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 ing pathway, like Bruton tyrosine kinase and phosphatidylinositol 3 kinase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 , and the induction of CXCL11-CXCR3 axis and phosphatidylinositol 3-kinase/AKT pathways.

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

25 Phosphatidylinositol 3-kinase/Akt signaling acting downs

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

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

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

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

30 ation and survival through activation of the phosphatidylinositol 3-kinase/AKT-, RAS/MAPK-, and STAT5

31 rotocol 2, whereas it additionally inhibited phosphatidylinositol 3-kinase/Akt/endothelial nitric oxi

32 We demonstrate that the phosphatidylinositol 3-kinase/AKT/GSK-3beta pathway inte

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

34 The phosphatidylinositol 3-kinase/Akt/mammalian target of ra

35 ciently controls IL-23- and IL-1beta-induced phosphatidylinositol 3-kinase/AKT/mTOR activation indepe

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

37 an target of rapamycin (mTOR) and associated phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway

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

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

40 on stress response, TP53, androgen receptor, phosphatidylinositol-3-kinase/AKT, and MYC signaling.

41 Phosphatidylinositol 3-kinase alpha is an attractive tar

42 Overexpressing phosphatidylinositol 3-kinase-an enzyme essential for os

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

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

45 R2 encodes the p85beta regulatory subunit of phosphatidylinositol 3-kinase and is frequently amplifie

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

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

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

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

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

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

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

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

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

55 lin via a pathway including IGF1 or insulin, phosphatidylinositol 3-kinase, and AKT.

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

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

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

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

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

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

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

63 found that local synthesis of PI(3,4)P(2) by phosphatidylinositol 3-kinase C2alpha at plasma membrane

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

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

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

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

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

69 regulates the assembly of the endolysosomal phosphatidylinositol 3-kinase complex (PI3KC3-C2)-which

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

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

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

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

74 Atg5, and Vps34, and other components of the phosphatidylinositol 3-kinase complex.

75 inositide PI(3)P by the autophagic class III phosphatidylinositol-3 kinase complex I (PI3KC3-C1) and

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

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

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

79 The phosphatidylinositol 3-kinase delta (PI3K-delta) inhibit

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

81 ext-generation, potent, and highly selective phosphatidylinositol 3-kinase delta (PI3Kdelta) inhibito

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

83 The phosphatidylinositol 3-kinase delta (PI3Kdelta) pathway

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

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

86 Phosphatidylinositol-3-kinase delta (PI3Kdelta) mediates

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

88 Activated phosphatidylinositol 3-kinase-delta (PI3K-delta) syndrom

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

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

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

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

93 e blood with isoform selective inhibitors of phosphatidylinositol 3-kinase dose dependently modulate

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

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

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

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

98 Toll-like receptor 9 (TLR9) and Phosphatidylinositol-3-kinase gamma (PI3Kgamma) are very

99 Phosphatidylinositol 3-kinase-gamma (PI3Kgamma) is highl

100 , downregulation of the androgen receptor -> phosphatidylinositol-3-kinase -> Akt pathway, upregulati

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

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

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 ulin-induced effect on FOXO1 nuclear efflux, phosphatidylinositol 3-kinase inhibitors, which we show

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

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

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

114 hat regulates the steady-state levels of all phosphatidylinositol 3-kinase-like protein kinases, incl

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 repair genes (eg, BRCA2 and ATM) in 60%, and phosphatidylinositol 3-kinase/mitogen-activated protein

118 Targeting the B-cell receptor and phosphatidylinositol 3-kinase/mTOR signaling pathways ha

119 Inhibition of phosphatidylinositol 3-kinase, or its downstream effecto

120 Phosphatidylinositol 3-kinase p110delta isoform (PI3K p1

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

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

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

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

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

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

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 yrosine kinase (TK) inhibitor, genistein and phosphatidylinositol 3-kinase (PI-3K) inhibitor, wortman

130 inducible factor 2alpha (HIF-2alpha) and the Phosphatidylinositol-3 kinase (PI(3) -Kinase)/AKT/Serum

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

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

133 ted the mitogen-activated protein kinase and phosphatidylinositol 3-kinase (PI3'K) pathways with the

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

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

136 Phosphatidylinositol 3 kinase (PI3K) inhibition also abo

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

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

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

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

141 keletal muscle insulin resistance, decreased phosphatidylinositol 3-kinase (PI3K) activation and alte

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

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

144 and identified high-value targets, including phosphatidylinositol 3-kinase (PI3K) and cyclin-dependen

145 In HNSCC, genetic aberrations in phosphatidylinositol 3-kinase (PI3K) and epidermal growt

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

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

148 70 coopted replicase assembly factors, Vps34 phosphatidylinositol 3-kinase (PI3K) and the membrane-be

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

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

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

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

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

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

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

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

157 ibited the activating phosphorylation of the phosphatidylinositol 3-kinase (PI3K) effector Akt induce

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

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

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

161 of autophagosome elongation by the class III phosphatidylinositol 3-kinase (PI3K) inhibitor 3-methyla

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

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

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

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

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

167 uced transcription factor that downregulates phosphatidylinositol 3-kinase (PI3K) levels to activate

168 signaling, including that of MET, downstream phosphatidylinositol 3-kinase (PI3K) mediates both cell

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

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

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

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

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

174 Phosphatidylinositol 3-kinase (PI3K) pathway activation

175 Phosphatidylinositol 3-kinase (PI3K) pathway activation

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

177 Phosphatidylinositol 3-kinase (PI3K) pathway activity wa

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

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

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

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

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

183 Phosphatidylinositol 3-kinase (PI3K) promotes cancer cel

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

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

186 Phosphatidylinositol 3-kinase (PI3K) signaling is highly

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

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

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

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

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

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

193 Targeting both CD20 and phosphatidylinositol 3-kinase (PI3K), a protein that is

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

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

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

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

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

199 g: 3' phosphatase and tensin homolog (PTEN), phosphatidylinositol 3-kinase (PI3K), or 5' Src homology

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

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

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

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

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

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

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

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

208 onetheless requires actin dynamics, Syk, and phosphatidylinositol 3-kinase (PI3K).

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

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

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

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

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

214 y enlarged brains, and overactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt (protein kinase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 t have the ability to simultaneously bind to phosphatidylinositol-3 kinase (PI3K) and/or cyclin-depen

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

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

236 ia represents a major advance, including the phosphatidylinositol-3'-kinase (PI3K) p110delta inhibito

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

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

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

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

241 The activation of the phosphatidylinositol-3-kinase (PI3K) pathway is a known

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

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

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

245 ogether function as a prototypical class III phosphatidylinositol-3-kinase (PI3K).

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

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

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

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

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

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

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

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

254 with beclin 1 and ATG14-containing class III phosphatidylinositol-3-kinase (PI3KC3) complex 1 (PI3KC3

255 Phosphatidylinositol 3-kinases (PI3Ks) and phosphatidyli

256 Phosphatidylinositol 3-kinases (PI3Ks) are a family of l

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

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

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

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

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

262 ied in more than one tissue, including PI3K (phosphatidylinositol 3-kinase/protein kinase-B) signalin

263 tumor resistance due to redundancies in the phosphatidylinositol-3'-kinase/protein kinase B and KRAS

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

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

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

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

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

269 of FUS's prion-like domain (PrLD) by nuclear phosphatidylinositol 3-kinase-related kinase (PIKK)-fami

270 site phosphorylation, activates the cellular phosphatidylinositol 3-kinase-related kinase ATM to caus

271 ivers of the DDR are multiple members of the phosphatidylinositol 3-kinase-related kinase family, inc

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

273 Ca(2+)-sensing proteins and SMG1, encoding a phosphatidylinositol 3-kinase-related kinase.

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 -dependent protein kinase (DNA-PK), like all phosphatidylinositol 3-kinase-related kinases (PIKKs), i

277 ses, small nucleolar ribonucleoparticles and 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 For nearly 30 years, the conserved phosphatidylinositol 3-kinase-related protein kinases (P

282 The phosphatidylinositol 3-kinase-related protein kinases ar

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

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

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

286 ociated with reductions in integrin-paxillin-phosphatidylinositol 3-kinase signaling in vivo.

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

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

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

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

291 Pro-rich peptide ligand to the SH3 domain of phosphatidylinositol 3-kinase unfolded in the presence o

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

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

294 Phosphatidylinositol 3-kinase Vps34 complexes regulate i

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

296 Dia2 and an endosomal effector protein, the phosphatidylinositol 3-kinase Vps34.

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

298 generating hyperactive alleles of the yeast phosphatidylinositol 3-kinase, Vps34.

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