ライフサイエンスコーパス: PI 3-kinase

1 tion-3 (STAT3) and phosphoinositol-3 kinase (PI 3-kinase).

2 entry is type IA phosphoinositide 3-kinase (PI 3-kinase).

3 n and class I phosphatidylinositol 3-kinase (PI 3-kinase).

4 activation of phosphatidylinositol 3-kinase (PI-3 kinase).

5 nocking out phosphatidylinositide 3-kinases (PI 3-kinases).

6 bstrate of CISK that functions downstream of PI 3-kinase.

7 at Ser-636/639, and favorably interacts with PI 3-kinase.

8 protein kinases that function downstream of PI 3-kinase.

9 stimulated by ERK1/2 and the second wave of PI 3-kinase.

10 In both pathways, p38 acts downstream to PI 3-kinase.

11 P, as was macropinocytosis, which depends on PI 3-kinase.

12 enuate leptin-induced activation of STAT3 or PI 3-kinase.

13 sruption of signaling from growth factors to PI 3-kinase.

14 as mediated differentially by Rho kinase and PI 3-kinase.

15 egulators or downstream effectors of type IA PI 3-kinase.

16 insulin signaling pathway via activation of PI 3-kinase.

17 in controlling gene expression downstream of PI 3-kinase.

18 t SAHA directly inhibited kinase activity of PI 3' kinase.

19 ctive dual inhibitor of mTORC1/2 and class I PI 3-kinases.

20 Thr187 in parallel to phosphatidylinositol (PI) 3-kinase.

21 enzymes, including type I phosphoinositide (PI) 3-kinases.

22 L-1 5-phosphatase and a wortmannin-sensitive PI 3-kinase act antagonistically to regulate the convers

23 Class I phosphoinositide (PI) 3-kinases act through effector proteins whose 3-PI s

24 PI 3'kinase activates Akt through its production of 3' p

25 aling through phosphatidylinositol 3-kinase (PI 3-kinase) activates the protein kinase Akt through ph

26 suggest that RacC plays an important role in PI 3-kinase activation and WASP activation for dynamic r

27 In contrast to Ca(2+), PI 3-kinase activation by C5a was inhibited by UDP, as w

28 of two distinct modes of retinal class I(A) PI 3-kinase activation that occurs in response to PDGF r

29 further examine the contributions of Src and PI 3-kinase activation to RV-induced Akt activation and

30 k-mediated signaling pathway as Rck-mediated PI 3-kinase activation was blocked by PP2, and PI 3-kina

31 of up to five- to tenfold in IGF-stimulated PI 3-kinase activation, a failure to activate the ERK ki

32 is stimulated by PI(4,5)P(2), which leads to PI 3-kinase activation, and PI(4,5)P(2) phosphorylation.

33 dance, and Ras siRNA abrogated Ad-36-induced PI 3-kinase activation, GLUT4 protein abundance, and glu

34 antly reduced membrane localization, MAP and PI 3-kinase activation, thymidine incorporation into DNA

35 TRAF binding domain previously implicated in PI 3-kinase activation.

36 st and prostate carcinoma cells with minimal PI(3) kinase activation adopt an immunoresistant phenoty

37 r of T-cell function, B7-H1, correlates with PI(3) kinase activation in breast and prostate cancer pa

38 fore, melanoma cells require either B-RAF or PI-3 kinase activation for protection from anoikis.

39 PI-3 kinase activation required a putative Src-homology

40 pathways that regulate NKG2D ligands include PI-3 kinase activation, histone acetylation, and the int

41 osphorylation and IRS-1-and IRS-2-associated PI 3-kinase activities.

42 bl significantly suppressed BMP-2-stimulated PI 3-kinase activity and its downstream Akt phosphorylat

43 receptor phosphorylation, and IRS-associated PI 3-kinase activity in skeletal muscle (P < 0.01, P < 0

44 lusion, GH regulates p85alpha expression and PI 3-kinase activity in WAT and provides a potential exp

45 An increase in PI 3-kinase activity was found in 12-LOX-transfected PC-

46 fter which the expression disappeared, while PI 3-kinase activity was observed up to 4 hours after IL

47 The insulin-induced increase in PI 3-kinase activity was robust in mice with GH deficien

48 nsulin receptor substrate (IRS)-1-associated PI 3-kinase activity were measured in white adipose tiss

49 pattern of subunit-specific basal class I(A) PI 3-kinase activity, which was stimulated in a temporal

50 ylated with normal kinetics in cells lacking PI 3-kinase activity.

51 rgistic in stimulating phosphatidylinositol (PI) 3-kinase activity, leading to receptor macropinocyto

52 pendent of both receptor phosphorylation and PI-3-kinase activity, suggestive of a novel mechanism.

53 membrane, and phosphatidylinositol 3-kinase (PI 3-kinase) activity in an insulin-independent manner.

54 d by activated Cdc42 and inactivated Rho via PI 3-kinase after FGF-2 stimulation and that Cdc42 activ

55 Activation of phosphatidylinositol 3-kinase (PI 3-kinase)/Akt signaling by BMP-2 leads to osteoblast

56 bitors of the phosphatidylinositol 3-kinase (PI 3-kinase)/Akt-1 and signal transducer and activator o

57 /MEK/ERK) and phosphatidylinositol 3-kinase (PI-3 kinase)/Akt signaling pathways.

58 V39 with Src, p85alpha PI 3-kinase, p110beta PI 3-kinase, Akt and Cit-Akt-PH, a fluorescent Akt pleck

59 ponse element-binding protein (CREB) via the PI 3-kinase-Akt pathway and that RNS60 up-regulated Ikap

60 tion of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4

61 Given the key role of PI 3-kinase-Akt signaling in myelination, we investigate

62 i-inflammatory property of RNS60 via type IA PI 3-kinase-Akt-CREB-mediated up-regulation of IkappaBal

63 il in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests

64 The RGC complex thus connects PI 3-kinase/Akt activity to the transport machineries re

65 Neither inhibition of PI 3-kinase/AKT nor IKKalphaT23A overexpression affected

66 ulin- and IGF-1-stimulated activation of the PI 3-kinase/Akt pathway and increased streptozotocin (ST

67 Activation of the PI 3-kinase/Akt pathway in beta-cells was impaired in pa

68 tes the activation of RalA downstream of the PI 3-kinase/Akt pathway.

69 olecular mechanisms by which mTORC1 inhibits PI 3-kinase/Akt signaling at the level of IRS-1 and sugg

70 ing and abrogate PTEN-mediated inhibition of PI 3-kinase/AKT signaling.

71 determine basal and PDGF-induced class I(A) PI 3-kinase/Akt survival signaling, in comparison with i

72 s novel pathway is a parallel pathway to the PI 3-kinase/AKT upstream of NFkappaB and both are involv

73 Inhibition of the PI 3-kinase/Akt-1 or STAT-3 pathways significantly reduc

74 and phosphorylation of AS160 and TBC1D1 in a PI 3-kinase/Akt-dependent manner, 2) contraction stimula

75 ut not PAS-TBC1D1 or glucose transport) in a PI 3-kinase/Akt-dependent manner, and 3) contraction sti

76 Taken together, we have discovered a novel PI 3-kinase/AKT-dependent pathway in response to IL-1, e

77 o characterize gene regulation downstream of PI 3-kinase/Akt/GSK-3 signaling in response to growth fa

78 nd cell cycle regulatory genes downstream of PI 3-kinase/Akt/GSK3 signaling.

79 nt pathway in response to IL-1, encompassing PI 3-kinase/AKT/IKKalphaT23 upstream of AP-1.

80 This mutant enhanced PI(3) kinase/AKT activation after receptor engagement by

81 n in altering baseline phosphatidylinositol (PI) 3-kinase/Akt activity.

82 proliferation, and the phosphatidylinositol (PI) 3-kinase/Akt pathway mediates insulin and IGF-1 acti

83 gene expression by the phosphatidylinositol (PI) 3-kinase/Akt pathway plays an important role in mamm

84 nditions mTOR inhibits phosphatidylinositol (PI) 3-kinase/Akt signaling by phosphorylating insulin re

85 Phosphatidylinositol (PI) 3-kinase/Akt signaling plays a critical role in cell

86 ial cells to stimulate phosphatidylinositol (PI) 3-kinase/Akt/endothelial nitric-oxide synthase leadi

87 Up-regulation of the Raf/MEK/ERK and PI-3 kinase/Akt pathways by NO was found to be mediated

88 man aortic VSMC apoptosis (via activation of PI-3 kinase/Akt signalling) and proliferation.

89 siRNA against p110beta PI 3-kinase also inhibited IL-8 expression.

90 lation resulted in significant inhibition of PI 3 kinase and Erk1/2 MAPK activity.

91 atrol inhibited PDGFR phosphorylation at the PI 3 kinase and Grb-2 binding sites tyrosine-751 and tyr

92 infection activates phosphatidylinositol 3 (PI 3)-kinase and the serine threonine kinase Akt minutes

93 Accordingly, inhibition of PI 3-kinase and AKT by chemical inhibitors abrogated gem

94 Inhibition of PI 3-kinase and Akt by either chemical inhibitors or dom

95 s after infection and that the activation of PI 3-kinase and Akt is required for maximal interleukin-

96 wo signaling pathways involving noncanonical PI 3-kinase and canonical Smads to integrate BMP-2-induc

97 Under these conditions, activation of PI 3-kinase and Cdc42 were observed in the migratory cel

98 cell survival signaling pathway mediated by PI 3-kinase and CISK.

99 ereas it stimulates cell proliferation using PI 3-kinase and ERK1/2 in parallel pathways.

100 e authors then determined cross-talk between PI 3-kinase and extracellular signal-regulated kinase (E

101 -2 stimulates proliferation of hCECs through PI 3-kinase and its downstream target ERK1/2 pathways.

102 quires intact insulin signaling via both the PI 3-kinase and MEK signaling cascades and the cSrc-fami

103 Ras and Cdc42, leading to the activation of PI 3-kinase and NFkappaB, provide a mechanism by which E

104 stimulation of CECs with IL-1beta activated PI 3-kinase and p38 in a biphasic fashion.

105 t pathways: the second wave of activation of PI 3-kinase and p38 was involved in cell migration, wher

106 induced FGF-2 facilitates cell migration via PI 3-kinase and p38, whereas it stimulates cell prolifer

107 roduce FGF-2 by IL-1beta stimulation through PI 3-kinase and p38.

108 Membrane translocation of PI 3-kinase and PI 3,4,5-trisphosphate reporter is absen

109 o assess the role of the p85alpha subunit of PI 3-kinase and PI 3-kinase signaling in GH-mediated ins

110 activation of type IA phosphatidylinositol (PI) 3-kinase and Akt and rapidly up-regulated IkappaBalp

111 activation of type IA phosphatidylinositol (PI) 3-kinase and AKT.

112 TRPC1 channel activity through activation of PI-3-kinase and generation of PIP(3).

113 eptor (EGFR), phosphatidylinositol-3 kinase (PI 3-kinase), and Akt.

114 d MAP kinase, phosphatidylinositol 3-kinase (PI 3-kinase), and extracellular-regulated kinase (ERK)-M

115 ding the Jak-STAT, phosphoinositol 3-kinase (PI 3-kinase), and mitogen-activated protein kinase (MAPK

116 inase (MAPK), phosphatidylinositol 3-kinase (PI-3 kinase), and protein kinase C (PKC) involvement wer

117 8 promoter and that RV colocalizes with Src, PI 3-kinase, and Akt in lipid rafts.

118 ining phospholipase Cdelta and Akt peptides, PI 3-kinase, and Akt inhibition in wild-type and NHE1-nu

119 ultiple protein kinases, including Syk, Btk, PI 3-kinase, and GSK3.

120 olve sequential activation of Gbetagamma(i), PI 3-kinase, and the Ca2+-independent MLCK, integrin-lin

121 n that interacts with membranes in activated PI 3-kinases, and its mutation abrogates the requirement

122 -dependent activation of the Ras-MAP kinase, PI-3 kinase, and mTOR pathways in these cells.

123 DHEA stimulates phosphorylation of FoxO1 via PI 3-kinase- and PKA-dependent pathways in endothelial c

124 kinase [Btk], phosphatidylinositol 3-kinase [PI 3-kinase], and GSK3) associated with RA and inhibited

125 he context of RV infection, Src and p110beta PI 3-kinase are upstream activators of Akt and the IL-8

126 Because PI 3-kinases are key mediators of insulin action, we inv

127 Ras proteins activate Raf and PI-3 kinases, as well as exchange factors for RalA and R

128 signalling processes that are downstream of PI 3-kinase associated changes in inositol phospholipids

129 TM physically associates with the homologous PI 3-kinase, ATR.

130 response to DHEA treatment was augmented by PI 3-kinase blockade and inhibited by MAPK blockade.

131 LOX-transfected PC-3 cells and inhibition of PI 3-kinase by LY294002 significantly reduced VEGF expre

132 The tumor suppressor Beclin1 is part of the PI(3) kinase class III (PI(3)KC3) lipid-kinase complex t

133 direct myotubularin binding to the type III PI 3-kinase complex hVps34/hVps15 leads to phosphatase i

134 understanding the mechanism by which type IA PI 3-kinase controls bacterial internalization.

135 8 (MyD88) and Phosphatidylinositol 3-kinase (PI-3 kinase)-dependent pathway.

136 e associated with insulin resistance through PI 3-kinase-dependent and -independent mechanisms.

137 Several PI 3-kinase-dependent feedback mechanisms have been iden

138 Balance between PI 3-kinase-dependent inhibition and MAPK-dependent stim

139 Insulin stimulates the activity of RalA in a PI 3-kinase-dependent manner.

140 tudy we hypothesized that DHEA may stimulate PI 3-kinase-dependent phosphorylation of FoxO1 in endoth

141 tumors have chronically elevated activity of PI 3-kinase-dependent signaling pathways, caused largely

142 hese data indicate that chronically elevated PI 3-kinase-dependent signaling to the degree seen in ma

143 heregulin-beta1 stimulation of Bmx was also PI 3-kinase-dependent.

144 oxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.

145 tected melanoma cells from anoikis through a PI-3 kinase-dependent pathway.

146 ockdown of ARE-BPs that are not regulated by PI 3-kinase did not affect degradation of these mRNAs.

147 II production of ROS prevented activation of PI 3-kinase during macronutrient perturbation, whereas p

148 at the c-Src signal molecule was upstream of PI 3-kinase during the Rck-mediated signaling pathway as

149 PIKE-A (phosphoinositide 3-kinases (PI 3)-kinase enhancer) is a ubiquitously expressed GTPas

150 PI 3-kinase enhancer A (PIKE-A) is critical for the acti

151 hosphorylation of GSK3beta were dependent on PI 3-kinase, Erk, and mTOR.

152 d expression of IRAK and TRAF6 and activated PI 3-kinase; expression of IRAK and TRAF6 reached maximu

153 al members of the phosphoinositide 3-kinase (PI 3-kinase) family, which contribute to various aspects

154 ECs ERK1/2 works as a downstream effector to PI 3-kinase for cell proliferation induced by FGF-2, whe

155 Here we show that macrophage PI 3-kinase gamma controls a critical switch between imm

156 C5aR and C3aR mediated their effects via PI-3 kinase-gamma-dependent AKT phosphorylation, providi

157 Although the ability of Ras to control PI 3-kinase has been well established in manipulated cel

158 ntigen (EEA) 1 and the phosphatidylinositol (PI) 3-kinase hVps34, which generates PI(3)P, a phospholi

159 or 6 (TRAF6), phosphatidylinositol 3-kinase (PI 3-kinase), IkappaB kinase (IKK), IkappaB, NF-kappaB,

160 le of the interaction of endogenous Ras with PI 3-kinase in normal and malignant cell growth in vivo

161 ssion profiling indicated that inhibition of PI 3-kinase in proliferating cells led to induction of g

162 t were downregulated following inhibition of PI 3-kinase in proliferating T98G cells.

163 rosine phosphorylation downstream of Src and PI 3-kinase in PTEN-deficient LNCaP and PC3 PCa cells an

164 wnstream target of the constitutively active PI 3-kinase in PTEN-deficient PCa cells and further show

165 sequential activation of Rho GTPases through PI 3-kinase in response to FGF-2 stimulation.

166 e cell periphery following the activation of PI 3-kinase in Swiss 3T3 fibroblasts, consistent with th

167 However, the role of PI 3-kinase in T-cell movement is unclear, and its impor

168 ate the involvement of c-Src upstream of the PI 3-kinase in the Zipper entry process mediated by Rck.

169 of the Vps34 class III phosphatidylinositol (PI) 3-kinase in autophagy.

170 constitutively active phosphatidylinositol (PI) 3-kinase in PTEN-deficient prostate cancer (PCa) cel

171 uption of the p85alpha regulatory subunit of PI 3-kinase increases insulin sensitivity, whereas eleva

172 t chain complex III ROS production activated PI 3-kinase independent of nutrient input.

173 and activation of Bmx in response to EGF was PI 3-kinase-independent.

174 O3a protected cells from apoptosis following PI 3-kinase inhibition.

175 3-kinase activation was blocked by PP2, and PI 3-kinase inhibitor had no effect on the Src phosphory

176 (t-butyl)pyrazolo [3,4-d]pyrimidine} and the PI 3-kinase inhibitor LY294002 each inhibited Akt phosph

177 Pretreatment of cells with a PI 3-kinase inhibitor or insulin receptor silencing with

178 ither the mTORC2 inhibitor rapamycin nor the PI 3-kinase inhibitor wortmannin affects paxillin tyrosi

179 Incubation with the PI 3-kinase inhibitor wortmannin eliminates insulin pote

180 ed by pretreatment of cells with wortmannin (PI 3-kinase inhibitor) or H89 (protein kinase A (PKA) in

181 y Gallein (betagamma inhibitor), Wortmannin (PI 3-kinase inhibitor), SecinH3 (cytohesin ARF GEF inhib

182 Y27632 were completely blocked by LY294002 (PI 3-kinase inhibitor).

183 A newly identified PI 3-kinase inhibitor, PIK93 that selectively inhibits t

184 ns were blocked by the phosphatidylinositol (PI) 3-kinase inhibitor LY294002.

185 ch can be blocked by a phosphatidylinositol (PI) 3-kinase inhibitor.

186 LY294002) or p110 isoform-selective (PI-103) PI 3-kinase inhibitors (versus Akt inhibitor) to assess

187 nd is inhibited by pan-phosphatidylinositol (PI)3-kinase inhibitors.

188 ively inhibited by phosphoinositol-3-kinase (PI-3-kinase) inhibitors wortmannin (50 nM) and PI-828 an

189 ATM is a PI 3-kinase involved in DNA double-strand break repair.

190 ppreciation not only of the finer details of PI 3-kinase involvement in T-cell migration, but also of

191 Regulation of the class IA PI 3-kinase involves inhibition and stabilization of the

192 Phosphoinositide (PI) 3-kinase is involved in insulin-mediated effects on

193 Activation of phosphoinositide 3-kinase (PI 3-kinase) is known to trigger many insulin-stimulated

194 ays, caused largely by oncogenic mutation of PI 3-kinase itself or loss of the opposing tumor suppres

195 Inhibition of PI 3-kinase led to a loss of Max/Mnt binding and transcr

196 and prostate carcinoma cells with activated PI(3) kinase lose the immunoresistant phenotype after tr

197 l as inhibitors of Akt (Akt inhibitor VIII), PI 3-kinase (LY294002 and wortmannin), and mTOR (rapamyc

198 y blocked by pathway-specific inhibitors for PI 3-kinase (LY294002) and MEK1/2 (U0126), respectively.

199 s to NF-kappaB activation (sulfasalazine) or PI 3-kinase (LY294002), and both inhibitors greatly bloc

200 uppressed by inhibitors of EGFR (AG1478) and PI 3-kinase (LY294002).

201 Selective inhibitors of MAPK (PD98059) and PI-3 kinase (LY294002) suppressed HGF-induced RVP by 86%

202 about the role of either rictor or mTORC2 in PI-3 kinase-mediated physiological processes in adult an

203 3,4,5-trisphosphate (PIP(3)), the product of PI-3-kinase-mediated phosphorylation of phosphatidylinos

204 Phosphatidylinositol (PI) 3-kinase mediates multiple pathways that regulate ma

205 ession involved activation of NADPH-oxidase, PI-3 kinase, mitogen-activated protein kinase, NF-kappaB

206 nd imatinib mesylate differentially regulate PI 3' kinase/mTOR-dependent signaling cascades in BCR-AB

207 locked by inhibitors of fatty-acid synthase, PI 3-kinase, mTORC, or an antibody against the carboxyl-

208 curred via activation of phosphoinositide-3 (PI-3) kinase, nicotinamide adenine dinucleotide phosphat

209 Neither phosphatidylinositol (PI) 3-kinase nor protein kinase C was required for syner

210 of these genes were regulated via effects of PI 3-kinase on mRNA stability.

211 Exposure of serum-deprived RGC-5 cells to PI 3-kinase or Akt inhibitors increased susceptibility t

212 a and other epithelial malignancies in which PI 3-kinase or EGF receptor family pathways are activate

213 Use of specific inhibitor to PI 3-kinase or IRAK demonstrated that IRAK activates PI

214 ment of cells with LY294002, an inhibitor of PI 3-kinase, or mutations of the PX domain reduces tyros

215 n) colocalization of RV39 with Src, p85alpha PI 3-kinase, p110beta PI 3-kinase, Akt and Cit-Akt-PH, a

216 Pharmacologic inhibitors were used to block PI 3-kinase, p38, or ERK1/2.

217 n of superoxide to H(2)O(2) does not inhibit PI 3-kinase pathway activation during nutrient perturbat

218 The Rho/PI 3-kinase pathway also differentially mediated matrix

219 ide anions and H(2)O(2), transduction of the PI 3-kinase pathway and steatosis.

220 ucose uptake in HSKM cells via Ras-activated PI 3-kinase pathway in an insulin-independent manner.

221 Additionally, we show that the PI 3-kinase pathway is key for both the induction of CYP

222 reen indicate that at least 9 members of the PI 3-kinase pathway play important roles in Listeria upt

223 rition involving mitochondrial ROS-dependent PI 3-kinase pathway regulation, leading to steatosis.

224 screen to identify components of the type IA PI 3-kinase pathway that control the entry of Listeria i

225 Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is

226 interfering RNA independently activated the PI 3-kinase pathway.

227 e ERK1/2 pathway in rCECs is parallel to the PI 3-kinase pathway.

228 tance can be attenuated by inhibitors of the PI(3) kinase pathway, and is dependent on S6K1-mediated

229 dependent regulation of the phosphoinositol (PI) 3-kinase pathway in steatosis induced by exposure of

230 ptor substrate (IRS)-1/phosphatidylinositol (PI) 3-kinase pathway, resulting in diminished glucose up

231 L-3 receptor+ NIH 3T3 cells utilize the Gab2/PI-3 kinase pathway activated by Jak2, and the Stat5 pat

232 anslation inhibition by blocking the mTOR or PI-3 kinase pathway could significantly reduce the fluor

233 through both the MAP kinase pathway and the PI-3 kinase pathway in Xenopus tissue explants.

234 equired for Cdx gene expression, whereas the PI-3 kinase pathway is not.

235 orylation of Akt, a downstream target of the PI-3-kinase pathway.

236 This may reflect both inhibition of PI-3 kinase pathways and mammalian target of rapamycin (

237 This phosphorylation depends on the PI 3-kinase/PDK1 axis but is Akt-independent.

238 K (mitogen-activated protein kinase) and and PI-3 kinase (phosphatidylinositol 3-kinase) pathways, an

239 The PI 3-kinase (PI 3-K) signaling pathway is essential for

240 The role of Src kinases, PI-3 kinase (PI-3K), Rac1, and CD47 was determined by in

241 the direct, tumor cell-intrinsic effects of PI 3-kinase (PI3K) has been a key focus of research to d

242 PI 3-kinase (PI3K) inhibitors (LY294002 or wortmannin),

243 Increased PI 3-kinase (PI3K) signaling in pancreatic ductal adenoc

244 Inactivation of PI 3-kinase (PI3K) signalling is critical for tumour sup

245 Currently, the Class III PI 3-kinase (PI3K) Vps34 is regarded as the only kinase

246 Insulin increased IRS-1-associated PI 3-kinase (PI3K), extracellular signal-regulated kinas

247 erotrimeric G-protein, phosphatidylinositol (PI) 3-kinase (PI3K), cytohesin ARF GEF and ARF GAP funct

248 In adult retinas, IGF1 activates PI-3 kinase (PI3K), but in neonatal retinas its action i

249 Tat could be attributed to activation of the PI-3-kinase (PI3K)/Akt pathway in the microglial cell li

250 PDGF-induced PI 3-kinase/PIP3/Akt axis may provide new therapeutic ap

251 ation of the small GTPase RalA downstream of PI 3-kinase plays a critical role in this process by mob

252 Blocking macropinocytosis by inhibition of PI 3-kinase prevented the increase in receptor activity

253 In contrast, blockade of PI 3-kinase prevents leptin-induced sympathetic activati

254 Phosphatidylinositol 3-kinase (PI 3-kinase), previously thought by some to be essential

255 The molecular mechanism by which PI 3-kinase promotes bacterial internalization is not un

256 Results suggest that FGF-2 uses both PI 3-kinase/Rac1 and ERK pathways for cell proliferation

257 In both PI 3-kinase/Rac1 and ERK1/2 pathways, Ser10 of p27 is ph

258 ET-BR expression occurred via activation of PI-3 kinase, reactive oxygen species and hypoxia inducib

259 These results show that PI 3-kinase regulation of mRNA stability, predominantly

260 tervening roles for kinases including GSK3B, PI 3-kinase, SGK3 and AMPK.

261 m of PTEN, our data introduce the concept of PI 3-kinase signal activation on the vast plasma membran

262 e ROS-dependent signal cascade amplifies the PI 3-kinase signal by maintaining phosphatase and tensin

263 titative PCR for components of the SHIP/PTEN/PI 3'kinase signaling circuit.

264 module integrates select IQGAP proteins with PI 3-kinase signaling and constitutes a novel, atypical

265 transcription factors and genes regulated by PI 3-kinase signaling have been identified.

266 e of the p85alpha subunit of PI 3-kinase and PI 3-kinase signaling in GH-mediated insulin resistance

267 assays to compare cardiac LTCC function and PI 3-kinase signaling in insulin-deficient diabetic mice

268 Decreased PI 3-kinase signaling in myocytes from type 1 diabetic m

269 had a cardiac contractility defect, reduced PI 3-kinase signaling in the heart, and decreased L-type

270 sts, but not matched skin fibroblasts, via a PI 3-kinase signaling pathway.

271 aling combines the canonical pathway and the PI 3-kinase signaling to upregulate FGF-2 production thr

272 early genes whose induction was dependent on PI 3-kinase signaling, 12 were induced directly by inhib

273 affected in diabetic animals due to reduced PI 3-kinase signaling.

274 chromosome 10 (PTEN)-dependent activation of PI 3-kinase signaling.

275 cal event, we analyzed phosphatidylinositol (PI) 3'kinase signaling, implicated as a critical pathway

276 tudies have shown that phosphatidylinositol (PI) 3-kinase signaling modulates LTCC function.

277 on with the CXCR4 ligand SDF1alpha activated PI-3 kinase signaling, and promoted growth and invasion

278 NF1), NF-kappaB signaling (PRKCB, CSNK1A1), PI-3-kinase signaling (PIK3R1, VAV1), RHOA/cytoskeleton

279 n, alterations in phosphoinositide-3 kinase (PI-3 kinase) signaling that lead to activation of AKT ar

280 These studies identify a MyD88-dependent PI-3 kinase-signaling pathway in T cells that differenti

281 ense oligodeoxynucleotides (ODNs) of Src and PI 3-kinase significantly decreased H-2g-induced monocyt

282 ed by Src and phosphatidylinositol 3-kinase (PI 3-kinase), since inhibitors and antisense oligodeoxyn

283 for recruitment of the phosphatidylinositol (PI) 3-kinase subunit Atg14 but is not required for Atg1

284 3-kinase C2alpha (PI3K-C2alpha) is a type II PI-3-kinase that has been implicated in several importan

285 In addition to transducing PI 3-kinase, the ROS-dependent signal cascade amplifies

286 ase or IRAK demonstrated that IRAK activates PI 3-kinase, the signaling of which phosphorylates IKKal

287 proteins can reduce their ability to attract PI 3-kinase, thereby minimizing its activation.

288 We investigated whether FGF-2 uses PI 3-kinase to facilitate phosphorylation of p27 on seri

289 quires the class III phosphatidylinositol 3 (PI(3))-kinase Vps34, but the mechanisms by which this ki

290 as blocked in a rod-specific knockout of the PI-3 kinase Vps34, resulting in failure of endosomal and

291 shion mesenchyme matrix compaction, but only PI 3-kinase was required for the enhanced matrix compact

292 oduction, but phosphatidylinositol 3-kinase (PI 3-kinase) was required for selective CCL5 induction.

293 Both Rho and PI 3-kinase were involved in normal cushion mesenchyme m

294 ctivate p110alpha/beta-associated class I(A) PI 3-kinase, which in turn enhanced Akt phosphorylation.

295 rtmannin (inhibitor of phosphatidylinositol [PI] 3-kinase, which is upstream of Akt) before and durin

296 Inhibition of PI 3-kinase with LY294002 prevented steatosis.

297 nteraction also precludes interaction of the PI 3-kinase with Rab GTPase activators.

298 tated in this motif abrogated association of PI-3 kinase with MyD88, phosphorylation of protein kinas

299 cy and loss-of-function alleles of the age-1/PI 3-kinase, with the asm-3; age-1 double mutant animals

300 Inhibiting phosphatidylinositol 3-kinase (PI 3-kinase) (wortmannin), mitogen-activated protein kin