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

1 LPA receptor antagonists, and inhibitors of phosphoinositide 3 kinase.

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

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

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

5 lcium, protein kinase C, and to some extent, phosphoinositide 3-kinase.

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

7 te that this BPA effect involves ERalpha and phosphoinositide 3-kinase.

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

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

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

11 activator of transcription-5 (JAK2-STAT5) or phosphoinositide 3-kinase-Akt (PI3K-Akt) pathways to med

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

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

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

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

16 rophy, insulin resistance and reduced muscle phosphoinositide 3-kinase-Akt signalling are common char

17 gh activation of estrogen receptor (ER)alpha-phosphoinositide 3-kinase-Akt-Foxo1 signaling, which can

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

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

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

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

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

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

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

31 3CA are frequent in human breast cancer, and phosphoinositide 3-kinase alpha (PI3Kalpha) inhibitors h

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

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

34 osolic calcium, and downstream activation of phosphoinositide 3-kinase and extracellular signal-regul

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

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

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

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

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

40 se tensin homolog), thereby activating PI3K (phosphoinositide-3-kinase) and mTOR (mammalian target of

41 Activation of ERK, phosphoinositide 3-kinase, and NADPH oxidase-mediated re

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

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

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

45 Phosphoinositide 3-kinase beta (PI3Kbeta) is regulated b

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

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

48 ys, including calcium, protein kinase C, and phosphoinositide 3-kinase but not extracellular signal-r

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

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

51 Bruton's tyrosine kinase, phospholipase and phosphoinositide-3-kinase, calcium, and phosphoinositide

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

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

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

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

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

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

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

61 Phosphoinositide-3-kinase delta (PI3Kdelta) is a critica

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

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

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

65 sib, a first-in-class oral dual inhibitor of phosphoinositide 3-kinase-delta,-gamma, in RR iNHL in a

66 Phosphoinositide-3-kinase-delta (PI3Kdelta), a lipid kin

67 We investigated a next-generation phosphoinositide-3-kinase-delta inhibitor (PI3K-deltai),

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 contrast, inhibition of phospholipase C and phosphoinositide 3-kinase did not prevent stimulating ef

72 sib is a second-generation oral inhibitor of phosphoinositide-3 kinase, downstream of the B-cell rece

73 d phospholipase C (PLC)-driven (females) and phosphoinositide 3-kinase-driven (males) phospholipid me

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

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

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

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

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

79 ung fibroblasts through its interaction with phosphoinositide 3-kinase gamma (PI3Kgamma), forming nan

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

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

82 dependent on activation of G(i), ERK1/2, and phosphoinositide 3-kinase gamma/Akt at a molecular level

83 38alpha kinase, c-Jun N-terminal kinase-1/2, phosphoinositide 3-kinase-gamma, and p50 and p65 nuclear

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

85 ived neurons, enriched in pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI

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

87 endent on the activities of the lipid kinase phosphoinositide 3-kinase in addition to the Rho GTPases

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

89 s (phospholipases Cepsilon and Cgamma1), and phosphoinositide 3-kinase, in nociceptors.

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

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

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

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

94 However, treatment with the phosphoinositide 3-kinase inhibitor wortmannin did not d

95 a detoxified TLR4 agonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, prevented the LPS-m

96 can then be reactivated by the addition of a phosphoinositide 3-kinase inhibitor, which has previousl

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

98 cluding several chemoimmunotherapy regimens, phosphoinositide 3-kinase inhibitors, and lenalidomide p

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

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

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

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

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

104 le protein inhibitor), gedatolisib (PKI-587, phosphoinositide 3-kinase/mammalian target of rampamycin

105 mic aberrations in neurofibromin 1 (NF1) and phosphoinositide 3-kinases/mammalian target of rapamycin

106 3-RAF1 aberrantly activate both the MAPK and phosphoinositide-3 kinase/mammalian target of rapamycin

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

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

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

110 Here we demonstrate that phosphoinositide 3-kinase p110alpha in the fetus and the

111 Although phosphoinositide 3-kinase pathway alterations are presen

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

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

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

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

116 1 (SHIP1) is an endogenous inhibitor of the phosphoinositide-3-kinase pathway that is involved in th

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

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

119 oss of HACE1 impaired KSHV infection-induced phosphoinositide 3-kinase (PI3-K), protein kinase C-zeta

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

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

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

123 FR1 on alcohol drinking are mediated via the phosphoinositide 3 kinase (PI3K) signaling pathway.

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

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

126 B cell adaptor for phosphoinositide 3-kinase (PI3K) (BCAP) is a signaling a

127 of connexin channels in a system mediated by phosphoinositide 3-kinase (PI3K) activation, which allow

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

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

130 Phosphoinositide 3-kinase (PI3K) activity is stimulated

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

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

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

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

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

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

137 The phosphoinositide 3-kinase (PI3K) and RAS signaling pathw

138 tin A was recently shown to strongly inhibit phosphoinositide 3-kinase (PI3K) and the mammalian targe

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

140 enetics screen of kinase inhibitors revealed phosphoinositide 3-kinase (PI3K) as a central player tra

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

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

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

144 PIK3CD encodes the phosphoinositide 3-kinase (PI3K) catalytic subunit, p110

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

146 Phosphoinositide 3-kinase (PI3K) comprised of the p110be

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

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

149 orylation of the P85 subunit in the P85-P110 phosphoinositide 3-kinase (PI3K) heterodimer, which redu

150 Depletion of CD2AP or phosphoinositide 3-kinase (PI3K) inhibition results in l

151 Phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 abo

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

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

154 120 (Buparlisib) is one of the most advanced phosphoinositide 3-kinase (PI3K) inhibitors for the trea

155 ated protein kinase kinase MEK1/2, MEK5, and phosphoinositide 3-kinase (PI3K) inhibitors.

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

157 ches, we found that the p110delta isoform of phosphoinositide 3-kinase (PI3K) is involved in anterogr

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

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

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

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

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

163 sly documented that systemic inactivation of phosphoinositide 3-kinase (PI3K) p110alpha, the principa

164 s identified known interactions of BCAP with phosphoinositide 3-kinase (PI3K) p85 subunit and NCK ada

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

166 th factor receptor (EGFR) and its downstream phosphoinositide 3-kinase (PI3K) pathway are commonly de

167 Defects in the phosphoinositide 3-kinase (PI3K) pathway are shared char

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

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

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

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

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

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

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

175 in-1 to initiate signaling by the downstream phosphoinositide 3-kinase (PI3K) pathway, with consequen

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

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

178 therapies is constitutive activation of the phosphoinositide 3-kinase (PI3K) pathway.

179 ng, and FGFR3 preferentially used downstream phosphoinositide 3-kinase (PI3K) pathways, whereas FGFR2

180 hat inactivation of the p110delta isoform of phosphoinositide 3-kinase (PI3K) reduces anterograde axo

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

182 ith distinct genetic bases for perturbed BCR/phosphoinositide 3-kinase (PI3K) signaling and dysregula

183 To study the role of phosphoinositide 3-kinase (PI3K) signaling in pericyte b

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

185 Class IA phosphoinositide 3-kinase (PI3K) signaling is critical f

186 e sought to dissect the effects of increased phosphoinositide 3-kinase (PI3K) signaling on CD4(+) T-c

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

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

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

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

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

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

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

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

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

196 turn, the Gbetagamma complex signals through phosphoinositide 3-kinase (PI3K) to regulate kinocilium

197 (PDGF) signaling recruits the p85 subunit of Phosphoinositide 3-kinase (PI3K) to regulate mammalian l

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

199 adipose tissue, specifically at the level of phosphoinositide 3-kinase (PI3K), a key IIS effector mol

200 d to activation of the catalytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that co

201 vated by CD44, including phospholipase C and phosphoinositide 3-kinase (PI3K), also attenuated HMWH-i

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

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

204 encoding the p110delta catalytic subunit of phosphoinositide 3-kinase (PI3K), have highly penetrant

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

206 encoding the catalytic p110delta subunit of phosphoinositide 3-kinase (PI3K), result in hyperactivat

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

208 ind that growth factor signaling through the phosphoinositide 3-kinase (PI3K)-Akt pathway induces acu

209 INSM1 modulates the phosphoinositide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT

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

211 The ubiquitous, growth factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network

212 1 report a novel regulatory role of class II phosphoinositide 3-kinase (PI3K)-C2alpha in the morpholo

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

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

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

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

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

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

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

220 CD133, but not GLIS3 or WNT, is required for phosphoinositide 3-kinase (PI3K)/AKT Ser/Thr kinase (AKT

221 Hyperactivated phosphoinositide 3-kinase (PI3K)/Akt serine/threonine ki

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

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

224 t vitreous activate the signaling pathway of phosphoinositide 3-kinase (PI3K)/Akt, which plays a crit

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

226 We also identify active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in

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

228 Prior studies suggest that phosphoinositide 3-kinase (PI3K)/mammalian target of rap

229 The phosphoinositide 3-kinase (PI3K)/mechanistic target of r

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

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

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

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

234 The phosphoinositide 3-kinase (PI3K)beta isoform is uniquely

235 Class Ia phosphoinositide 3-kinases (PI3K) are critical mediators

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

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

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

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

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

241 a 4-gene predictive signature containing the phosphoinositide-3 kinase (PI3K) inhibitor, PTEN, for id

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

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

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

245 re we report that the regulatory subunits of phosphoinositide-3 kinase (PI3K)-p85alpha (PIK3R1) and p

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

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

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

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

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

251 (2+) overload was partially prevented by the phosphoinositide-3-kinase (PI3K) inhibitor, LY294002.

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

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

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

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

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

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

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

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

260 4,5-trisphosphate (PIP3) by the lipid kinase phosphoinositide-3-kinase (PI3K).

261 erine/threonine protein kinase that mediates phosphoinositide-3-kinase (PI3K)/AKT signalling.

262 The phosphoinositide-3-kinase (PI3K)/mammalian target of rap

263 Phosphoinositide 3-kinase/PI3K functioned as an essentia

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

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

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

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

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

269 Phosphoinositide 3-kinases (PI3Ks) are ubiquitous lipid

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

271 Phosphoinositide 3-kinases (PI3Ks) regulate several cell

272 ted protein kinases (MAPKs) ERK and p38, the phosphoinositide 3-kinases (PI3Ks), and the kinase mTOR.

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

274 Phosphoinositide-3-kinases (PI3Ks) are part of signal tr

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

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

277 hat GPER1 mediates the effects of E2 via the phosphoinositide 3-kinase-protein kinase B-mechanistic t

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

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

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

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

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

283 phosphoinositide 3-kinase/protein kinase B/mammalian tar

284 The survival signaling pathway phosphoinositide-3-kinase/protein kinase B that regulate

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

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

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

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

289 3 require its phosphorylation by a family of phosphoinositide-3-kinase-related-kinases (PIKKs), which

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

291 mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase signaling but in different for

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

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

294 links TCR signaling to mTORC2 activation via phosphoinositide 3-kinase signaling.

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

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

297 Phosphoinositide 3-kinase signalling in particular is kn

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

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

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