ライフサイエンスコーパス: PI3K

1 PI3K status in tumour tissue was determined via central

2 PI3K-delta/gamma inhibition may directly inhibit maligna

3 PI3K/Akt and NF-kappaB pathways account for the anti-inf

4 PI3Ks have dual kinase specificity: a lipid kinase activ

5 on of the relative gene expression of IRS-1, PI3K and Akt in the insulin signaling pathway, while 2.7

6 UT8 expression, respectively, through IGF-1R/PI3K/Akt signaling pathway in human endometrial cells.

7 ceptor (LR/37/67 kDa) and downstream ERK1/2, PI3K/AKT and FAK signalling pathways.

8 ngs reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also

9 olved in the MAPK pathway [31.2% (138/442)], PI3K signaling [18.1% (80/442)], and the cell-cycle mach

10 whereas combination therapy of aspirin and a PI3K inhibitor further attenuated tumor growth.

11 stream of HGF-mediated c-Met activation in a PI3K dependent manner.

12 is activated by Trio downstream of PDGF in a PI3K- and Src-dependent manner.

13 ta1 treatment enhanced TRPV4 activation in a PI3K-dependent manner in normal human lung fibroblasts i

14 sa3 translocates to the plasma membrane in a PI3K-dependent manner upon activation of human platelets

15 rent study is to determine the efficacy of a PI3K/mTOR dual inhibitor, LY3023414, on established EAC

16 n, we find potentially clinically actionable PI3K signalling mutations in 16% of cases.

17 Activated PI3K Delta Syndrome (APDS) is a primary immunodeficiency

18 gulates CXCR4 and FAK expression, activating PI3K/AKT and ERK1/2 FAK-downstream pathways in MCL.

19 ncy or expression of a constitutively active PI3K rescued function of B cells in infected mice.

20 vates the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway, signal transducer and activator of tr

21 romosome 9q loss, resulting in increased AKT/PI3K/mTOR signaling.

22 class II phosphoinositide 3-OH kinase alpha (PI3K-C2alpha) acting as limiting scaffold protein organi

23 of pathway checkpoints, p-mTOR (p=0.03) and PI3K-alpha (P = 0.04) were downregulated in treatment re

24 of muscle atrophy via targeting of IGF-1 and PI3K(p85alpha), and that suppression of miR-29b may repr

25 of Adcy1 normalizes the aberrant ERK1/2- and PI3K-mediated signalling, attenuates excessive protein s

26 nhibitory reciprocal feedback between AR and PI3K/AKT signaling pathways, pAKT levels were increased

27 study supports the evaluation of aspirin and PI3K pathway inhibitors as a combination therapy for tar

28 expression is sufficient to activate BCR and PI3K/Akt signaling pathways and further enhances signali

29 ulatory function requires Ca(2+) binding and PI3K-Ibeta activation.

30 s-activation between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a RasPIK3IP1PI3K signaling ne

31 its effectors, including the Raf/Mek/Erk and PI3K/Akt/mTORC1 signaling cascades, and also the WNT/bet

32 A/TSG-6 effect is mediated by RhoA, ERK, and PI3K/Akt signaling.

33 Additionally, specific FAK and PI3K inhibitors reduce SOX11-enhanced MCL cell migration

34 e in Akt phosphorylation was Gbetagamma- and PI3K-dependent, and the increase in eNOS phosphorylation

35 esistance to combined inhibition of HER2 and PI3K.

36 tor of endoplasmic reticulum homeostasis and PI3K/AKT signaling, is overexpressed in the acini and PD

37 , and activation of epithelial NF-kappaB and PI3K signaling pathways are restricted by the M-ILK defi

38 lation as well as inhibitors of the MAPK and PI3K pathways, we found that MAPK and PI3K regulate dent

39 PK and PI3K pathways, we found that MAPK and PI3K regulate dental epithelial stem cell activity, tran

40 l transduction events involving Ras/MAPK and PI3K/Akt pathways.

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

42 Dual targeting of the MEK and PI3K/AKT pathways downstream of KRAS by selumetinib plus

43 e aim of this trial was to block the MEK and PI3K/AKT pathways downstream of the KRAS protein as an a

44 proliferation and apoptosis via the PIM and PI3K kinases.

45 pression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon plus ins

46 Using DREAM-null platelets and PI3K isoform-specific inhibitors, we observed that plate

47 /TRAIL-R can promote metastasis via Rac1 and PI3K.

48 results in actin cytoskeleton remodeling and PI3K/Akt and Erk signaling in an IgD-BCR-dependent manne

49 downstream signaling events, such as rho and PI3K activation.

50 disruption of B-cell receptor signalling and PI3K-AKT-mTOR axis leads to release of MCL cells from TM

51 receptor activation, new TrkB synthesis, and PI3K/Akt signaling (the S pathway).

52 dimers bound to active receptors, augmenting PI3K signaling and oncogenic transformation.

53 dently enhanced degradation of Mdm2, blocked PI3K/Akt/Mdm2 pathway and suppressed HCC cell survival.

54 r of breast cancer, indicating that blocking PI3K-AKT pathway-dependent beta-catenin accumulation may

55 of RNF157 on the same residues modulated by PI3K and MAPK signaling.

56 Randomisation was stratified by PI3K pathway activation status (activated vs non-activat

57 n ECSHIP2(Delta/+) ECs and was suppressed by PI3K and NADPH oxidase 2 inhibitors.

58 sulin by upregulating GLUT4 translocation by PI3K mediated activation of Akt signaling pathways.

59 8, 0044281, 0007155) and pathways in cancer, PI3K-Akt signaling pathway, metabolic pathways (pathway

60 I2-CD40L axis, and GLI2 is required for CCR3-PI3K-AKT-mediated regulation of the CD40L promoter.

61 We found that the CCR3-PI3K-AKT signaling modulates the GLI2-CD40L axis, and GL

62 In UN-KC-6141 cells, PI3K and MEK signaling increased expression of KLF5; a h

63 ssed in tumors with Pten loss, circumventing PI3K-mediated repression of the androgen axis.

64 Moreover, combining PI3K and MEK inhibition was effective against imatinib-r

65 the latter further potentiated by concurrent PI3K/MEK inhibition, consistent with a role for RNF157 i

66 puts from the TCR and a TLR2-MyD88-dependent PI3K signaling pathway.

67 In vivo, raft-dependent PI3K signaling is up-regulated in klotho-deficient mouse

68 hed in lipid rafts to inhibit raft-dependent PI3K signaling.

69 Ph-like genomic alterations with 4 discrete PI3K pathway protein inhibitors and observed marked leuk

70 te the dual activity of BKM120 into discrete PI3K and tubulin inhibitors.

71 NGF treatment displaced PI3K C2A from the Golgi and optogenetic recruitment of t

72 Specific FAK inhibition blocks downstream PI3K/AKT- and ERK1/2-mediated phosphorylation.

73 e klotho down-regulates growth factor-driven PI3K signaling, contributing to extension of lifespan, c

74 -bearing Kit(V558Delta/+) mice with the dual PI3K/mTOR inhibitor voxtalisib, the pan-PI3K inhibitor p

75 Treatment with dual PI3K/mTOR inhibitor gedatolisib resulted in near eradica

76 for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signaling.

77 gulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, contributing to a more aggr

78 FTR and TLR4 signaling, and is necessary for PI3K/AKT signaling induction in response to MPhi activat

79 extra- and intracellular sources apart from PI3K, microtubules, and dynamin-2.

80 These data serve as a basis for future PI3K-based immune therapies for transplantation.Phosphat

81 eous mutation profiles accumulating in GPCR, PI3K-Akt and FGFR signaling pathways.

82 promoting the tonic B-cell receptor (BCR)-->PI3K pathway (TCF3 and ID3) did not differ by age, where

83 d survival of thyroid cancer cells harboring PI3K-activating mutations.

84 ome Atlas (TCGA) data was analyzed for HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations from sarco

85 y developmental stages, physiologically high PI3K-Akt-mTORC1 signaling suppresses expression of Krox2

86 nalling circuitry including Shh, Wnt, Hippo, PI3K and MAPK pathways.

87 However, PI3K inhibitors primarily induce cell cycle arrest, leav

88 t the catalytic subunit p110delta of class I PI3K played a role in induction of antiviral immune resp

89 Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3.

90 We screened all class IA PI3K isoforms and found that HRas activates both p110alp

91 show how a functional dichotomy in Class IA PI3K isoforms in these two subsets of CD4(+) T cells can

92 Class IA PI3Ks are activated downstream of the Ras superfamily of

93 n, and aggregation through PI3K class Ibeta (PI3K-Ibeta).

94 ics in each of these contexts, we identified PI3K/Akt regulation of glycolysis as a multifaceted modu

95 Taken together, our results identify PI3K C2A as being required and sufficient for deltaR exp

96 ithfully reports the mitotic action of IGF1R-PI3K-Akt-Tor signaling in epithelial cells in real-time.

97 The class III PI3K Vacuolar protein sorting 34 (Vps34) plays a role in

98 sulin-like growth factor (IGF)/insulin (IIS)-PI3K-AKT-TOR signaling pathway is linked to major human

99 In PI3K pathway-activated patients (n=372), median progress

100 Previous mutants were defective in PI3K because they failed to bind the enzyme and bring th

101 sults support an important role for Rasa3 in PI3K-dependent integrin alphaIIbbeta3-mediated outside-i

102 iolisib led to a dose-dependent reduction in PI3K/AKT pathway activity assessed ex vivo and improved

103 nt with TC14012 also significantly increased PI3K/Akt phosphorylation, and tube formation was blocked

104 el role of calpain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS activation through Ezrin.

105 ld not generate sufficient anti-inflammatory PI3K activity, similar to what is observed in CF.

106 hted in this review, started to interconnect PI3K pathway activation to Ca(2+) signaling.

107 ploys single-molecule imaging to investigate PI3K activation in a six-component pathway reconstituted

108 ncies, whereas select combinations involving PI3K, CSF1R, or bromodomain inhibitors showed preferenti

109 teraction with phosphatidylinositol 3-kinase PI3K, leading to activated Akt and increased cell prolif

110 ls, inhibition of phosphoinositide-3 kinase (PI3K) activity blocked export of newly synthesized delta

111 -Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediates their interaction.

112 ctivation of phosphatidylinositol 3- kinase (PI3K) and contributes to arterial thrombosis.

113 itively regulates phosphoinositide 3-kinase (PI3K) activity during platelet activation.

114 , an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylas

115 by regulating phosphatidylinositol-3-kinase (PI3K) activity, but the participation of PTEN in host de

116 The phosphatidylinositol-3-kinase (PI3K) alpha/delta (PI3Kalpha/delta) inhibitor AZD8835 sh

117 ignaling from phosphatidylinositol 3-kinase (PI3K) and AKT to mechanistic target of rapamycin (mTOR)

118 Phosphoinositide 3-kinase (PI3K) and the proteasome pathway are both involved in ac

119 ractions with phosphatidylinositol 3-kinase (PI3K) and the Rac1 guanine nucleotide exchange factor Ti

120 Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha gene (PIK3CA) are frequent

121 osphorylated phosphatidylinositide 3-kinase (PI3K) increased both in 5-FU-tolerant subpopulations acc

122 the most advanced phosphoinositide 3-kinase (PI3K) inhibitors for the treatment of cancer, but it int

123 Phosphoinositide 3-kinase (PI3K) is deregulated in a wide variety of human tumors a

124 ing that Gi/o and phosphoinositide 3-kinase (PI3K) mediate the increase independently of epidermal gr

125 ling and increased phosphoinositol-3-kinase (PI3K) pathway signaling in isoform 2 overexpressing cell

126 Effectors of the phosphoinositide 3-kinase (PI3K) signal transduction pathway contribute to the hypo

127 (ABL), and/or phosphatidylinositol 3-kinase (PI3K) signaling and poor clinical outcomes.

128 cells, activates phosphoinositide 3-kinase (PI3K) signalling by binding to the p85alpha subunit of P

129 orylation and phosphatidylinositol 3-kinase (PI3K) signals.

130 kinases, Shc, phosphatidylinositol 3-kinase (PI3K), and phospholipase C-gamma1 (PLCgamma1) have all b

131 inase C (PKC) and phosphoinositide-3-kinase (PI3K), and subsequently to phosphorylation of MARCKS.

132 he sole class III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs) and platelets, we created

133 UL46-encoded phosphatidylinositol 3-kinase (PI3K)-Akt activator, was dependent upon the Ser/Thr kina

134 regulator in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway that have been shown to play

135 inhibitor of phosphatidylinositol 3-kinase (PI3K)-delta/gamma isoforms currently in clinical develop

136 latory subunit of phosphoinositide-3-kinase (PI3K).

137 sphorylation in a phosphoinositide 3-kinase (PI3K)/Akt-dependent manner, resulting in ERG enrichment

138 The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapam

139 downstream of phosphatidylinositol 3-kinase (PI3K); its role in vascular function is poorly understoo

140 The phosphatidyl-inositol-3 kinases (PI3K) pathway regulates a variety of cellular processes,

141 nsplantation.Phosphatidylinositol-3-kinases (PI3K) gamma and delta are key regulators of T cell signa

142 The phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases central to regulati

143 unit of class IA phosphoinositide 3-kinases (PI3Ks).

144 In patients with known PI3K status (n=851), median progression-free survival wa

145 g pathway) for adenoma evolution, and LAMA1 (PI3K-Akt signaling pathway) and ADCY3 (FGFR signaling pa

146 glucose homeostasis downstream of the leptin-PI3K pathway in POMC neurons.

147 Many PI3K pathway-targeted therapies have been tested in onco

148 Mechanistically, PI3K blockade by BKM120 attenuated HR competency with ga

149 tion of these pathways by the small-molecule PI3K inhibitor pictilisib (GDC-0941) and the MEK inhibit

150 tyrosine phosphatase (PTPase) at the nephrin-PI3K binding site and renders PI3K for IRS-1, thereby ac

151 We also identified novel PI3K effectors that were commonly-regulated, including p

152 Reduced abundance of PI3K-C2alpha in breast cancer models initially impairs t

153 ignaling intermediates for the activation of PI3K by both the insulin-like growth factor 1 receptor (

154 ct of ibrutinib and reciprocal activation of PI3K-AKT-mTOR and integrin-beta1 signalling.

155 e binding of BRD4 and the kinase activity of PI3K.

156 The activity of PI3K/protein kinase B (AKT) and insulin receptor substra

157 n high-grade glial brain tumors, blockade of PI3K or AKT minimally affects downstream mTOR activity i

158 -BCR signaling, resulting in deactivation of PI3K/Akt signaling.

159 Downregulation of PI3K-C2alpha causes spindle alterations, delayed anaphas

160 P3, the product used to signal downstream of PI3K.

161 oration with a constitutively active form of PI3K rescued migration.

162 While this can limit the impact of PI3K-targeted therapies, these findings also open the op

163 The importance of PI3K activity and tyrosine phosphorylation are two examp

164 The concomitant inhibition of PI3K and BRD4 blocks MYC expression and activation, prom

165 Here we show that although inhibition of PI3K-AKT-mTOR signaling markedly decreased glycolysis an

166 Inhibition of PI3K-dependent exocytosis of TRPC6 is thought to be the

167 se RNF157 as a target at the intersection of PI3K and MAPK signaling.

168 enrichment analysis revealed involvement of PI3K/Akt, mechanistic target of rapamycin (mTOR), and ME

169 The p110beta isoform of PI3K plays a particularly important role in the pathogen

170 i was effectively blocked in the presence of PI3K inhibitors.

171 Presence of PI3K pathway aberration was associated with a significan

172 CD8+ T cells was assessed in the presence of PI3K-alpha, -beta, or -delta inhibitors.

173 tyrosine phosphorylation and recruitment of PI3K, are not inhibited by microtubule disruption, indic

174 wild type that point to novel regulation of PI3K signaling.

175 rs that mediate soluble klotho regulation of PI3K signaling.

176 c kinase to activate a negative regulator of PI3K signaling, SHIP-1 via phosphorylation, providing a

177 results clearly define an antiviral role of PI3K by modulating immune responses and demonstrate diff

178 RNA-seq analysis reveals a divergent role of PI3K/AKT/mTORC signalling, specifically of the mTORC2 su

179 BCAP also interacts with the p85 subunit of PI3K and phospholipase Cgamma, enzymes that deplete plas

180 alling by binding to the p85alpha subunit of PI3K and that K-80003, an anti-cancer agent, inhibits th

181 , the gene encoding the catalytic subunit of PI3K, PI3K inhibitors have yielded little clinical benef

182 levels of c-Met and the p85alpha subunit of PI3K.

183 findings were associated with suppression of PI3K/Akt/mTOR activation and STAT3 phosphorylation upon

184 ment (ARE)-binding protein BRF1, a target of PI3K-Akt.

185 nase 2 (CDK2), itself a downstream target of PI3K/MAPK signaling, leads to increased phosphorylation

186 Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and Akt.

187 cancer, PSMA initiates signaling upstream of PI3K through G protein-coupled receptors, specifically v

188 focal adhesion kinase activation upstream of PI3K-mTOR, and induces transcriptional changes that incl

189 rlisib supports the rationale for the use of PI3K inhibitors plus endocrine therapy in patients with

190 Many viruses depend on PI3K signaling for replication.

191 ne-resident HRas and evaluated its effect on PI3K signaling in lipid kinase assays and through analys

192 il-containing protein kinase (ROCK), ERK, or PI3K.

193 Inhibition of ROCK, ERK, or PI3K/Akt blocked sHA/TSG-6-mediated AHR.

194 p38 MAPK (SB203580), JNK MAPK (SP600125), or PI3K (LY294002) were used to determine the involvement o

195 Overall, PI3K/mTOR inhibition potently decreased ALL burden in vi

196 Pan-PI3K and p110alpha-selective pharmacological inhibition

197 Buparlisib, a pan-PI3K inhibitor, has shown preclinical antitumour activit

198 ase 3 study assessed the efficacy of the pan-PI3K inhibitor buparlisib plus fulvestrant in patients w

199 Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and resto

200 dual PI3K/mTOR inhibitor voxtalisib, the pan-PI3K inhibitor pilaralisib, and the PI3K-alpha-restricte

201 ls responsive to combined inhibition of PARP/PI3K, with concomitantly induced DNA damage accumulation

202 broblast growth factor (FGF)-ERK1/2 pathway, PI3K-AKT, the leukemia inhibitory factor (LIF)-JAK-STAT3

203 Pharmacological PI3K/AKT pathway manipulation recapitulated cellular phe

204 gene encoding the catalytic subunit of PI3K, PI3K inhibitors have yielded little clinical benefit for

205 Inhibition of PKA, PI3K, Akt, and mammalian target of rapamycin complex 1 (

206 -(o-tolyl)quinazolin-4(3H)-one)] is a potent PI3K inhibitor selective for the delta isoform.

207 xplain why rigid collagen fibrils potentiate PI3K activation to promote malignancy and offer a perspe

208 ritical role in adenocarcinomas by promoting PI3K/Akt signaling.

209 and modulate, through activation of the PTEN/PI3K/Akt signaling pathway, different molecules involved

210 model identifies calcium, actin, Ras, Raf1, PI3K, and JAK as key regulators of cardiac mechano-signa

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

212 tide-3 kinase/mammalian target of rapamycin (PI3K/mTOR) signaling pathways.

213 m of the Ras superfamily of GTPases, and Ras-PI3K interaction plays a key role in promoting tumor for

214 ing the detailed molecular events in the Ras-PI3K interaction has been challenging because it occurs

215 These mutants recruit PI3K activity like the wild type, but fail to elevate th

216 or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels.

217 at the nephrin-PI3K binding site and renders PI3K for IRS-1, thereby activating mTORC1.

218 in, we described the evolution of a reported PI3K inhibitor into a moderate PI3Kalpha inhibitor with

219 oted SC migration by a pathway that required PI3K and ERK1/2.

220 Use of more selective PI3K inhibitors, such as alpha-specific PI3K inhibitor,

221 tive PI3K inhibitors, such as alpha-specific PI3K inhibitor, is warranted to further improve safety a

222 Studies employing isoform-specific PI3K inhibitors and a PI3Kdelta-deficient mouse strain r

223 anchorage as well as signaling through Src, PI3K, and Rac1, and increasingly stiff collagen promoted

224 CAPE inhibits FGF-stimulated PI3K/Akt signaling, and neural crest defects in CAPE-tre

225 phosphoinositide 3-kinase catalytic subunit PI3K(p110alpha), which can promote tumor growth, was rem

226 Together, these results suggest PI3K inhibition may be a plausible approach to expand th

227 e feedback loop that is essential to sustain PI3K/Akt signaling in breast cancer.

228 a positive feedback mechanism that sustains PI3K/Akt signaling in tumor cells, further illuminating

229 ochordal transcription factor brachyury (T), PI3K signalling mutations, and mutations in LYST, a pote

230 phase onset, and aneuploidy, indicating that PI3K-C2alpha expression is required for genomic stabilit

231 Here we report that PI3K signaling is critical for the control of West Nile

232 Collectively, our results show that PI3K delta is essential for survival during sepsis.

233 ATION: The results from this study show that PI3K inhibition combined with endocrine therapy is effec

234 preciated roles of PIK3CA mutation show that PI3K signalling can contribute to the generation of irre

235 The PI3K-protein kinase B (PKB; also known as Akt) signaling

236 The PI3K/Akt/mTOR pathway mediates signals from multiple rec

237 The PI3K/phosphoinositide-dependent kinase (PDK) 1 pathway r

238 Among the PI3K-Akt targets, 75% could be explained by a deactivati

239 the pan-PI3K inhibitor pilaralisib, and the PI3K-alpha-restricted inhibitor alpelisib each diminishe

240 gulation of FOXO4 is primed, in part, by the PI3K/AKT effector axis of oncogenic RAS signalling.

241 importance of phosphatases that control the PI3K pathway, we assessed Treg cell induction in vitro,

242 lation, we hypothesized that cotargeting the PI3K and proteasome pathways might synergistically inhib

243 cemia and hyperinsulinemia also impaired the PI3K/Akt while enhancing the ERK/p38MAPK/JNK pathways in

244 tissue was evaluated for aberrations in the PI3K pathway.

245 other key signaling pathways, including the PI3K/Akt/mTOR and MAPK pathways, and with other receptor

246 oteins with related functions, including the PI3K/mTOR pathway, altered in 60% of lines; BRCA DNA rep

247 chanism for these effects which involves the PI3K/Akt signaling and apoptotic pathway.

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

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

250 duction of ROS, H2O2, and NO, modulating the PI3K/Akt, MAPK, NFkappaB and Nrf2 pathways and their dow

251 ed by either inhibition or activation of the PI3K and MAPK pathways.

252 the Golgi and optogenetic recruitment of the PI3K C2A kinase domain to the TGN-induced deltaR export

253 reast cancer, including an evaluation of the PI3K pathway activation status as a biomarker for clinic

254 Pharmacologic inhibition of the PI3K pathway in tumor-bearing Kit(V558Delta/+) mice with

255 riments targeting HER2 and components of the PI3K pathway supported proteogenomic response prediction

256 ing infection and identify regulation of the PI3K pathway, a mechanism previously shown to silence au

257 ownstream signaling toward activation of the PI3K, and recruitment of F-actin and of the actin-branch

258 Activation of the PI3K-AKT signaling cascade is a common critical event du

259 ur data demonstrate that deregulation of the PI3K-AKT/ mTORC1/ p70S6K pathways, an event frequently o

260 Perturbation of the PI3K-PKB pathway, or the loss of negative regulators of

261 ly, CTLA4 binding promoted activation of the PI3K/Akt/mTOR axis and FoxO1 nuclear exclusion in DCs, l

262 Activation of the PI3K/AKT/mTOR pathway occurs frequently in breast cancer

263 ly upregulating PIK3IP1, a suppressor of the PI3K/Akt/mTOR pathway.

264 to monitor drug-induced perturbation of the PI3K/mTOR pathway in sarcomas.

265 ic changes that occur with inhibition of the PI3K/mTOR pathway.

266 mutations that occur in genes regulating the PI3K/Akt/mTOR pathway-a key pathway in neuronal growth a

267 Finally, IL-15 robustly stimulated the PI3K/Akt/mTOR and MEK/ERK pathways in CD56bright compare

268 mors driven by genetic lesions targeting the PI3K cascade.

269 d IL-15, but only an inhibitor targeting the PI3K/Akt/mTOR pathway blocked proliferation induced by I

270 Our results support the notion that the PI3K signaling pathway might be activated, both dependen

271 Altogether, these data indicate that the PI3K-PKB-GSK-3 pathway is a novel regulatory axis that i

272 RF72-ALS cases, we also demonstrate that the PI3K/Akt cell survival signalling pathway is dysregulate

273 However, given that the PI3K/Akt/mechanistic target of rapamycin (mTOR) pathway

274 ch promotes glioma proliferation through the PI3K-mTOR pathway.

275 ioma proliferation and apoptosis through the PI3K/AKT pathways was demonstrated by supplementation wi

276 ted to stress responses mediated through the PI3K/TOR or MAPK signaling cascades, which act to protec

277 enriched in signalling pathways in which the PI3K-Akt signalling pathway was identified as a hub.

278 RK1/2-MAPK pathway, which converges with the PI3K/Akt/mTOR (mechanistic target of rapamycin) pathway

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

280 These PI3K lipid kinases phosphorylate the constitutive lipid

281 nstrate differential mode of action of three PI3K inhibitors on IFN-I.

282 Ca(2+) mobilization, and aggregation through PI3K class Ibeta (PI3K-Ibeta).

283 ast to wild-type platelets is insensitive to PI3K inhibitors.

284 erapeutically to target tumours resistant to PI3K/mTOR inhibition.

285 es trastuzumab and pertuzumab but respond to PI3K inhibitor buparlisib (TPB).

286 experiments in vitro suggested that unequal PI3K/mechanistic target of rapamycin signaling drives in

287 5) whose suppression induced cell death upon PI3K inhibition.

288 eased proliferation of PDGFRalpha+ cells via PI3K/Akt signaling pathway.

289 s effect was preserved in vivo after ex vivo PI3K-delta inhibition in CD8(+) T cells destined for ado

290 tion within hours of hypoxic exposure, where PI3K-Akt signalling was suggested to have a nodal role b

291 striction or growth factor starvation, where PI3K/mTOR signalling is decreased, matrix-attached human

292 Treatment of cancer cells with PI3K inhibitors or taxane causes FOXO1 localization in t

293 by demonstrating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway that is associated wit

294 PSMA expression correlated with PI3K-Akt signaling in cells, animal models, and patients

295 e showed that suppressing these 5 genes with PI3K inhibition induced tumor regression.

296 y by the combination of a MEK inhibitor with PI3K or cyclin-dependent kinase 4/6 inhibitors.

297 normal association of the E349K mutant with PI3K, cells expressing the mutant failed to elevate phos

298 ective response was limited to patients with PI3K pathway aberration.

299 s of the PIM2 and ZAK kinases synergize with PI3K inhibition.

300 eir oncogenic dependencies when treated with PI3K and AKT inhibitors.