ライフサイエンスコーパス: phosphoinositide 3-kinase

1 ate sodium current (INa-L) via inhibition of phosphoinositide 3-kinase.

2 ity, but this was not mediated by inhibiting phosphoinositide 3-kinase.

3 ndent on FcRgamma, Toll-like receptor 4, and phosphoinositide 3-kinase.

4 pression of insulin receptor substrate 1 and phosphoinositide 3-kinase.

5 utation in p110alpha, a catalytic subunit of phosphoinositide 3-kinase.

6 Interestingly, inhibition of phosphoinositide 3-kinase abolished GRK2-mediated betaAR

7 clusion, this study identifies Met-dependent phosphoinositide 3-kinase activation in proximal tubules

8 Our findings suggest that phosphoinositide 3-kinase activation promotes PKM2 phosp

9 PI3K (phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-act

10 IGF1R can provide protection independent of phosphoinositide 3-kinase-Akt and heat-shock protein 70;

11 ex 2 is independent of the classical insulin-phosphoinositide 3-kinase-Akt pathway, highlighting a no

12 rylation, which is mediated primarily by the phosphoinositide 3-kinase-Akt pathway.

13 e findings further support engagement of the phosphoinositide 3-kinase-AKT signaling axis by H-Ras.

14 is response was mediated in part through the phosphoinositide 3-kinase-AKT signaling pathway.

15 aling mechanism whereby lipolysis blocks the phosphoinositide 3-kinase-Akt-mTOR pathway, resulting in

16 kinase 1 and 2 (MAPK/ERK1/2) inhibition, and phosphoinositide 3 kinase/Akt (IP3/Akt) inhibition, indi

17 s/extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/AKT and signal transducer and

18 ur results demonstrate the importance of the phosphoinositide 3-kinase/AKT pathway in modulating the

19 ha (HIF-1alpha) stabilization, including the phosphoinositide 3-kinase/Akt pathway, Siah1, and Siah2,

20 Nonsignificant effects on phosphoinositide 3-kinase/Akt signal transduction were o

21 First, phosphoinositide 3-kinase/Akt signaling is hyperactivate

22 n through phosphatase and tensin homolog and phosphoinositide 3-kinase/Akt signaling pathways.

23 specially those with sustained activation of phosphoinositide 3-kinase/AKT signaling.

24 of HCK reduced survival and attenuated BTK, phosphoinositide 3-kinase/AKT, and mitogen-activated pro

25 inactivation served to unmask a prosurvival phosphoinositide 3-kinase/AKT-dependent signaling pathwa

26 Rac1 and downregulating p22(phox) through a phosphoinositide 3-kinase/Akt-mediated mechanism.

27 ion of mitogen-activated protein kinases and phosphoinositide 3-kinase/Akt.

28 r signaling pathway, the ABL kinase, and the phosphoinositide 3-kinase/AKT/mammalian target of rapamy

29 pattern of mutations in the RTK-RAS-RAF and phosphoinositide 3-kinase/AKT/mammalian target of rapamy

30 nd protein synthesis, the latter through the phosphoinositide 3-kinase/Akt/nuclear factor kappaB path

31 tiple signaling pathways, including the PTEN/phosphoinositide-3-kinase/AKT axis, WNT/beta-catenin sig

32 ve been proposed, such as activations of the phosphoinositide-3-kinase/Akt pathway and p38 mitogen-ac

33 VEGF receptor-2 signaling via the phosphoinositide-3-kinase/Akt pathway was required for t

34 ating mutations in PIK3CA, the gene encoding phosphoinositide-(3)-kinase alpha (PI3Kalpha), are frequ

35 Depletion of class II phosphoinositide-3 kinase alpha (PI3K C2A), but not inhi

36 subtype that showed increased sensitivity to phosphoinositide 3-kinase and fibroblast growth factor r

37 ifloxacin, an IKr blocker with no effects on phosphoinositide 3-kinase and INa-L prolonged APD acutel

38 ations indicated that CLPTM1L interacts with phosphoinositide 3-kinase and is essential for Ras-induc

39 pairs KIT signaling pathways, thus affecting phosphoinositide 3-kinase and MAPK pathways in human mas

40 in alpha5 at the junctions to suppress local phosphoinositide 3-kinase and Rac activity.

41 ics of chemoattractant-induced activation of phosphoinositide 3-kinase and Rac effectors.

42 Phosphoinositide 3-kinase and Rac polarization depend sp

43 Phosphoinositide 3-kinase and the small GTPase Rac displ

44 implications for cancer treatments targeting phosphoinositide 3-kinases and Akt because they may impa

45 vation of mitogen-activated protein kinases, phosphoinositide 3-kinase, and NF-kappaB.

46 requires the multimodular B-cell adaptor for phosphoinositide 3-kinase (BCAP).

47 Class IA phosphoinositide 3-kinase beta (PI3Kbeta) is considered

48 Inhibition of IGF1R or phosphoinositide 3-kinase blocked PR-B-dependent CTSD mR

49 oughput virtual screening (HTVS) study using phosphoinositide 3-kinase (both PI3Kgamma and PI3Kdelta)

50 Also, inhibition of phosphoinositide 3-kinase but not NF-kappaB had a simila

51 Here, we studied the function of class II phosphoinositide 3-kinase-C2alpha (PI3K-C2alpha) in rena

52 The protein expression of phosphoinositide 3-kinase catalytic subunit PI3K(p110alp

53 n, but requires concurrent activation of the phosphoinositide 3-kinase catalytic subunit, PIK3CA.

54 cterize Beclin1, a proximal component of the phosphoinositide 3-kinase class III lipid-kinase complex

55 Specifically, phosphoinositide-3 kinases (class I PI3Ks, beta and gamm

56 lture, we show that the p110delta isoform of phosphoinositide 3-kinase co-localizes with focal adhesi

57 lated GRP78 then bound to VPS34, a class III phosphoinositide-3 kinase, consequently preventing the s

58 Phosphoinositide 3-kinase delta (PI3Kdelta) controls int

59 Aberrant signaling of phosphoinositide 3-kinase delta (PI3Kdelta) has been imp

60 Inhibition of phosphoinositide 3-kinase delta (PI3Kdelta) is an appeal

61 n-of-function variants in the genes encoding phosphoinositide 3-kinase delta (PI3Kdelta) lead to accu

62 p110delta protein, the catalytic subunit of phosphoinositide 3-kinase delta (PI3Kdelta), encoded by

63 which can be achieved with theophylline and phosphoinositide 3-kinase delta inhibitors.

64 ular profile characterized by an increase in phosphoinositide 3-kinase delta, macrophage migration in

65 lls from patients treated with idelalisib, a phosphoinositide-3-kinase delta inhibitor recently appro

66 adding idelalisib, a first-in-class targeted phosphoinositide-3-kinase delta inhibitor, to bendamusti

67 Duvelisib is an oral dual inhibitor of phosphoinositide 3-kinase-delta (PI3K-delta) and PI3K-ga

68 estin-1 to the plasma membrane, and promoted phosphoinositide 3-kinase-dependent activation of protei

69 The enhanced respiratory burst was phosphoinositide 3-kinase-dependent but delayed apoptosi

70 enhances the glycine-activated current in a phosphoinositide 3-kinase-dependent manner, a positive f

71 Phosphoinositide 3-kinase enhancer (PIKE) is a group of

72 Conversely, depleting phosphoinositide-3 kinase enhancer (PIKE) expression by

73 Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is require

74 Furthermore, the dependence on phosphoinositide 3-kinase for P-TEFb recruitment to IL1B

75 Phosphoinositide 3-kinase gamma (PI3Kgamma) has profound

76 We show that phosphoinositide 3-kinase gamma (PI3Kgamma) is a key pla

77 Phosphoinositide 3-kinase gamma (PI3Kgamma) is an attrac

78 mediated G-protein-coupled receptor kinase 2-phosphoinositide 3-kinase gamma membrane recruitment, an

79 Using an established enzyme phosphoinositide 3-kinase gamma, we discuss the insights

80 its ability to directly bind InsR, IRS1, and phosphoinositide 3-kinase, GIV serves as a key hub in th

81 an oral reversible inhibitor of all class I phosphoinositide-3-kinases, has shown antitumoral activi

82 Class I phosphoinositide 3-kinases have an established role in t

83 as independent of the regulatory function of phosphoinositide 3-kinase in mediating the metabolic act

84 cted findings cast doubt over the utility of phosphoinositide 3-kinase inhibition in acute respirator

85 to include time and INa-L in evaluating the phosphoinositide 3-kinase inhibition-derived proarrhythm

86 phenotype of patient cells was resistant to phosphoinositide 3-kinase inhibition.

87 acellular signal-regulated kinase) and PI3K (phosphoinositide-3-kinase) inhibition, we find the FGF r

88 athways that activate macropinocytosis, with phosphoinositide 3-kinase inhibitor activation stimulati

89 Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mT

90 uggest that chronic (hours) drug exposure to phosphoinositide 3-kinase inhibitors used in cancer can

91 nal phenotype, and this could be reversed by phosphoinositide 3-kinase inhibitors.

92 ownregulation of the PI3K inhibitor PIK3IP1 (phosphoinositide-3-kinase interacting protein 1), leadin

93 Vps34 (the human class III phosphoinositide 3-kinase) is a lipid kinase involved in

94 n the co-receptor ICOS and the activation of phosphoinositide-3 kinase leading to the expression of k

95 tion of the 5' to 3' exonuclease EXO1 by the phosphoinositide 3-kinase-like kinases ATM (ataxia telan

96 on of the essential NMD effector UPF1 by the phosphoinositide-3-kinase-like kinase (PIKK) SMG-1 is a

97 veral pathways [including, among others, the phosphoinositide 3-kinase/mammalian target of rapamycin

98 3-RAF1 aberrantly activate both the MAPK and phosphoinositide-3 kinase/mammalian target of rapamycin

99 In this study, we tested whether the dual phosphoinositide 3-kinase/mechanistic target of rapamyci

100 resulted in dose-dependent inhibition of the phosphoinositide 3-kinase/mechanistic target of rapamyci

101 tracellular signal-regulated kinase/RSK1 and phosphoinositide-3 kinase/mTOR pathway, which synergizes

102 Although phosphoinositide 3-kinase pathway alterations are presen

103 location biosensor for signaling through the phosphoinositide 3-kinase pathway, along with a cytosoli

104 trisphosphate, a downstream effector for the phosphoinositide 3-kinase pathway, in the pipette inhibi

105 arrhythmias by augmenting INa-L through the phosphoinositide 3-kinase pathway.

106 TEN) is a critical negative regulator of the phosphoinositide-3 kinase pathway, members of which play

107 Tumor blocks were collected for phosphoinositide-3-kinase pathway mutation analysis.

108 1 (SHIP1) is an endogenous inhibitor of the phosphoinositide-3-kinase pathway that is involved in th

109 t kinase 7 pathway as revealed by the use of phosphoinositide 3-kinase -pathway-specific inhibitors a

110 For example, the PI3K (phosphoinositide 3-kinase) pathway connected to the prod

111 as focal adhesion kinase (FAK), Src, c-Cbl, phosphoinositide 3-kinase (PI-3K), and Rho-GTPases.

112 Phosphoinositide 3-kinase (PI3-K) is involved in both In

113 rain neuroblasts (NBs) in Drosophila utilize Phosphoinositide 3-kinase (PI3-kinase) and DE-cadherin t

114 RAS signalling through phosphoinositide 3-kinase (PI3-Kinase) has been shown to

115 Phosphoinositide 3 kinase (PI3K) is a direct upstream ac

116 could be a result of down-regulation of the phosphoinositide 3 kinase (PI3K)/AKT protein kinase/insu

117 Mutations that deregulate Notch1 and Ras/phosphoinositide 3 kinase (PI3K)/Akt signalling are prev

118 sing this model, we report that constitutive phosphoinositide 3-kinase (PI3K) activation caused by PT

119 led that platelet DREAM positively regulates phosphoinositide 3-kinase (PI3K) activity during platele

120 Phosphoinositide 3-kinase (PI3K) activity is important f

121 Phosphoinositide 3-kinase (PI3K) activity is stimulated

122 evels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased

123 (PTEN), a tumor suppressor that counteracts phosphoinositide 3-kinase (PI3K) activity, is one of the

124 In the developing vasculature, the phosphoinositide 3-kinase (PI3K) alpha isoform integrate

125 ectly on cells through pathways, such as the phosphoinositide 3-kinase (PI3K) and Janus kinase-signal

126 fication or ligand overexpression maintained phosphoinositide 3-kinase (PI3K) and MEK/ERK signaling e

127 lls results in cooperative activation of the phosphoinositide 3-kinase (PI3K) and mitogen-activated p

128 )/LYN complexes, which allows recruitment of phosphoinositide 3-kinase (PI3K) and phosphorylation of

129 Phosphoinositide 3-kinase (PI3K) and the proteasome path

130 ed, in silico screen nominated inhibitors of phosphoinositide 3-kinase (PI3K) as NFE2L2 antagonists.

131 Phosphoinositide 3-kinase (PI3K) beta signaling is requi

132 ficient of SHP2 binding (PDGFRalpha-F720) or phosphoinositide 3-kinase (PI3K) binding (PDGFRalpha-F73

133 Inhibition of phosphoinositide 3-kinase (PI3K) by Ly294002 or inhibiti

134 (I/R) injury inactivates the p85 subunit of phosphoinositide 3-kinase (PI3K) by nitration and divert

135 he up-regulation of the p110gamma subunit of phosphoinositide 3-kinase (PI3K) class IB and increased

136 ct on Gbetagamma-mediated phospholipase C or phosphoinositide 3-kinase (PI3K) gamma activation in vit

137 Phosphoinositide 3-kinase (PI3K) generation of PI(3,4,5)

138 relin were blocked by co-administration of a phosphoinositide 3-kinase (PI3K) inhibitor (LY294002).

139 N-acetylcysteine and phosphoinositide 3-kinase (PI3K) inhibitor restored the

140 demonstrated that concomitant use of MEK and phosphoinositide 3-kinase (PI3K) inhibitors (MEKi/PI3Ki)

141 120 (Buparlisib) is one of the most advanced phosphoinositide 3-kinase (PI3K) inhibitors for the trea

142 Phosphoinositide 3-kinase (PI3K) is deregulated in a wid

143 Class IA phosphoinositide 3-kinase (PI3K) is essential for clonal

144 Inhibitors of the class I phosphoinositide 3-kinase (PI3K) isoform PI3Kalpha have

145 rgic responses and (2) to define the role of phosphoinositide 3-kinase (PI3K) isoforms in sequential

146 to the functions of the ubiquitous class IA phosphoinositide 3-kinase (PI3K) isoforms, p110alpha and

147 but not by AG1478, indicating that Gi/o and phosphoinositide 3-kinase (PI3K) mediate the increase in

148 sphorylation and renal tumor growth by other phosphoinositide 3-kinase (PI3K) or AKT inhibitor treatm

149 nsulin regulates ER stress via the metabolic/phosphoinositide 3-kinase (PI3K) or alternate signaling

150 itors or knockdown of PGE2 receptor 4 (EP4), phosphoinositide 3-kinase (PI3K) p85alpha, extracellular

151 The phosphoinositide 3-kinase (PI3K) pathway is believed to

152 Because regulation of the phosphoinositide 3-kinase (PI3K) pathway is critical for

153 Activation of the phosphoinositide 3-kinase (PI3K) pathway occurs frequent

154 Activation of the phosphoinositide 3-kinase (PI3K) pathway occurs widely i

155 The phosphoinositide 3-kinase (PI3K) pathway plays an integr

156 The phosphoinositide 3-kinase (PI3K) pathway regulates multi

157 ubtype frequently harbors aberrations in the phosphoinositide 3-kinase (PI3K) pathway, raising the po

158 suppressor in normal cells to inactivate the phosphoinositide 3-kinase (PI3K) pathway, thus suppressi

159 The phosphoinositide 3-kinase (PI3K) pathway, with downstrea

160 roliferation through directly inhibiting the phosphoinositide 3-kinase (PI3K) pathway.

161 ed prosurvival signaling via an EGF receptor/phosphoinositide 3-kinase (PI3K) pathway.

162 on by high dose LPS, potentially through the phosphoinositide 3-kinase (PI3K) pathway.

163 We found that inhibition of phosphoinositide 3-kinase (PI3K) reduced OSR1 activation

164 Here we examined how signaling downstream of phosphoinositide 3-kinase (PI3K) regulates different ste

165 Effectors of the phosphoinositide 3-kinase (PI3K) signal transduction pat

166 Upregulation of phosphoinositide 3-kinase (PI3K) signaling is a common a

167 Self-amplification of phosphoinositide 3-kinase (PI3K) signaling is believed t

168 Activating mutations in the phosphoinositide 3-kinase (PI3K) signaling pathway are f

169 Insulin activation of phosphoinositide 3-kinase (PI3K) signaling regulates glu

170 e demonstrate that CUX1 deficiency activates phosphoinositide 3-kinase (PI3K) signaling through direc

171 Diabetes is associated with a reduction in phosphoinositide 3-kinase (PI3K) signaling, which regula

172 of insulin-like growth factor-1R/INSR-driven phosphoinositide 3-kinase (PI3K) signaling.

173 al branching mechanism that is stabilized by phosphoinositide 3-kinase (PI3K) signaling.

174 ads to HER3-mediated oncogenic activation of phosphoinositide 3-kinase (PI3K) signaling.

175 hanisms such as tyrosine phosphorylation and phosphoinositide 3-kinase (PI3K) signaling.

176 sally associated with increased constitutive phosphoinositide 3-kinase (PI3K) signaling; untreated ne

177 Ralpha), produced in tumour cells, activates phosphoinositide 3-kinase (PI3K) signalling by binding t

178 d mGluR I subsequently induces activation of phosphoinositide 3-kinase (PI3K) through phosphorylation

179 We investigated the contributions of phosphoinositide 3-kinase (PI3K) to KRAS-initiated tumor

180 we examine the Rag GTPases and the class III phosphoinositide 3-kinase (PI3K) Vps34, two mediators of

181 Both myosin II and phosphoinositide 3-kinase (PI3K) were found to hold stri

182 tic signaling by the pre-TCR/Notch effector, phosphoinositide 3-kinase (PI3K), and by inositol-trisph

183 of mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and interferon regulat

184 encoding the p110alpha catalytic subunit of phosphoinositide 3-kinase (PI3K), have been shown to tra

185 ncover the role of Vps34, the sole class III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs

186 , the gene encoding the catalytic subunit of phosphoinositide 3-kinase (PI3K), occur with high freque

187 Ras/mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), p63, and Wnt signaling

188 ibuted to failure of the antibody to inhibit phosphoinositide 3-kinase (PI3K), which is activated by

189 The phosphoinositide 3-kinase (PI3K), which phosphorylates p

190 ras, early Eomes induction in vitro required phosphoinositide 3-kinase (PI3K)-AKT but not extracellul

191 FR-independent activation of the MEK-ERK and phosphoinositide 3-kinase (PI3K)-AKT pathways.

192 inase 1 (PDK1) is a pivotal regulator in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway t

193 To test if phosphoinositide 3-kinase (PI3K)-alpha (PIK3CA), another

194 1 report a novel regulatory role of class II phosphoinositide 3-kinase (PI3K)-C2alpha in the morpholo

195 Phosphoinositide 3-kinase (PI3K)-dependent activation of

196 cells, SCF strongly induced pAKT(S473) in a phosphoinositide 3-kinase (PI3K)-dependent manner, which

197 bly, nearly all KRAS deficient cells exhibit phosphoinositide 3-kinase (PI3K)-dependent mitogen-activ

198 We hypothesized that a phosphoinositide 3-kinase (PI3K)-dependent signaling pat

199 iphosphate at the plasma membrane to enhance phosphoinositide 3-kinase (PI3K)-dependent tumor cell in

200 HER3 amplifies phosphoinositide 3-kinase (PI3K)-driven tumorigenesis an

201 red systolic contractility and activated the phosphoinositide 3-kinase (PI3K)-pathway in the heart.

202 t contain mutant Keap1, by inhibition of the phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB)/

203 c cells show activation of Ras-signaling and phosphoinositide 3-kinase (PI3K)-signaling pathways and

204 that include focal adhesion kinase (FAK) and phosphoinositide 3-kinase (PI3K).

205 ctivated during the polarization process, is phosphoinositide 3-kinase (PI3K).

206 00-fold selectivity for cellular mTOR versus phosphoinositide 3-kinase (PI3K).

207 Genes in the phosphoinositide 3-kinase (PI3K)/AKT pathway are the mos

208 Activation of the phosphoinositide 3-kinase (PI3K)/AKT pathway in neurobla

209 Intrinsic resistance to agents targeting phosphoinositide 3-kinase (PI3K)/AKT pathway is one of t

210 ete on chromosome 10 (PTEN) and promoted the phosphoinositide 3-kinase (PI3K)/Akt pathway, which in t

211 tly contributes to activating the consequent phosphoinositide 3-kinase (PI3K)/Akt signaling pathway.

212 PTEN inhibits phosphoinositide 3-kinase (PI3K)/Akt signaling, a common

213 w that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K)/Akt-dependent manner, r

214 Dysfunctional signaling through the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway leads

215 n the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rap

216 The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)

217 Of these, the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)

218 activities of bone morphogenetic protein and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)

219 The androgen receptor (AR) and the phosphoinositide 3-kinase (PI3K)/protein kinase B/mammal

220 Moreover, a Phosphoinositide 3-kinase (PI3K)alpha inhibitor disrupte

221 ted kinases [Bruton's tyrosine kinase (BTK), phosphoinositide 3-kinase (PI3K)delta], which will chang

222 Class I phosphoinositide 3-kinases (PI3K) are heterodimers compo

223 inflammatory molecules and the activation of phosphoinositide 3-kinases (PI3K) in a process that requ

224 e elucidation of the biological functions of phosphoinositide 3-kinases (PI3K) was realized years ago

225 In PC12 cells, inhibition of phosphoinositide-3 kinase (PI3K) activity blocked export

226 Phosphoinositide-3 kinase (PI3K) generates PtdIns(3,4,5)

227 , which expresses a constitutively activated phosphoinositide-3 kinase (PI3K) in the intestinal epith

228 SMG-1 is a phosphoinositide-3 kinase (PI3K) involved in mediating n

229 The phosphoinositide-3 kinase (PI3K) pathway is deregulated

230 a tumor suppressor and an antagonist of the phosphoinositide-3 kinase (PI3K) pathway.

231 f activated AKT owing to the deregulation of phosphoinositide-3 kinase (PI3K) signaling, and depletio

232 ed myosin II (MyoII), increased and extended phosphoinositide-3-kinase (PI3K) activity, and extended

233 el hepatocyte growth factor (HGF) stimulated phosphoinositide-3-kinase (PI3K) and mitogen activated p

234 ase-mediated ectodomain shedding, activating phosphoinositide-3-kinase (PI3K) and mitogen-activated p

235 d by the activation of different isoforms of phosphoinositide-3-kinase (PI3K) and the downstream sign

236 h encodes the p110alpha catalytic subunit of phosphoinositide-3-kinase (PI3K) are frequently found in

237 Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha

238 genic mutations in PIK3CA, which encodes the phosphoinositide-3-kinase (PI3K) catalytic subunit p110a

239 increased stem-cell-factor activation of the phosphoinositide-3-kinase (PI3K) effectors Akt/mammalian

240 (2+) overload was partially prevented by the phosphoinositide-3-kinase (PI3K) inhibitor, LY294002.

241 a fly-human cross-species comparison of the phosphoinositide-3-kinase (PI3K) interactome in a drosop

242 The role of the phosphoinositide-3-kinase (PI3K) pathway was characteriz

243 thway, which was mediated by RET through the phosphoinositide-3-kinase (PI3K) pathway.

244 thereby uncoupling STAT5 phosphorylation and phosphoinositide-3-kinase (PI3K) pathways.

245 a clear degenerating axons slowly due to low phosphoinositide-3-kinase (PI3K) signalling and, subsequ

246 holipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kinase (PI3K), and subsequently to ph

247 ame intracellular signaling kinases, such as phosphoinositide-3-kinase (PI3K), protein kinase C (PKC)

248 r commonly deregulated pathway in CRC is the phosphoinositide-3-kinase (PI3K)-AKT pathway.

249 Phosphoinositide-3-kinase (PI3K)-alpha inhibitors have s

250 s in PIK3R1 encoding a regulatory subunit of phosphoinositide-3-kinase (PI3K).

251 4,5-trisphosphate (PIP3) by the lipid kinase phosphoinositide-3-kinase (PI3K).

252 Phosphoinositide 3-kinase/PI3K functioned as an essentia

253 Classically Class IB phosphoinositide 3-kinase (PI3Kgamma) plays a role in ex

254 rmacologic targeting of the gamma isoform of phosphoinositide 3-kinase (PI3Kgamma), highly expressed

255 We examined the role of phosphoinositide 3-kinases (PI3Ks) and Src-family kinase

256 The physiologic roles of the class II phosphoinositide 3-kinases (PI3Ks) and their contributio

257 Phosphoinositide 3-kinases (PI3Ks) are a family of lipid

258 The phosphoinositide 3-kinases (PI3Ks) are a family of lipid

259 Phosphoinositide 3-kinases (PI3Ks) are ubiquitous lipid

260 Phosphoinositide 3-kinases (PI3Ks) control many importan

261 sphosphate [PI(3,4,5)P3, or PIP3] by class I phosphoinositide 3-kinases (PI3Ks) is a major signaling

262 Phosphoinositide 3-kinases (PI3Ks) regulate several cell

263 f p110alpha, p110gamma, and p110delta type I phosphoinositide 3-kinases (PI3Ks), interacting via an a

264 lpha regulatory (PIK3R1) subunit of class IA phosphoinositide 3-kinases (PI3Ks).

265 Mutations in the catalytic subunit of phosphoinositide 3-kinase (PIK3CA) and other PI3K-AKT pa

266 either mitogen-activated protein kinases or phosphoinositide 3-kinase prevented the MP-induced endot

267 SF induces cardiomyocyte proliferation via a phosphoinositide 3-kinase-protein kinase B-cycle-depende

268 se proliferative effects were modulated by a phosphoinositide 3-kinase-protein kinase B-cycle-depende

269 a putative signaling protein upstream of the phosphoinositide 3-kinase-protein kinase B/AKT-mammalian

270 mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pa

271 Furthermore, LMP1 activated and triggered phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pa

272 ion, and invasion of Huh-7 cells through the phosphoinositide 3-kinase/protein kinase B pathway and i

273 through the aberrant expression of the TYRO3/phosphoinositide 3-kinase/protein kinase B signal transd

274 s (e.g., Ca(2+) -dependent protein kinase C, phosphoinositide 3-kinase/protein kinase B, mitogen-acti

275 everal signal transduction pathways, such as phosphoinositide 3-kinase/protein kinase B, which are cr

276 onical pathway involved in the activation of phosphoinositide 3-kinase/protein kinase K (PI3K/Akt) si

277 tive role for Phosphotase and tensin homolog/phosphoinositide 3-kinase (PTEN/PI3K) as a key point of

278 activation, signal transduction through the phosphoinositide-3 kinase-RAC-alpha serine/threonine-pro

279 Integrins promote high phosphoinositide 3-kinase/Rac activities at the free end

280 couples with distinct effectors to polarize phosphoinositide 3-kinase/Rac and myosin II light chain/

281 ic lymphocytic leukemia/lymphoma 10 (BCL10), phosphoinositide-3 kinase regulatory subunit 1 (PIK3R1),

282 factor 1 (IGF1), IGF1 receptor (IGF1R), and phosphoinositide-3-kinase, regulatory subunit 1 (alpha)

283 ghly conserved 3744-residue protein from the Phosphoinositide 3-Kinase-related kinase (PIKK) family a

284 The mammalian target of rapamycin (mTOR), a phosphoinositide 3-kinase-related protein kinase, contro

285 3 require its phosphorylation by a family of phosphoinositide-3-kinase-related-kinases (PIKKs), which

286 Inhibition of phosphoinositide 3-kinases, responsible for the synthesi

287 thways, including cell-cycle, p53 signaling, phosphoinositide 3-kinase signaling, mitogen-activated p

288 IVIg also induces suppression of phosphoinositide 3-kinase signaling, which plays a centr

289 YO16), which has been implicated in neuronal phosphoinositide 3-kinase signaling.

290 tream EGF receptor, SRC tyrosine kinase, and phosphoinositide 3-kinase signaling.

291 racellular signal-regulated kinase 1/2, p38, phosphoinositide-3 kinase signaling pathways.

292 nst the mitogen-activated protein kinase and phosphoinositide-3-kinase signaling pathways significant

293 (mitogen-activated protein kinase) and PI3K (phosphoinositide 3-kinase) signaling pathways, we discov

294 Phosphoinositide 3-kinase signalling in particular is kn

295 sely to sepsis and burns datasets but not to phosphoinositide 3-kinase signatures.

296 that synaptic PIP3 is generated by class IA phosphoinositide 3-kinases that associate with T cell re

297 Here we investigated the role of the phosphoinositide-3-kinase/v-akt murine thymoma viral onc

298 Here, we show that the class III phosphoinositide 3-kinase vacuolar protein sorting 34 (V

299 eted by specific inhibition of the class III phosphoinositide 3-kinase VPS34, results in prolonged ly

300 rther studies demonstrated an interaction of phosphoinositide 3-kinase with MARCKS, but not with phos