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

1 des the catalytic subunit p110alpha of PI3K (phosphatidylinositol 3-kinase).

2 rosine kinase, Bruton's tyrosine kinase, and phosphatidylinositol 3-kinase achieve promising clinical

3 , both of which target FOG2, an inhibitor of phosphatidylinositol 3-kinase activation.

4 GFR2 and MEK1/2 activation but not on p38 or phosphatidylinositol 3-kinase activation.

5 as a ubiquitous Rab7 effector that inhibits phosphatidylinositol 3-kinase activity on endosomes and

6 increased growth and activation of the PI3K (phosphatidylinositol-3 kinase)-AKT pathway in A375 but n

7 reduced cell migration and suppressed PI3K (phosphatidylinositol 3'-kinase)/Akt phosphorylation and

8 ptional activation of HIF1alpha mRNA and the phosphatidylinositol 3 kinase-AKT pathway to enhance HIF

9 (mut) on the Golgi signals and activates the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway, si

10 ling pathways, such as calcium mobilization, phosphatidylinositol 3-kinase-AKT activation, cortactin-

11 ess, E2-induced NRF2 accumulation depends on phosphatidylinositol 3-kinase-AKT activation.

12 xtracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase-Akt signaling pathways, wh

13 survival pathways including Jak/Stat, MapK, phosphatidylinositol 3-kinase-Akt, Ras-Raf-1, MEK1/extra

14 -based therapies, inhibitors that target the phosphatidylinositol 3-kinase-Akt-mammalian target of ra

15 Specifically, we show that the canonical phosphatidylinositol 3-kinase-Akt-mTOR signaling pathway

16 Inhibiting the phosphatidylinositol 3 kinase/AKT pathway, using NVP-BKM

17 last-derived NRG- and HGF-mediated PI3K/AKT (phosphatidylinositol 3'-kinase/AKT) survival signaling i

18 ncers, and its depletion results in enhanced phosphatidylinositol 3-kinase/Akt (PI3K/Akt) activation

19 DHCR24 expression, which, in turn, activates phosphatidylinositol 3-kinase/Akt and induces HO-1.

20 a mechanism involving decreased activity of phosphatidylinositol 3-kinase/AKT axis.

21 mmation, oxidative stress, and NF-kappaB and phosphatidylinositol 3-kinase/AKT pathway activation.

22 elay the oncogenic signals from the upstream phosphatidylinositol 3-kinase/Akt pathway in human cance

23 ignaling of the insulin-like growth factor 1/phosphatidylinositol 3-kinase/AKT pathway in skeletal mu

24 The phosphatidylinositol 3-kinase/Akt pathway, which is stro

25 PU.1 promoter activity via Syk, Src, and the phosphatidylinositol 3-kinase/Akt pathway.

26 disabled-1 and consecutive activation of the phosphatidylinositol 3-kinase/Akt pathway.

27 growth factor receptor and activation of the phosphatidylinositol 3-kinase/AKT pathway.

28 Inhibition of phosphatidylinositol 3-kinase/Akt reduced the (A-I)rHDL-

29 Furthermore, inhibition of the phosphatidylinositol 3-kinase/Akt self-renewal signaling

30 Phosphatidylinositol 3-kinase/Akt signaling acting downs

31 ic mutations in the receptor tyrosine kinase/phosphatidylinositol 3-kinase/Akt signaling cascade.

32 loss results in increased activation of the phosphatidylinositol 3-kinase/Akt signaling pathway, whi

33 1/2 mitogen-activated protein kinase and the phosphatidylinositol 3-kinase/AKT were attenuated in VSM

34 for the presence of a cross-talk among Smad, phosphatidylinositol 3-kinase/Akt, and Ca(2+) signaling

35 ne synergism, and glucolipotoxicity, through phosphatidylinositol 3-kinase/Akt- and extracellular sig

36 The phosphatidylinositol 3-kinase/AKT/mammalian target of ra

37 Phosphatidylinositol 3-kinase/AKT/mammalian target of ra

38 In conclusion, UDH displays mutations of the phosphatidylinositol 3-kinase/AKT/mTOR axis at different

39 ls, including the insulin receptor substrate/phosphatidylinositol-3 kinase/Akt (IRS-PI3K-Akt) pathway

40 Recent studies have shown that the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) pathway pla

41 vation of IRS1 downstream signaling pathways phosphatidylinositol-3-kinase/AKT and Erk mitogen-activa

42 gulation through integrins and activation of phosphatidylinositol-3-kinase/Akt and mitogen-activated

43 294002, which is a specific inhibitor of the phosphatidylinositol-3-kinase/Akt pathway.

44 Phosphatidylinositol 3-kinase alpha is an attractive tar

45 in betagamma subunits mediated activation of phosphatidylinositol 3-kinase and Akt to regulate eNOS a

46 )-related kinases spleen tyrosine kinase and phosphatidylinositol 3-kinase and inhibits vascular endo

47 Combinations with phosphatidylinositol 3-kinase and mammalian target of ra

48 f mHtt could be inhibited efficiently by the phosphatidylinositol 3-kinase and neutral sphingomyelina

49 tt secretion can be reduced significantly by phosphatidylinositol 3-kinase and neutral sphingomyelina

50 involved in cell-cycle regulation as well as phosphatidylinositol-3 kinase and receptor tyrosine kina

51 PP activated DFCP1 punctation in a class III phosphatidylinositol-3-kinase and calcium dependent mann

52 receptor 3 (CR3) and the signaling proteins phosphatidylinositol-3-kinase and caspase recruitment do

53 h the major oncogenic Ras effector pathways, phosphatidylinositol-3-kinase and mitogen-activated prot

54 from degradation, and modulates HGF-induced phosphatidylinositol-3-kinase and mitogen-activated prot

55 th erlotinib and by dual inhibition of PI3K (phosphatidylinositol 3'-kinase) and MEK.

56 tein, Ras, mitogen-activated protein kinase, phosphatidylinositol 3 kinase, and Ca(2+)/calcineurin si

57 rb2, leading to activation of enzymes Vav-1, phosphatidylinositol 3' kinase, and phospholipase C-gamm

58 signaling cascades, such as protein kinase, phosphatidylinositol 3-kinase, and extracellular recepto

59 tentiation in the hippocampus, activates the phosphatidylinositol 3-kinase, and increases GluA1 AMPAR

60 IR] tyrosine phosphorylation, IR substrate 1-phosphatidylinositol-3-kinase, and Akt phosphorylation a

61 spleen tyrosine kinase, Src family kinases, phosphatidylinositol-3-kinase, and p38 mitogen-activated

62 PTEN platelet-derived growth factor receptor/phosphatidylinositol 3-kinase axis as a novel regulator

63 intracellular calcium, protein kinase C, and phosphatidylinositol 3-kinases-based signaling.

64 B-cell adaptor for phosphatidylinositol 3-kinase (BCAP) is a signaling adap

65 sue of Blood, Laurent et al demonstrate that phosphatidylinositol 3-kinase beta (PI3Kbeta) activity i

66 s (eg, inhibitors of spleen tyrosine kinase, phosphatidylinositol 3-kinase, Bruton tyrosine kinase, a

67 ion between TIMP1 and CD63 and signaling via phosphatidylinositol 3-kinase, but not TIMP1 protease in

68 nterfering RNA screening identified class II phosphatidylinositol 3-kinase C2beta (PI3KC2beta) as the

69 ases such as Bruton tyrosine kinase (BTK) or phosphatidylinositol 3-kinase can induce mobilization of

70 RAS and phosphatidylinositol 3-kinase catalytic subunit alpha (P

71 CMV) replication and identified the class II phosphatidylinositol 3-kinase class II alpha (PI3K-C2A)

72 he top hit from our screen, the lipid kinase phosphatidylinositol 3-kinase class II alpha (PI3K-C2A),

73 lator, from the Beclin-1 complex, activating phosphatidylinositol 3-kinase class III activity and the

74 depletion of WNK1 stimulates focal class III phosphatidylinositol 3-kinase complex (PI3KC3) activity,

75 The class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) is c

76 The class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) is r

77 The class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) that

78 kinase complex and the PI3KC3-C1 (class III phosphatidylinositol 3-kinase complex I) lipid kinase co

79 utophagy-specific regulator of the class III phosphatidylinositol 3-kinase complex, promotes membrane

80 The Barkor/ATG14(L)-VPS34 (a class III phosphatidylinositol 3-kinase) complex and its product p

81 catalytic subunit in the class III PtdIns3 (phosphatidylinositol 3) kinase complexes, mediates the p

82 BECN1 is a core component of class III phosphatidylinositol-3-kinase complexes responsible for

83 Idelalisib is an oral phosphatidylinositol 3-kinase delta (PI3Kdelta) inhibito

84 We further show that SYK, BTK, and phosphatidylinositol 3-kinase delta (PI3Kdelta) inhibito

85 The phosphatidylinositol 3-kinase delta (PI3Kdelta) pathway

86 Inhibition of phosphatidylinositol 3-kinase delta (PI3Kdelta), a linch

87 Given synergistic preclinical activity with phosphatidylinositol 3-kinase delta and spleen tyrosine

88 Phosphatidylinositol-3-kinase delta (PI3Kdelta) mediates

89 Idelalisib, an oral inhibitor of phosphatidylinositol-3-kinase delta (PI3Kdelta), was eva

90 sib (GS-1101, CAL-101), an oral inhibitor of phosphatidylinositol 3-kinase-delta, was evaluated in a

91 vitro, high glucose conditions prompted the phosphatidylinositol 3 kinase-dependent upregulation of

92 n a p38 mitogen-activated protein kinase and phosphatidylinositol 3'-kinase-dependent manner.

93 nding to Rab8A is stimulated by insulin in a phosphatidylinositol 3-kinase-dependent manner, whereas

94 lation at Thr-308 occurred within 5 min, was phosphatidylinositol 3-kinase-dependent, and occurred in

95 owth- and survival-factor signalling through phosphatidylinositol 3-kinase effectors such as AKT and

96 growth factor receptor kinase or downstream phosphatidylinositol 3 kinase eliminated retinal ganglio

97 uces the dissociation of the Vps34 class III phosphatidylinositol-3-kinase from these organelles as t

98 nalysis of AAK, Aurora B kinase, MYC, BCL-2, phosphatidylinositol 3-kinase gamma, and Notch1 expressi

99 it-interacting peptide betaark-ct and by the phosphatidylinositol 3-kinase-gamma (PI3Kgamma) inhibito

100 The phosphatidylinositol 3-kinase hotspot mutation (E545K) w

101 ilar to the "butterfly effect" described for phosphatidylinositol 3-kinase Ialpha, whereby through ap

102 b, an oral inhibitor of the delta isoform of phosphatidylinositol 3-kinase, in combination with ritux

103 of mammary epithelial cells (MECs) with the phosphatidylinositol 3-kinase inhibitor BKM120 abolishes

104 The phosphatidylinositol 3-kinase inhibitor GDC-0941 was ine

105 HGF effects were blocked by phosphatidylinositol-3 kinase inhibitor and by MET-block

106 r types lends credence to the development of phosphatidylinositol 3-kinase inhibitors alongside the u

107 Macrophages were incubated with pan-phosphatidylinositol 3-kinase inhibitors or PI3Kp110alph

108 HDACIs also synergize with phosphatidylinositol 3-kinase inhibitors to inhibit tumo

109 e kinase, mammalian target of rapamycin, and phosphatidylinositol 3-kinase inhibitors, but not protea

110 mal pool of PI3P, generated by the class III phosphatidylinositol 3-kinase, is important for the Cb-m

111 elangiectasia mutated (ATM), a member of the phosphatidylinositol 3 kinase-like kinase family, is a m

112 are responsible for activating the two major phosphatidylinositol 3-kinase-like kinases (PI3KKs) invo

113 nt biochemical and cellular activity against phosphatidylinositol-3 kinase-like kinase (PIKK) family

114 proach, and an shRNA screen converged on the phosphatidylinositol 3-kinase/mammalian target of rapamy

115 ream regulation by insulin/IGF signaling via phosphatidylinositol-3 kinase/mammalian target of rapamy

116 Compounds targeting phosphatidylinositol-3-kinase/mammalian target of rapamy

117 These results suggest that the phosphatidylinositol 3-kinase/mTOR pathway is involved i

118 les critical for macropinocytosis, including phosphatidylinositol 3-kinases, myosin light-chain kinas

119 Phosphatidylinositol 3-kinase p110delta isoform (PI3K p1

120 nase kinase 1/2 pathway activates, while the phosphatidylinositol 3 kinase pathway represses SHP in a

121 s a key signaling molecule downstream of the phosphatidylinositol 3-kinase pathway and is a master re

122 stinct consequences on the activation of the phosphatidylinositol 3-kinase pathway in endometrial epi

123 rations in one of the three key genes of the phosphatidylinositol 3-kinase pathway, PIK3CA, PTEN, and

124 onocyte migration by activation of the PI3K (phosphatidylinositol 3'-kinase) pathway.

125 d through activation of the inflammasome and phosphatidylinositol 3-kinase pathways.

126 ion), or MAPK/PI3K (mitogen-activated kinase/phosphatidylinositol-3 kinase) pathways were found in al

127 e potent inhibitors of Plasmodium falciparum phosphatidylinositol-3-kinase (PfPI3K), revealing an une

128 eptor-ras signaling pathways, as well as the phosphatidylinositol 3-kinase/phosphatase and tensin hom

129 nce most glioblastomas (GBMs) show increased phosphatidylinositol-3 kinase (PI-3K) signaling, we soug

130 eficient cells, hyperinvasiveness involves a phosphatidylinositol 3-kinase-PI(3,4)P2 signaling axis w

131 Instead, we establish a critical role for phosphatidylinositol 3-kinase (PI3-kinase) signaling in

132 alization of R-Ras2 and its interaction with phosphatidylinositol 3-kinase PI3K, leading to activated

133 MP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediate

134 The phosphatidylinositol 3'-kinase (PI3K) pathway is dysregu

135 et aggregation by favoring the activation of phosphatidylinositol 3- kinase (PI3K) and contributes to

136 the regulatory and catalytic subunits of the phosphatidylinositol 3-kinase (PI3K) (p85alpha and p110a

137 a cytoplasmic tyrosine kinase that regulates phosphatidylinositol 3-kinase (PI3K) activation and acti

138 Btk and Csk function downstream of phosphatidylinositol 3-kinase (PI3K) activation during I

139 hocytic leukemia (CLL) displays constitutive phosphatidylinositol 3-kinase (PI3K) activation resultin

140 but occurred only upon stimulation requiring phosphatidylinositol 3-kinase (PI3K) activity.

141 Although signaling from phosphatidylinositol 3-kinase (PI3K) and AKT to mechanis

142 ted kinase (ERK) 1/2, and to a lesser extent phosphatidylinositol 3-kinase (PI3K) and nuclear factor

143 omolog (PTEN) is a negative regulator of the phosphatidylinositol 3-kinase (PI3K) and protein kinase

144 also demonstrate an important role for both phosphatidylinositol 3-kinase (PI3K) and STAT3 in the up

145 brane identity through its interactions with phosphatidylinositol 3-kinase (PI3K) and the Rac1 guanin

146 Crosstalk between the phosphatidylinositol 3-kinase (PI3K) and the transformin

147 Previous studies have identified phosphatidylinositol 3-kinase (PI3K) as the main downstr

148 ial cells by binding and activating cellular phosphatidylinositol 3-kinase (PI3K) at the plasma membr

149 electively inhibits the alpha isoform of the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (

150 d whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (

151 s on the negative transcriptional control of phosphatidylinositol 3-kinase (PI3K) class IA subunits.

152 re we show that small-molecule inhibitors of phosphatidylinositol 3-kinase (PI3K) currently in the cl

153 ee types of lipid kinases that belong to the phosphatidylinositol 3-kinase (PI3K) family.

154 ensitivity and that the p110delta subunit of phosphatidylinositol 3-kinase (PI3K) further promotes th

155 reatic cancer cell lines and that concurrent phosphatidylinositol 3-kinase (PI3K) inhibition caused s

156 B activation underlie acquired resistance to phosphatidylinositol 3-kinase (PI3K) inhibitors in breas

157 Interestingly, phosphatidylinositol 3-kinase (PI3K) inhibitors or P2Y12

158 e Unc-51-like kinase and is sensitive to the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmann

159 Inhibition of phosphatidylinositol 3-kinase (PI3K) is a promising appr

160 ion or loss of the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is emerging as a tr

161 action of the p85alpha regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is to associate wit

162 growth factor receptor (EGFR) and downstream phosphatidylinositol 3-kinase (PI3K) mediates viral entr

163 TP transiently activated Akt and, inhibiting phosphatidylinositol 3-kinase (PI3K) or Akt as well as d

164 lia neurons with pertussis toxin, as well as phosphatidylinositol 3-kinase (PI3K) or extracellular si

165 lia neurons with pertussis toxin, as well as phosphatidylinositol 3-kinase (PI3K) or extracellular si

166 ants lacking binding sites for its effectors phosphatidylinositol 3-kinase (PI3K) or SRC homology 2-c

167 insulin receptor or the regulatory subunits phosphatidylinositol 3-kinase (PI3K) p85alpha or p85beta

168 Phosphatidylinositol 3-kinase (PI3K) pathway activation

169 Phosphatidylinositol 3-kinase (PI3K) pathway activation

170 quire GAB2 for survival and show evidence of phosphatidylinositol 3-kinase (PI3K) pathway activation,

171 Phosphatidylinositol 3-kinase (PI3K) pathway activity wa

172 are dependent on GAB2 for activation of the phosphatidylinositol 3-kinase (PI3K) pathway and are sen

173 Aberrant activation of the phosphatidylinositol 3-kinase (PI3K) pathway has been sh

174 One outcome of activation of the phosphatidylinositol 3-kinase (PI3K) pathway is increase

175 The phosphatidylinositol 3-kinase (PI3K) pathway regulates a

176 tations and potentially by activation of the phosphatidylinositol 3-kinase (PI3K) pathway.

177 OR)/Unc-51-like kinase 1 (ULK1) and Beclin-1/phosphatidylinositol 3-kinase (PI3K) pathways were evalu

178 r signal-regulated kinase (RAS/MEK/ERK), and phosphatidylinositol 3-kinase (PI3K) pathways.

179 Phosphatidylinositol 3-kinase (PI3K) promotes cancer cel

180 vated JAK/STAT, Abelson kinase (ABL), and/or phosphatidylinositol 3-kinase (PI3K) signaling and poor

181 In this study, we aimed to demonstrate that phosphatidylinositol 3-kinase (PI3K) signaling is an imp

182 In glioblastoma, phosphatidylinositol 3-kinase (PI3K) signaling is freque

183 The phosphatidylinositol 3-kinase (PI3K) signaling pathway i

184 The ubiquitous phosphatidylinositol 3-kinase (PI3K) signaling pathway r

185 fferentially use the Janus kinase (Jak2) and phosphatidylinositol 3-kinase (Pi3k) signaling pathways,

186 (PTEN), a tumor suppressor that antagonizes phosphatidylinositol 3-kinase (PI3K) signaling, is frequ

187 s the receptor from CD19 phosphorylation and phosphatidylinositol 3-kinase (PI3K) signals.

188 Dual inhibition of MAP/ERK kinase (MEK) and phosphatidylinositol 3-kinase (PI3K) with the potent and

189 ed to endosomes depending on the activity of phosphatidylinositol 3-kinase (PI3K), a key enzyme for f

190 sisting of focal adhesion kinase (FAK), Src, phosphatidylinositol 3-kinase (PI3K), Akt, and mTOR medi

191 ion of BKM120, a small-molecule inhibitor of phosphatidylinositol 3-kinase (PI3K), alleviated dyslipi

192 P2A), YAP, Src family tyrosine kinases, Shc, phosphatidylinositol 3-kinase (PI3K), and phospholipase

193 osphorylation was sensitive to inhibition of phosphatidylinositol 3-kinase (PI3K), basal AKT1 phospho

194 l nodes insulin receptor substrate (IRS) and phosphatidylinositol 3-kinase (PI3K), exhibit divergent

195 although 2-OHE2 and 4-OHE2 rapidly activate phosphatidylinositol 3-kinase (PI3K), its activation is

196 odel is dependent on the p110beta isoform of phosphatidylinositol 3-kinase (PI3K), while breast cance

197 icantly influenced by the HSV-1 UL46-encoded phosphatidylinositol 3-kinase (PI3K)-Akt activator, was

198 Activating mutations in genes encoding phosphatidylinositol 3-kinase (PI3K)-AKT pathway compone

199 olipid syndrome stimulated mTORC through the phosphatidylinositol 3-kinase (PI3K)-AKT pathway.

200 E. chaffeensis infection activated the phosphatidylinositol 3-kinase (PI3K)-Akt-mTOR (mechanist

201 itogen activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI3K)-AKT.

202 Duvelisib (IPI-145) is an oral inhibitor of phosphatidylinositol 3-kinase (PI3K)-delta/gamma isoform

203 al-related kinase 1/2 (Erk1/2)-dependent and phosphatidylinositol 3-kinase (PI3K)-independent pathway

204 ein kinase (MAPK; 37%), cell cycle (20%) and phosphatidylinositol 3-kinase (PI3K)-mTOR (15%) pathways

205 n formation by converging onto regulation of phosphatidylinositol 3-kinase (PI3K).

206 moting effect was abolished by inhibitors of phosphatidylinositol 3-kinase (PI3K).

207 mannin and LY294002, which are inhibitors of Phosphatidylinositol 3-Kinase (PI3K).

208 mation by constitutively activating cellular phosphatidylinositol 3-kinase (PI3K).

209 ulin and growth factor signals downstream of phosphatidylinositol 3-kinase (PI3K).

210 the p85 subunit and subsequent activation of phosphatidylinositol 3-kinase (PI3K).

211 The tumors displayed dysregulated phosphatidylinositol 3-kinase (PI3K)/Akt and Lkb1/Ampk s

212 Conversely, activation of the phosphatidylinositol 3-kinase (PI3K)/Akt and the canonic

213 is important for HCMV-mediated activation of phosphatidylinositol 3-kinase (PI3K)/Akt during virus en

214 Phosphatidylinositol 3-kinase (PI3K)/AKT pathway aberrat

215 tion of p65 at Ser-536 is independent of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway during

216 The phosphatidylinositol 3-kinase (PI3K)/Akt pathway integra

217 he liver, insulin-mediated activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is at t

218 PD-1 abrogates activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, but th

219 ll surface protein, is known to regulate the phosphatidylinositol 3-kinase (PI3K)/AKT pathway.

220 llular signal-regulated kinase (MEK/ERK) and phosphatidylinositol 3-kinase (PI3K)/AKT pathways are of

221 activators of transcription (JAK/STAT3) and phosphatidylinositol 3-kinase (PI3K)/AKT pathways in tum

222 egulated protein kinases 1/2 (ERK1/2) and/or phosphatidylinositol 3-kinase (PI3K)/Akt signaling incre

223 HBx can activate the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathw

224 cells was dependent on the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathw

225 PK/p90 ribosomal S6 kinase (p90RSK), but not phosphatidylinositol 3-kinase (PI3K)/AKT signaling.

226 en-activated protein (MAP) kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian targe

227 cellular transformation and to activate the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathway.

228 In this study, we show that the dual phosphatidylinositol 3-kinase (PI3K)/mTOR inhibitor PF-0

229 evel of DEAD-box helicase p68 (DDX5) through phosphatidylinositol 3-kinase (PI3K)/p300 signaling and

230 rget of rapamycin complex 2 (mTORC2) and the phosphatidylinositol 3-kinase (PI3K)/phosphoinositide-de

231 , a new agent that specifically disrupts the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (A

232 The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (A

233 rake on myelination, which downregulates the phosphatidylinositol 3-kinase (PI3K)/v-AKT murine thymom

234 hat inhibits insulin signaling downstream of phosphatidylinositol 3-kinase (PI3K); its role in vascul

235 e of the brain through which an inhibitor of phosphatidylinositol-3 kinase (PI3K) (wortmannin) was ad

236 tracellular signal-regulated kinases 1/2 and phosphatidylinositol-3 kinase (PI3K)/AKT in sensitive ce

237 Signaling through the phosphatidylinositol-3 kinase (PI3K)/Akt pathway, which

238 complex, the core component of the class III phosphatidylinositol-3 kinase (PI3K-III), binds Atg14L o

239 EN controls cell proliferation by regulating phosphatidylinositol-3-kinase (PI3K) activity, but the p

240 The phosphatidylinositol-3-kinase (PI3K) alpha/delta (PI3Kal

241 models, we demonstrate that inactivation of phosphatidylinositol-3-kinase (PI3K) catalytic subunit p

242 Inhibition of the phosphatidylinositol-3-kinase (PI3K) pathway as an antic

243 Importance: Molecular aberrations in the phosphatidylinositol-3-kinase (PI3K) pathway drive tumor

244 Dysregulation of the phosphatidylinositol-3-kinase (PI3K) pathway in a wide r

245 The phosphatidylinositol-3-kinase (PI3K) pathway is commonly

246 tivation of the signaling pathways involving phosphatidylinositol-3-kinase (PI3K), Akt, and mammalian

247 LY294002, a specific inhibitor of phosphatidylinositol-3-kinase (PI3K), significantly impa

248 CD133 and DNA-PK may increase MDR1 via the phosphatidylinositol-3-kinase (PI3K)-Akt signal pathway.

249 Mutations of genes within the phosphatidylinositol-3-kinase (PI3K)-AKT-MTOR pathway ar

250 itment of the p85alpha regulatory subunit of phosphatidylinositol-3-kinase (PI3K).

251 erfamily that stimulate specific isoforms of phosphatidylinositol-3-kinase (PI3K).

252 Moreover, we identify phosphatidylinositol-3-kinase (PI3K)/AKT as a downstream

253 nt PIK3CA resulted in a robust activation of phosphatidylinositol-3-kinase (PI3K)/AKT signaling but a

254 Clenbuterol activated the phosphatidylinositol-3-kinase (PI3K)/Akt/mechanistic tar

255 activated protein kinase (MAPK) pathway, the phosphatidylinositol-3-kinase (PI3K)/mammalian target of

256 K-based immune therapies for transplantation.Phosphatidylinositol-3-kinases (PI3K) gamma and delta ar

257 Phosphatidylinositol-3-kinases (PI3K) gamma and delta ar

258 s how interactions between autophagy and the phosphatidylinositol 3-kinase(PI3K)/Akt/mammalian target

259 , the gene encoding the p110alpha subunit of phosphatidylinositol 3-kinase (PI3Kalpha), are frequent

260 Phosphatidylinositol 3-kinases (PI3Ks) and phosphatidyli

261 es between the activation mechanisms of ATM, phosphatidylinositol 3-kinases (PI3Ks), and the other PI

262 ecific conditional knockout of the class III phosphatidylinositol 3-kinase, Pik3c3.

263 cal PKC (aPKC) isoforms are activated by the phosphatidylinositol 3-kinase product phosphatidylinosit

264 ilaments, actin-related protein 2/3 complex, phosphatidylinositol-3'-kinase, protein tyrosine kinases

265 protein (YAP) proteins via inhibition of the phosphatidylinositol 3 kinase/protein kinase B (Akt) pat

266 investigated its therapeutic effects on the Phosphatidylinositol 3 kinase/Protein kinase B (PI3K/Akt

267 Inhibitors of the phosphatidylinositol 3-kinase/protein kinase B/mammalian

268 we found that pharmacological inhibition of phosphatidylinositol 3-kinase (PtdIns 3-kinase) activity

269 arly, differences in the activation state of phosphatidylinositol 3-kinase (PtdIns3K) correlated with

270 or PtdIns(4)P5K alone, or treatment with the phosphatidylinositol 3-kinase (PtdInsI3K) inhibitor wort

271 negative regulators of insulin signaling via phosphatidylinositol 3-kinase regulation.

272 s of the tumor-promoting and HSF1-associated phosphatidylinositol 3-kinase-related kinase (PIKK) fami

273 zation of ATM and other members of the PIKK (phosphatidylinositol 3-kinase-related kinase) family kin

274 damage response (DDR), activating all three phosphatidylinositol 3-kinase-related kinases (PI3KKs):

275 ree proteins regulate the cellular levels of phosphatidylinositol 3-kinase-related kinases (PIKKs) an

276 ses, small nucleolar ribonucleoparticles and phosphatidylinositol 3-kinase-related kinases.

277 to the highly conserved eukaryotic family of phosphatidylinositol 3-kinase-related kinases.

278 omplex, a co-chaperone for maturation of the phosphatidylinositol 3-kinase-related protein kinases (P

279 Two large phosphatidylinositol 3-kinase-related protein kinases (P

280 Phosphatidylinositol 3-kinases (PI3Ks) and phosphatidylinositol 3-kinase-related protein kinases (P

281 The phosphatidylinositol 3-kinase-related protein kinases ar

282 r substrate 2alpha or the survival-promoting phosphatidylinositol-3-kinase, respectively, to be ubiqu

283 ors of mitogen-activated protein kinase 1 or phosphatidylinositol 3-kinase, reversed the aggressive p

284 ed axon conduction, and did not activate the phosphatidylinositol 3-kinase/serine-threonine-specific

285 on chromosome 10 (PTEN) negatively regulates phosphatidylinositol 3-kinase signaling and downstream t

286 hatase type II (INPP4B) negatively regulates phosphatidylinositol 3-kinase signaling and is a tumor s

287 e of Erk amplification without alteration of phosphatidylinositol 3-kinase signaling in Nf1(+/-) neoi

288 uantify the local concentration of actin and phosphatidylinositol 3-kinase signaling on the surfaces

289 and receptor association to Src-kinases and phosphatidylinositol-3-kinase signalling pathways, but i

290 Here, we have shown that phosphatidylinositol 3-kinase-targeted (PI3K-targeted) t

291 te, thereby opposing the activity of class I phosphatidylinositol 3-kinases that mediate growth- and

292 G2 were reported to regulate the activity of phosphatidylinositol 3-kinase (the upstream activator of

293 ylation enhances ATG14L-associated class III phosphatidylinositol 3-kinase VPS34 activity by increasi

294 is required for correct localization of the phosphatidylinositol 3-kinase Vps34 and the production o

295 Phosphatidylinositol 3-kinase Vps34 complexes regulate i

296 phosphatase Pah1, which also lack Ypt7, the phosphatidylinositol 3-kinase Vps34, and the lipid phosp

297 nteracting proteins, including the class III phosphatidylinositol-3 kinase Vps34, play crucial roles

298 est this hypothesis by focusing on class III phosphatidylinositol 3-kinase (Vps34), which is an essen

299 f Akt and ERK, as well as the association of phosphatidylinositol 3-kinase with IRS-1, were significa

300 Inhibition of phosphatidylinositol 3-kinase with wortmannin or mTORC1