulate mTOR signaling remain poorly defined.

246 ither the TSC1 or TSC2 genes, which regulate mTOR kinase activity.

247 with metabolically active L-cysteine rescued mTOR activation and proliferation but not autophagy.

248 pregulation occurred in acquired resistance, mTOR in innate resistance, and pleiotrophin in both sett

249 Moreover, AZD4547 downregulated RTK, mTOR, and Wnt/beta-catenin signaling pathways in premali

250 Potent active-site mTOR inhibitors engender mitochondrial hyperfusion due t

251 h and activates mTORC1 through site-specific mTOR phosphorylation (on S2159) in response to certain g

252 Taken together, these data suggest mTOR signaling-dependent, mitogenic conditioning of AECI

253 Disruption of TACI-mTOR interaction by rapamycin, truncation of the MyD88-b

254 Our findings demonstrate that targeting mTOR-dependent M2 cells is critical for preventing chron

255 These results demonstrate that mTOR acts as a molecular rheostat of NK cell reactivity

256 Together, these findings demonstrate that mTOR signals play an essential role in antigen-specific

257 Recent studies indicate that mTOR can, in parallel, regulate the activity of stress t

258 We propose that mTOR folate sensing in trophoblast cells matches placent

259 Here we show that mTOR coordinates immunometabolic reconfiguration of marg

260 ited mTOR S2159A knock-in mice, we show that mTOR S2159 phosphorylation promotes mTORC1 signaling, IR

261 fect on PHT mTOR signalling, suggesting that mTOR senses low folate rather than high homocysteine.

262 The mTOR inhibitor rapamycin has been shown to attenuate the

263 ly, while CpG-stimulated cells activated the mTOR pathway via TLR9 receptor to induced MMP-7, beta-gl

264 optotic splicing isoforms and activating the mTOR pathway by modulating the alternative splicing of S

265 Liposomal doxorubicin, bevacizumab, and the mTOR inhibitors temsirolimus or everolimus using 21-day

266 the translational efficiency as well as the mTOR pathway.

267 ated after the Gln checkpoint and before the mTOR-mediated cell cycle checkpoint.

268 However, the mTOR activation remained unchanged.

269 ost-treatment with rapamycin, indicating the mTOR pathway is involved in mediating seizure-induced as

270 ve signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric

271 lasts results in decreased expression of the mTOR inhibitor DDIT4 (REDD1).

272 s acting both upstream and downstream of the mTOR kinase itself.

273 tion of IL-1R, leads to up-regulation of the mTOR pathway and increased levels of the epigenetic regu

274 was linked to a paracrine activation of the mTOR pathway in lymphatic endothelial cells.

275 isms of resistance include activation of the mTOR, histone deacetylase (HDAC), MAPK, and ERBB4 pathwa

276 tion, and thereby promotes activation of the mTOR-HIF1alpha pathway.

277 We report the mTOR activator gene RHEB as an ID gene that is associate

278 Here, we demonstrated that the mTOR complex 1 (mTORC1) is essential for this sustained

279 These findings suggest that the mTOR-mediated signaling pathway is not essential to beta

280 Using the mTOR activator MHY1485 we confirmed that the inhibitory

281 These mTOR defects in turn resulted from defective autophagy i

282 eactivity of hyporesponsive NK cells through mTOR activation.

283 Thus, mTOR drives innate-like antibody responses by linking pr

284 RHEB binds to mTOR distally from the kinase active site, yet causes a

285 P1 expression and sensitizes cancer cells to mTOR kinase inhibitors by enhancing 4E-BP1-mediated tran

286 echanism by which PML loss may contribute to mTOR activation and cancer progression via dysregulation

287 at Leishmania uses an alternative pathway to mTOR to induce autophagy in host macrophages.

288 h the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus en

289 ustained through adaptation or resistance to mTOR inhibition remains unknown.

290 ivity could be responsible for resistance to mTOR inhibitors and is a potential candidate for the dev

291 nked to cancer progression and resistance to mTOR inhibitors, but the mechanism underlying 4E-BP1 dow

292 ming that supports metastasis in response to mTOR inhibition.

293 er activity, and rendered it unresponsive to mTOR inhibition.

294 ced MMP-7, beta-glucan-stimulated cells were mTOR-independent and used Dectin-1 receptor.

295 While mTOR is known to be involved in the DNA damage response,

296 and potential therapeutic applications with mTOR inhibitors.

297 cin, incompletely block mTORC1 compared with mTOR kinase inhibitors (TORKi).

298 This receptor interacts with mTOR via the TLR adapter MyD88.

299 ect coordination, and the observed link with mTOR activity suggests a direct link between a robust bi

300 In lung cancer patients treated with mTOR inhibitor RAD001, we observed enhanced S184 Bax pho