ライフサイエンスコーパス: rapamycin

1 ion and the immunosuppressive mTOR inhibitor rapamycin.

2 p54p) to plasma membranes in the presence of rapamycin.

3 ive regulator of Ulk1, mechanistic target of rapamycin.

4 immunosuppresive antifungal drugs FK506 and rapamycin.

5 tor prevents trapping of ST-FRB in the ER by rapamycin.

6 local-regional release of EpoB, 17-AAG, and rapamycin.

7 monella or treatment with autophagy-inducing rapamycin.

8 i, the expression of which is decreased with rapamycin.

9 which was up-regulated after activation with rapamycin.

10 s was blocked by STAT3 inhibitors but not by rapamycin.

11 df) dwarfism, calorie restriction or dietary rapamycin.

12 th 0.5 mg/kg (38.5% and 14.7%) and 2.5 mg/kg rapamycin (90.3% and 82.9%), respectively, 2) connective

13 CD4(+) T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were

14 dress this issue, we examined the effects of rapamycin, a specific inhibitor of mTOR, on B cell and C

15 We observed that both trehalose and rapamycin activate autophagy in BV2 microglial cells and

16 ted protein kinase and mechanistic target of rapamycin activator (LAMTOR) complexes and show that epi

17 n dependent on 621-101 mechanistic target of rapamycin activity and net hydrogen ion exporters, parti

18 60 cancer cell lines indicated that although rapamycin activity was correlated with levels of MTOR, i

19 trapped in the ER even without Ii-FKBP upon rapamycin addition.

20 KO mice and in WT animals exposed to chronic rapamycin administration decreased glucagon content and

21 These deleterious effects were attenuated by rapamycin administration in mice.

22 ycling requires active mechanistic target of rapamycin (aka mammalian target of rapamycin) (mTORC1),

23 such as cyclosporine and tacrolimus but not rapamycin also inhibit BCR-mediated EBV activation.

24 n hepatic cleaved caspase 3 were reversed by rapamycin, an inhibitor of mTOR signaling.

25 uld be suppressed by combined treatment with rapamycin and an extracellular signal-regulated kinase (

26 ant regulator of Akt and mammalian target of rapamycin and as such plays a key role in neuronal funct

27 of wt LARP6 and STRAP is also attenuated by rapamycin and by raptor knockdown.

28 at least in part, the sensitizing effects of rapamycin and dexamethasone.

29 own regulator of the Akt/mammalian target of rapamycin and ERK signaling pathways in multiple cellula

30 that mutants in PHO84 are hypersensitive to rapamycin and in response to phosphate feeding, generate

31 is largely dependent on mammalian target of rapamycin and its subsequent inactivation of FoxO1.

32 Therefore, we grew NKKY101 cells on rapamycin and observed TOR1 hyperactivation, which leads

33 B or treatments with the autophagy enhancers rapamycin and Tat-Beclin-1 increased ureagenesis and pro

34 ticles were engineered to release TGF-beta1, Rapamycin, and IL-2, to locally sustain a microenvironme

35 rk1 trk2 mutants display hypersensitivity to rapamycin, and reciprocally, TORC1 inhibition reduces po

36 by overexpression of VAPB or PTPIP51 impairs rapamycin- and torin 1-induced, but not starvation-induc

37 Erythromycin, avermectin and rapamycin are clinically useful polyketide natural produ

38 tophagy activators, including mTOR-dependent rapamycin as well as mTOR-independent carbamazepine and

39 We found that rapamycin attenuated the consolidation of extinction mem

40 tment of the animals with the mTOR inhibitor rapamycin before mitogenic stimulation.

41 sed to FKBP (FK506-binding protein) and FRB (rapamycin-binding domain) pair and split GFP fragments.

42 ich we conclude is Avo3, occludes the FKBP12-rapamycin-binding site of Tor2's FRB domain rendering TO

43 ine/threonine kinase and mammalian target of rapamycin (both molecules involved in sensing amino acid

44 e markers through Akt2/mechanistic target of rapamycin-C1/70S6K pathway and activated the inflammasom

45 focal adhesion kinase, mechanistic target of rapamycin, C10 regulator of kinase II, and C10 regulator

46 to result in increased mechanistic target of rapamycin C2 (mTORC2) nucleation and activity leading to

47 ansplant patients, it has been reported that rapamycin can also stimulate pathogen-specific cellular

48 at are functionally related to the target of rapamycin complex (TOR).

49 lly, there was increased mammalian target of rapamycin complex 1 (mTORC1) activation, which has been

50 cient cells have reduced mammalian target of rapamycin complex 1 (mTORC1) activity, although the unde

51 n up-regulation of the mechanistic target of rapamycin complex 1 (mTORC1) activity, one of the major

52 including inhibition of mammalian target of rapamycin complex 1 (mTORC1) and activation of Akt, ulti

53 Mammalian target of rapamycin complex 1 (mTORC1) and cell senescence are int

54 eeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal-re

55 vestigated the role of mechanistic target of rapamycin complex 1 (mTORC1) and its effector p70 S6 kin

56 Mechanistic target of rapamycin complex 1 (mTORC1) controls biosynthesis and h

57 The mechanistic target of rapamycin complex 1 (mTORC1) controls cell growth and me

58 The activity of the mechanistic target of rapamycin complex 1 (mTORC1) decreases in DENV-infected

59 Mammalian target of rapamycin complex 1 (mTORC1) has an essential role in de

60 The mammalian target of rapamycin complex 1 (mTORC1) inhibitor rapamycin slows p

61 mbalance was reversed by mammalian target of rapamycin complex 1 (mTORC1) inhibitors.

62 The mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of c

63 Mechanistic target of rapamycin complex 1 (MTORC1) is a critical negative regu

64 The mechanistic target of rapamycin complex 1 (mTORC1) is a protein kinase complex

65 The mammalian target of rapamycin complex 1 (mTORC1) kinase promotes cell growth

66 The hypertrophy-inducing mammalian target of rapamycin complex 1 (mTORC1) pathway was activated in Cp

67 The mechanistic target of rapamycin complex 1 (mTORC1) protein kinase is a master

68 Here we show that mechanistic target of rapamycin complex 1 (mTORC1) regulates polyamine dynamic

69 The mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient sufficiency

70 Instead, mechanistic target of rapamycin complex 1 (mTORC1) signal transduction was unl

71 ferentiation, requires mechanistic target of rapamycin complex 1 (mTORC1) signaling and anabolic meta

72 bition, respectively, of mammalian target of rapamycin complex 1 (mTORC1) signaling.

73 d receptor 1 (PAR-1) and mammalian target of rapamycin complex 1 (mTORC1) signaling.

74 The mechanistic target of rapamycin complex 1 (mTORC1) supports proliferation thro

75 n of PKA, PI3K, Akt, and mammalian target of rapamycin complex 1 (mTORC1) suppressed the ability of g

76 h binds to and activates mammalian target of rapamycin complex 1 (mTORC1) when GTP loaded.

77 This event requires the mammalian target of rapamycin complex 1 (mTORC1), a signaling pathway that r

78 The mammalian target of rapamycin complex 1 (mTORC1), a transducer of local dend

79 ivity, activation of the mammalian target of rapamycin complex 1 (mTORC1), and subsequent increase in

80 cal scaffold protein for mammalian target of rapamycin complex 1 (mTORC1), was acutely deleted in int

81 fructose and glucose on mammalian target of rapamycin complex 1 (mTORC1), which appeared to have bot

82 ell help activates the mechanistic target of rapamycin complex 1 (mTORC1), which promotes the anaboli

83 inhibits signaling via mechanistic target of rapamycin complex 1 (mTORC1).

84 tion of cell growth by mechanistic target of rapamycin complex 1 (mTORC1).

85 uclear factor-kappaB and mammalian target of rapamycin complex 1 (mTORC1).

86 we show that overexpression of the target of rapamycin complex 1 (TORC1) effector NPR1 improves hal4

87 thogen Candida albicans Eukaryotic Target of Rapamycin complex 1 (TORC1) induces growth and prolifera

88 Mechanistic target of rapamycin complex 1 (TORC1) integrates nutrient signals

89 The target of rapamycin complex 1 (TORC1) is a highly conserved multip

90 master nutrient response regulator target of rapamycin complex 1 (TORC1), results in rapid desumoylat

91 atin expression, reduced mammalian target of rapamycin complex 1 function, and hyperammonemic stress

92 e found that Akt-mTORC1 (mammalian target of rapamycin complex 1) signaling was increased, and treatm

93 endent inhibition of the mammalian target of rapamycin complex 1, and deficiency of autophagy impairs

94 d the phosphorylation of mammalian target of rapamycin complex 1, ribosomal protein S6 kinase 1, and

95 In contrast to mechanistic target of rapamycin complex 1-dependent canonical autophagy, GC B

96 r ribonucleoproteins and mammalian target of rapamycin complex 1.

97 rtrophy was dependent on mammalian target of rapamycin complex 1.

98 lationship between the mechanistic target of rapamycin complex 1/2 protein subunit regulatory associa

99 ncreases the activity of mammalian target of rapamycin complex 2 (mTORC2) and thereby upregulates Sna

100 investigation shows that mammalian target of rapamycin complex 2 (mTORC2) contributes to BCR-mediated

101 etabolism machinery, the mammalian target of rapamycin complex 2 (mTORC2) has been well studied in ly

102 t important component of mammalian target of rapamycin complex 2 (mTORC2).

103 ing analyses suggest the mammalian target of rapamycin complex 2 (mTORC2)/Akt signaling pathway is hi

104 mproved treatment protocol that uses a lower rapamycin concentration and shorter treatment times, lea

105 and loss of loxP-flanked DNA sequences in a rapamycin controlled manner.

106 When Tm infected mice were treated with rapamycin, DCLK1 and IL-25 expression in enterocytes and

107 Two potential compounds, XAV939 and rapamycin, decreased proliferation in FAP-COs, but also

108 Patches delivering rapamycin developed less neointimal hyperplasia, less sm

109 d that despite this immunomodulatory effect, rapamycin did not affect HIV-1 gene expression induced b

110 In contrast, rapamycin did not prevent the FSS-induced increase in Na

111 lucose starvation, amino acid deprivation or rapamycin did not trigger micro-lipophagy and failed to

112 t BCR-mediated lytic induction but find that rapamycin does not inhibit BCR-mediated lytic induction.

113 or EpoB and its combinations with 17-AAG and rapamycin, enabling a platform for i.p. delivery, sustai

114 or by inhibition of the mammalian target of rapamycin, enhanced lysosomal clearance of C99.

115 Moreover, rapamycin-enhanced migration of TSC2-null cells was inhi

116 tivated in Cpt2M(-/-) hearts; however, daily rapamycin exposure failed to attenuate hypertrophy in Cp

117 model, relatively high-dose intraperitoneal rapamycin extended lifespan and improved markers of neur

118 hat B cells were the primary target cells of rapamycin for the impaired humoral immunity and that red

119 We hypothesized that delivery of rapamycin from nanoparticles (NP) covalently attached to

120 However, rapamycin further increased uPA expression in TSC2-null

121 , C-box mutations render MAF1 insensitive to rapamycin, further defining a regulatory role for this r

122 demonstrated that primary HCEC treated with rapamycin had lower proliferation but considerably longe

123 Additionally, we found that rapamycin had minimal effects on B cell responses activa

124 Rapamycin had the converse effect, linking MTOR signalin

125 The mTOR inhibitor rapamycin has been shown to attenuate the behavioral eff

126 Rapamycin has previously been shown to have anti-aging e

127 a TORC1 signaling defect but does not rescue rapamycin hypersensitivity.

128 hese findings raise the possibility of using rapamycin in conjunction with T cell-activating agents i

129 Allosteric mTOR inhibitors, such as rapamycin, incompletely block mTORC1 compared with mTOR

130 are prevented by pre- or post-treatment with rapamycin, indicating the mTOR pathway is involved in me

131 with an anti-apoptotic effect of autophagy, rapamycin-induced apoptosis and cytotoxicity were blocke

132 ator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increased intracellular kill

133 control GTA but do not significantly affect rapamycin-induced autophagy.

134 We developed a novel ubiquitination system, Rapamycin-Induced Degradation (RapiDeg), to test the sor

135 Inhibition of mTORC1 with rapamycin induces PIM3 transcript and protein levels in

136 activation of phospholipase C beta or with a rapamycin-inducible system in which various phosphatidyl

137 Mechanistic target of rapamycin inhibition by either nutrient starvation or us

138 flammatory status by the mammalian target of rapamycin inhibitor rapamycin on the different immune ce

139 evented by the selective mammalian target of rapamycin inhibitor temsirolimus and the protein synthes

140 De novo use of mammalian target of rapamycin inhibitors after kidney transplantation is ass

141 Over the past decade, mammalian target of rapamycin inhibitors have received considerable attentio

142 dylinositol 3-kinase and mammalian target of rapamycin inhibitors in breast cancer, and inhibitors of

143 Mammalian target of rapamycin inhibitors may confer cardioprotective advanta

144 unomodulatory drugs, and mammalian target of rapamycin inhibitors.

145 ng site of Tor2's FRB domain rendering TORC2 rapamycin insensitive and recessing the kinase active si

146 t infusion of the selective mTORC1 inhibitor rapamycin into the medial PFC (mPFC) blocks the antidepr

147 Rapamycin is a clinically important drug that is used in

148 ts provide evidence that mammalian target of rapamycin is a key player involved in prevention of TH2

149 ntibody responses is required in cases where rapamycin is used to stimulate vaccine-induced immunity.

150 Sirolimus (rapamycin) is an immunosuppressive drug used in transpla

151 Although its specific inhibitor, rapamycin, is currently used as an immunosuppressive dru

152 Target of rapamycin kinase complex 1 (TORC1) regulates Pol III act

153 f rapamycin (mTOR) (or mechanistic target of rapamycin), leading to dephosphorylation of Unc-51-like

154 Rapamycin may be a useful additive for ex vivo expansion

155 ggest that inhibition of B cell responses by rapamycin may play an important role in regulation of al

156 uPA-dependent pathway, when used along with rapamycin, might attenuate LAM progression and potential

157 nt inactivation of the mechanistic target of rapamycin mobilizes autophagy, which sequesters stressed

158 Our data demonstrate that rapamycin modulates global RNA homeostasis by NMD.

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

160 on of the protein kinase mammalian target of rapamycin (mTOR) (or mechanistic target of rapamycin), l

161 ess kinase activation, mechanistic target of rapamycin (mTOR) activation, loss of glutamate and potas

162 ermore, IL-10 suppresses mammalian target of rapamycin (mTOR) activity through the induction of an mT

163 IGF-I, is regulated by mechanistic target of rapamycin (mTOR) and casein kinase (CSNK)-2.

164 Inhibitors of the mechanistic target of rapamycin (mTOR) are currently used to treat advanced me

165 ntified c-Jun kinase and mammalian target of rapamycin (mTOR) as components of two distinct host sign

166 berrant signaling by the mammalian target of rapamycin (mTOR) contributes to the devastating features

167 Mechanistic target of rapamycin (MTOR) cooperates with Hedgehog (HH) signaling

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

169 While inhibition of mechanistic target of rapamycin (mTOR) effectively slows cyst expansions in an

170 Mechanistic target of rapamycin (mTOR) enhances immunity in addition to orches

171 Here we show that mechanistic target of rapamycin (mTOR) functions as a folate sensor in primary

172 The mechanistic target of rapamycin (mTOR) has a key role in the integration of va

173 s a novel way by which mechanistic target of rapamycin (mTOR) influences reprogramming.

174 s safety and efficacy of mammalian target of rapamycin (mTOR) inhibition in combination with liposoma

175 Mechanistic target of rapamycin (mTOR) inhibitors can attenuate TAV; therefore

176 The mammalian target of rapamycin (mTOR) inhibitors, sirolimus and everolimus, a

177 The mammalian target of rapamycin (mTOR) is a crucial signaling node that integr

178 Although the mammalian target of rapamycin (mTOR) is an essential regulator of developmen

179 nase (PI3K) and AKT to mechanistic target of rapamycin (mTOR) is prominently dysregulated in high-gra

180 ologic inhibition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, c

181 Mechanistic target of rapamycin (mTOR) links nutrient availability to cell gro

182 on assays; the effect of mammalian target of rapamycin (mTOR) manipulation in MSCs was studied in viv

183 ogenase (LDH) assay, and mammalian target of rapamycin (mTOR) pathway activation were evaluated.

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

185 vel regulator of the Akt/mammalian target of rapamycin (mTOR) pathway downstream of multiple TLRs.

186 results show that the mechanistic target of rapamycin (mTOR) pathway in neurons regulates CTGF produ

187 iven that the PI3K/Akt/mechanistic target of rapamycin (mTOR) pathway is also known to regulate myeli

188 protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway is one of the most commonly dys

189 cells by activating the mammalian target of rapamycin (mTOR) pathway.

190 ed periostin-induced Akt/mammalian target of rapamycin (mTOR) signaling and ADPKD cell proliferation

191 to clarify the role of mechanistic target of rapamycin (mTOR) signaling in hepatic ischemia/reperfusi

192 Mechanistic target of rapamycin (mTOR) signaling is necessary to generate a me

193 or TrkB, facilitation of mammalian target of rapamycin (mTOR) signaling pathway and inhibition of gly

194 ming, with NF-kappaB and mammalian target of rapamycin (mTOR) signaling strongly increased.

195 Further, the mammalian target of rapamycin (mTOR) signaling was implicated as being invol

196 acid (AMPA) receptor and mammalian target of rapamycin (mTOR) signaling, respectively.

197 Inhibition of the mechanistic target of rapamycin (mTOR) using rapamycin prevented the increase

198 g the kinase mammalian/mechanistic target of rapamycin (mTOR) with clinically available small-molecul

199 ipulations of insulin, mechanistic target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), a

200 lexes containing S6K1 or mammalian target of rapamycin (mTOR), and appears to represent an incomplete

201 volvement of PI3K/Akt, mechanistic target of rapamycin (mTOR), and MEK/ERK pathways in the regulation

202 nserved protein kinase mechanistic target of rapamycin (mTOR), existing in two complexes, mTORC1 and

203 d with upregulation of mechanistic target of rapamycin (mTOR), proinflammatory, and anti-apoptotic si

204 ted factor 6 (TRAF6) and mammalian target of rapamycin (mTOR), respectively.

205 receptors, which trigger mammalian target of rapamycin (mTOR)-dependent structural plasticity via bra

206 n kinase B (PKB/Akt) and mammalian target of rapamycin (mTOR).

207 educed activity of the mechanistic target of rapamycin (mTOR).

208 kappaB (NF-kappaB) and mechanistic target of rapamycin (mTOR).

209 lved in activating the mechanistic target of rapamycin (mTOR).

210 sistance mediated by the mammalian target of rapamycin (mTOR)/sphingosine-kinase-1 (SK1) pathway.

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

212 Furthermore, Rapamycin negated miR-96 mediated brain injury attenuati

213 ay, and that inhibition of this pathway with rapamycin not only reverses the observed changes in neur

214 ere undertaken to investigate the effects of rapamycin on primary human corneal epithelial cells in v

215 the mammalian target of rapamycin inhibitor rapamycin on the different immune cell subsets.

216 s increased, and treatment with 2.24 mg/kg.d rapamycin or 40% caloric restriction for 9 weeks partial

217 ilar effects are seen using mTORC1 inhibitor rapamycin or by knocking down raptor.

218 n caused by UBE2O loss, while treatment with rapamycin or inhibition of HIF1alpha ablates UBE2O-depen

219 Inhibition of mTOR activity by rapamycin or partially restoring autophagy delays neurod

220 Rapamycin or raptor deletion ameliorates the aberrant TF

221 Sequestration of FKBP12 by rapamycin or tacrolimus activates hepcidin both in vitro

222 ase in activity in the mechanistic target of rapamycin pathway, and that inhibition of this pathway w

223 ith the PI3K/Akt/mTOR (mechanistic target of rapamycin) pathway at the level of mTORC1 and also regul

224 by the universally conserved TOR (Target of Rapamycin) pathway to balance growth and development wit

225 inase (PI3K)-Akt-mTOR (mechanistic target of rapamycin) pathway, and activation was induced by three

226 AKT and complex 1 of the mammalian target of rapamycin pathways and activation of the AMPK pathway.

227 vated protein kinase and mammalian target of rapamycin pathways and the inverse correlation of CDC42E

228 ls of phosphorylation of mammalian target of rapamycin (phospho-mTOR).

229 kinase B, phosphorylated mammalian target of rapamycin, phosphorylated eukaryotic translation initiat

230 hatidylinositol-3-kinase/mammalian target of rapamycin (PI3K/mTOR) signaling are being investigated i

231 hosphoinositide-3 kinase/mammalian target of rapamycin (PI3K/mTOR) signaling pathways.

232 that Protein Kinase B-mechanistic Target of Rapamycin (PKB/AKT-mTOR) signaling controls the dynamics

233 jected in dHc with AAV-Cre, and in NBQX- and rapamycin-pretreated wild-type mice, these compounds blo

234 mechanistic target of rapamycin (mTOR) using rapamycin prevented the increase in cellular energy leve

235 Since combined delivery of antigen plus rapamycin (RAP) in nanoparticles is known to induce anti

236 eration, and the stimulation of autophagy by rapamycin (Rap) remarkably suppressed palmitic acid-indu

237 e were conditioned with anti-CD154 (MR1) and rapamycin (Rapa) plus 100 cGy total body irradiation (MR

238 r microspheres (TRI microspheres; TGF-beta1, Rapamycin (Rapa), and IL-2).

239 Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patien

240 The addition of rapamycin reconstituted a fluorescent enzyme, termed spl

241 The process was reversible as upon rapamycin removal, the split GFP-COase fluorescence was

242 er-associated MTOR mutants and the growth of rapamycin-resistant cancer cells.

243 In a SATAY screen for rapamycin-resistant mutants, we identify Pib2 (PhosphoIn

244 double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels of HMO1 mRNA, but on

245 RNA, well-studied age-related factors (i.e., rapamycin, resveratrol, TNF-alpha, and staurosporine), q

246 ells treated with the TOR-specific inhibitor rapamycin revealed that TOR not only dictates transcript

247 also provide evidence for the enhancement of rapamycin's inhibitory effect on IL-1beta secretion by t

248 rtant novel modulator of mammalian target of rapamycin signaling and autophagy in the vascular system

249 the nucleus can regulate mammalian target of rapamycin signaling and neuronal growth.

250 sted that unequal PI3K/mechanistic target of rapamycin signaling drives intraclonal cell fate heterog

251 th energy production and mammalian target of rapamycin signaling in human liver cancer cell lines and

252 tivation and inhibited mechanistic target of rapamycin signaling in mouse embryonic fibroblasts as we

253 d enriched activation of mammalian target of rapamycin signaling in outer radial glia.

254 ired to fully suppress mechanistic target of rapamycin signaling, a known effector of NF1 loss.

255 202) accumulation, Akt/mechanistic target of rapamycin signaling, levels of ionized calcium-binding a

256 ctivation of oncogenic mechanistic target of rapamycin signaling.

257 proteins associated with mammalian target of rapamycin signalling were detected in the PFC and with g

258 et of rapamycin complex 1 (mTORC1) inhibitor rapamycin slows progression of these diseases but is not

259 antigen-independent manner, suggesting that rapamycin specifically inhibits B cell responses induced

260 ient CD4(+) T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their ph

261 increased expression of mammalian target of rapamycin, suggesting reduced amino acid catabolism in M

262 bitors and inhibitors of mammalian target of rapamycin that have provided additional benefit to patie

263 Here, we administered low-dose oral rapamycin to a knock-in (KI) mouse model of authentic mt

264 meostasis and the energy-dependent Target of Rapamycin (TOR) kinase in meristematic activity, yet a p

265 Here, we discovered that the Target of Rapamycin (TOR) kinase phosphorylates PYL ABA receptors

266 The Target of Rapamycin (TOR) pathway regulates morphogenesis and resp

267 Target of rapamycin (TOR) promotes reinitiation at upstream ORFs (

268 The Target of Rapamycin (TOR) signalling network plays important roles

269 pheromone response pathway and the target of rapamycin (TOR)-regulated ribosomal biogenesis pathway,

270 ward for the identification of the target of rapamycin, TOR.

271 ell-known downstream phenomenon of target of rapamycin (TOR1) signaling, we suspected a link between

272 Rapamycin treated cells demonstrated less senescence by

273 Apoptosis was also lower in the rapamycin treated cells.

274 nd more selectively and less specifically in rapamycin treated mice.

275 Transcriptome analysis of rapamycin-treated cells reveals genome-wide changes in a

276 l immunity and that reduced Tfh formation in rapamycin-treated mice was due to lower GC B cell respon

277 ponses during acute viral infection and that rapamycin treatment alters the interplay of immune cell

278 Importantly, rapamycin treatment did not impair cytotoxic T lymphocyt

279 rcomas was evaluated by short- and long-term rapamycin treatment in sarcoma cell lines.

280 Rapamycin treatment increased FoxO3 activity as well as

281 s spectrometry demonstrated that hypoxia and rapamycin treatment increased IGFBP-1 phosphorylation at

282 These results indicate that rapamycin treatment of HCEC prevents the loss of corneal

283 Here we found that rapamycin treatment predominantly inhibited GC B cell re

284 Rapamycin treatment reduced inflammatory lesions formed

285 Rapamycin treatment resulted in suppression of virus-spe

286 Compared with control, hypoxia and rapamycin treatment showed markedly amplified PLA signal

287 These effects were suppressed by lysine or rapamycin treatment, suggesting that the enhanced argini

288 These effects were reversed by rapamycin treatment.

289 mpaired mTORC2-dependent pAKT-S473 following rapamycin treatment.

290 Rapamycin-treatment also causes depletion of PTC-contain

291 transcript exhibits a shorter half-life upon rapamycin-treatment as compared to the non-PTC isoform.

292 Rapamycin-treatment significantly reduces the levels of

293 Disruption of TACI-mTOR interaction by rapamycin, truncation of the MyD88-binding domain of TAC

294 Rapamycin was administered intraperitoneally daily for 1

295 Importantly, low-dose oral rapamycin was sufficient to extend Tk2KI/KI mouse lifesp

296 3-methyladenine (3MA) or rapamycin were used to determine the role of autophagy i

297 derstand the mechanism of action of the drug rapamycin, which approximately 25 y ago led to the disco

298 to iron and inflammation and among drugs, by rapamycin, which inhibits mTOR in complex with the immun

299 e, we compared RapaLink-1, a TORKi linked to rapamycin, with earlier-generation mTOR inhibitors.

300 has been associated with such inhibitors as rapamycin.-Xiong, M., Zhu, Z., Tian, S., Zhu, R., Bai, S