ライフサイエンスコーパス: phosphatidylinositol 3,4,5-trisphosphate

1 ylinositol 4,5-bisphosphate (PIP(2)) but not phosphatidylinositol 3,4,5-trisphosphate.

2 linositol 3-kinase (PI3Kgamma) to synthesize phosphatidylinositol 3,4,5-trisphosphate.

3 E3 (but not NHE1) is reversibly activated by phosphatidylinositol 3,4,5-trisphosphate.

4 specifically reduces the cellular levels of phosphatidylinositol 3,4,5-trisphosphate.

5 ation, as well as by binding newly generated phosphatidylinositol 3,4,5-trisphosphate.

6 n vitro showing slightly higher affinity for phosphatidylinositol 3,4,5-trisphosphate.

7 yl-phenylalanine, FcgammaR cross-linking, or phosphatidylinositol 3,4,5-trisphosphate.

8 eter), another 5-phosphatase that hydrolyzes phosphatidylinositol 3,4,5-trisphosphate.

9 se, as well as the localized accumulation of phosphatidylinositol 3,4,5-trisphosphate.

10 to phosphatidylinositol 3,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate.

11 ein partner PLCbeta(1) or a lipid regulator, phosphatidylinositol-3,4,5 trisphosphate.

12 d with macropinocytosis markers, dextran and phosphatidylinositol-3,4,5-trisphosphate.

13 ng by dephosphorylating its major substrate, phosphatidylinositol-3,4,5-trisphosphate.

14 product of phosphoinositide-3 kinase (PI3K), phosphatidylinositol-3.4,5-trisphosphate.

15 stead relies on its ability to bind membrane phosphatidylinositol (3,4,5)-trisphosphate.

16 unt of PtdIns(4,5)P(2) available to generate phosphatidylinositol (3,4,5)-trisphosphate.

17 rylation of PKB substrates, independently of phosphatidylinositol-(3,4,5)-trisphosphate.

18 h the dynamic coalescence of ILT3, BCRs, and phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1

19 K lesion severity was reflected by increased phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1

20 Including phosphatidylinositol 3,4,5-trisphosphate, a downstream e

21 Phosphatidylinositol 3,4,5-trisphosphate, a high-affinit

22 I3Ks) phosphorylate PtdIns(4,5)P(2) to yield phosphatidylinositol(3,4,5)-trisphosphate, activating si

23 osome 10 (PTEN) result in elevated levels of phosphatidylinositol (3,4,5)-trisphosphate, activation o

24 ferentiation, possibly through regulation of phosphatidylinositol [3,4,5]-trisphosphate activity.

25 s activate protein kinase-like ER kinase and phosphatidylinositol 3,4,5-trisphosphate/Akt signaling p

26 arose exhibited markedly elevated levels of phosphatidylinositol (3,4,5)-trisphosphate, along with A

27 id phosphatase control the level of cellular phosphatidylinositol (3,4,5)-trisphosphate, an activator

28 portant regulator of intracellular levels of phosphatidylinositol 3,4,5-trisphosphate, an important s

29 The pleckstrin homology domain of GRP1 binds phosphatidylinositol (3,4,5) trisphosphate and mediates

30 Both the lipid phosphatidylinositol (3,4,5) trisphosphate and the solub

31 ermore, the HCN1-specific peptide binds both phosphatidylinositol (3,4,5)-trisphosphate and phosphati

32 P-Rex1 is dually regulated by phosphatidylinositol (3,4,5)-trisphosphate and the Gbeta

33 o dephosphorylate the lipid second-messenger phosphatidylinositol 3,4, 5-trisphosphate and phosphatid

34 mor suppressor protein that dephosphorylates phosphatidylinositol 3,4,5 trisphosphate and antagonizes

35 dephosphorylating the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate and by doing so

36 singly, FcgammaRIIB-dependent degradation of phosphatidylinositol 3,4,5-trisphosphate and conversion

37 f phosphatidylinositol phosphates, including phosphatidylinositol 3,4,5-trisphosphate and most phosph

38 ich blocks binding of phosphoinositides like phosphatidylinositol 3,4,5-trisphosphate and phosphatidy

39 his enzyme hydrolyzes only lipid substrates, phosphatidylinositol 3,4,5-trisphosphate and phosphatidy

40 Phosphoinositides such as phosphatidylinositol 3,4,5-trisphosphate and phosphatidy

41 Although binding of 3'-phosphoinositides, phosphatidylinositol 3,4,5-trisphosphate and phosphatidy

42 -derived lymphocytes had increased levels of phosphatidylinositol 3,4,5-trisphosphate and phosphoryla

43 ikely contributes to the increased levels of phosphatidylinositol 3,4,5-trisphosphate and the excess

44 ol 1,3,4,5-tetrakisphosphate but did bind to phosphatidylinositol 3,4,5-trisphosphate and to a lesser

45 K-A expression facilitated crosstalk between phosphatidylinositol-(3,4,5)-trisphosphate and inhibitor

46 gly linked to its ability to dephosphorylate phosphatidylinositol-3,4,5 trisphosphate and, thereby, c

47 f phospho-Akt as a marker of the presence of phosphatidylinositol-3,4,5-trisphosphate and found that

48 ed by PI3Ks, which generate lipid messengers phosphatidylinositol-3,4,5-trisphosphate and phosphatidy

49 Surprisingly, K230R mutant strongly binds to phosphatidylinositol-3,4,5-trisphosphate and suppresses

50 neutropenia and normalizes levels of p-Akt, phosphatidylinositol 3,4,5-trisphosphate, and active cas

51 ., phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate, and increases

52 phosphorylation of Vav, Vav association with phosphatidylinositol 3,4,5-trisphosphate, and Vav guanin

53 terine cancers that acts as a phosphatase on phosphatidylinositol-3,4,5-trisphosphate, antagonizing t

54 fter phosphatidylinositol 4,5-biphosphate or phosphatidylinositol 3,4,5-trisphosphate application com

55 ) directly opposes PI3K by dephosphorylating phosphatidylinositol 3, 4, 5-trisphosphate at the 3' pos

56 ions to dephosphorylate the phosphoinositide phosphatidylinositol 3,4,5-trisphosphate at the plasma m

57 ion impair bone resorption, we conclude that phosphatidylinositol 3,4,5-trisphosphate-based protein i

58 y Ras/Rap1GAP Rasa3 (GAP1(IP4BP)) as a major phosphatidylinositol 3,4,5-trisphosphate-binding protein

59 In this work, we demonstrate that the phosphatidylinositol 3,4,5-trisphosphate-binding protein

60 sphosphate (PIP(2))-binding domain; (iii), a phosphatidylinositol-(3,4,5)-trisphosphate-binding domai

61 ssed on mast cells induces the production of phosphatidylinositol 3, 4, 5-trisphosphate by PI3K, whic

62 nd LY294002, completely inhibit formation of phosphatidylinositol 3,4,5-trisphosphate by collagen.

63 ch regulates the levels of the PI3K product, phosphatidylinositol 3,4,5-trisphosphate) caused mast ce

64 a thermal shift screen directed against the phosphatidylinositol (3,4,5) trisphosphate-dependent Rac

65 By investigating phosphatidylinositol (3,4,5)-trisphosphate-dependent Rac

66 Akt1 (K179A) mutant were phosphorylated in a phosphatidylinositol 3,4,5-trisphosphate-dependent manne

67 regulatory subunits (RIalpha) interact with phosphatidylinositol 3,4,5-trisphosphate-dependent Rac e

68 investigated whether Gbetagamma signaling to phosphatidylinositol 3,4,5-trisphosphate-dependent Rac e

69 nd is inhibited through its interaction with phosphatidylinositol 3,4,5-trisphosphate-dependent Rac e

70 Finally, we identified phosphatidylinositol 3,4,5-trisphosphate-dependent Rac e

71 ably expressing ectopic wild-type and mutant phosphatidylinositol-3,4,5-trisphosphate-dependent Rac e

72 whole-genome sequence data identified PREX2 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac e

73 rophages demonstrated increased constitutive phosphatidylinositol 3,4,5-trisphosphate formation, incr

74 steoclast podosomes, and here we demonstrate phosphatidylinositol 3,4,5-trisphosphate/gelsolin functi

75 SHIP2 dephosphorylates phosphatidylinositol 3,4,5-trisphosphate generated by th

76 In both mice, Phosphatidylinositol 3,4,5-trisphosphate generation by a

77 Here we show that phosphatidylinositol-3,4,5-trisphosphate generation and

78 Intriguingly, in plants, phosphatidylinositol (3,4,5)-trisphosphate has not been

79 HIP phosphorylation, recruitment of p52 Shc, phosphatidylinositol 3,4,5-trisphosphate hydrolysis, inh

80 ed infection can be alleviated by augmenting phosphatidylinositol (3,4,5)-trisphosphate in transfused

81 PTEN is capable of dephosphorylating phosphatidylinositol 3,4, 5-trisphosphate in vitro and d

82 phatidylinositol bisphosphates as well as of phosphatidylinositol 3,4,5-trisphosphate in mixed phosph

83 iochemical properties of gelsolin related to phosphatidylinositol 3,4,5-trisphosphate in osteoclast p

84 llular calcium mobilization and synthesis of phosphatidylinositol 3,4,5-trisphosphate in the nucleus.

85 Although a number of studies have implicated phosphatidylinositol-3,4,5-trisphosphate in cell migrati

86 se (PI3K), which catalyzes the production of phosphatidylinositol-3,4,5-trisphosphate, in cell surviv

87 SWAP-70, a phosphatidylinositol 3,4,5-trisphosphate-interacting, F-

88 and the PI phosphatase SHIP2, which converts phosphatidylinositol 3,4,5-trisphosphate into phosphatid

89 Phosphatidylinositol 3,4,5-trisphosphate is a major intr

90 )P2 is overproduced and does not change when phosphatidylinositol 3,4,5-trisphosphate is raised.

91 lipid second messenger PIP3/PtdIns(3,4,5)P3 (phosphatidylinositol (3,4,5)-trisphosphate) is potential

92 eased Akt activity correlates with increased phosphatidylinositol (3,4,5)-trisphosphate levels which

93 Thus, PTEN negatively regulates growth cone phosphatidylinositol 3,4,5-trisphosphate levels and medi

94 hatidylinositol 3-kinase inhibitor decreases phosphatidylinositol 3,4,5-trisphosphate levels and supp

95 Phosphatidylinositol 3,4,5-trisphosphate levels are sign

96 revealed rapid PTEN-dependent depression of phosphatidylinositol 3,4,5-trisphosphate levels in the g

97 ase phosphatidylinositol-3,4-bisphosphate or phosphatidylinositol 3,4,5-trisphosphate levels or induc

98 function led to an increase in intracellular phosphatidylinositol 3,4,5-trisphosphate levels, which s

99 ective Akt phosphorylation despite unaltered phosphatidylinositol 3,4,5-trisphosphate levels.

100 Phosphatidylinositol-3,4,5-trisphosphate levels were und

101 ctivity and probably involving regulation of phosphatidylinositol-3,4,5-trisphosphate levels.

102 During podosome formation, distinct phosphatidylinositol 3,4,5-trisphosphate lipid (PI(3,4,5

103 ation is blocked in presence of the specific phosphatidylinositol-3,4,5-trisphosphate lipid phosphata

104 proportional to the number of tightly bound phosphatidylinositol-(3,4,5)-trisphosphate lipids.

105 Microvesicles containing phosphatidylinositol 3,4,5-trisphosphate mimicked the ac

106 e) produced a modest gain in plasma membrane phosphatidylinositol 3,4,5-trisphosphate, moderate Akt a

107 milliseconds, sufficient to degrade several phosphatidylinositol-3,4,5 trisphosphate molecules.

108 = 8.8) and has the greatest affinity toward phosphatidylinositol 3,4,5-trisphosphate of known 5-phos

109 ector of PI3K), together with a PI3K product phosphatidylinositol 3,4,5-trisphosphate, onto membrane

110 PTEN [phosphatidylinositol (3,4,5)-trisphosphate phosphatase a

111 atase with sequence homology to tensin) is a phosphatidylinositol 3,4,5-trisphosphate phosphatase tha

112 g of PIP2 was specific, because PIP2 but not phosphatidylinositol 3,4,5-trisphosphate, phosphatidylin

113 n superoxide generation, the distribution of phosphatidylinositol 3,4,5-trisphosphate, phosphatidylin

114 mbination is mediated by displacement of the phosphatidylinositol 3,4,5-trisphosphate/phosphoinositid

115 is involved in T cell Ca(2+) signaling via a phosphatidylinositol 3,4, 5-trisphosphate PI(3,4,5)P(3)-

116 sphatidylinositol (4)-phosphate (PI(4)P) and phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P(3

117 respond to phosphatidylinositides, including phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P(3

118 inositol (4,5)-bisphosphate (PI(4,5)P(2)) or phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P(3

119 tions of the GRP1 PH domain interacting with phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P(3

120 mbrane and hydrolyzing the 3' phosphate from phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P3)

121 t increased abundance of membrane-associated phosphatidylinositol 3,4,5-trisphosphate (PI((3,4,5))P(3

122 icroscopy data showed that H(2)O(2) elevated phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3))

123 Membrane phospholipids, such as phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3))

124 PIPKH resulted in >8-fold increase in total phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3))

125 ediated Ca(2+) signaling in mast cells via a phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3))

126 Jurkat cells exhibited high basal levels of phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3);

127 ruffles to form macropinosomes enriched for phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) a

128 In chemotaxing cells, localization of phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) t

129 is a lipid phosphatase with activity against phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3),

130 een its pleckstrin homology domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

131 (PI3K), tensin homology protein (PTEN), and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

132 een its pleckstrin homology domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

133 iates specific binding to negatively charged phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

134 ell growth and survival by dephosphorylating phosphatidylinositol-(3,4,5)-trisphosphate (PI[3,4,5]P3)

135 s (SHIPs) dephosphorylate the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3) a

136 ion and survival by modulating intracellular phosphatidylinositol-3,4,5-trisphosphate (PI-3,4,5-P3) c

137 dylinositol-3,4-bisphosphate (PI-3,4-P2) and phosphatidylinositol-3,4,5-trisphosphate (PI-3,4,5-P3) l

138 of this enzyme reduced rather than increased phosphatidylinositol-3,4,5-trisphosphate (PI-3,4,5-P3) l

139 membranes containing its rare target lipid, phosphatidylinositol (3,4,5)-trisphosphate [PI(3,4,5)P(3

140 phages, enzymes that synthesize or hydrolyze phosphatidylinositol (3,4,5)-trisphosphate [PI(3,4,5)P(3

141 Production of the phosphoinositide lipid phosphatidylinositol (3,4,5)trisphosphate [PI(3,4,5)P3,

142 of SHIP(-/-) animals have elevated levels of phosphatidylinositol 3,4,5-trisphosphate [PI (3,4,5)P(3)

143 of AP-1B onto recycling endosomes containing phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P(3)]

144 T1 PH) binds the rare signaling phospholipid phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P(3)]

145 phils have shown that local accumulations of phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P(3)]

146 ted from the PM only when both PI(4,5)P2 and phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P3] w

147 RAP1 binds PIP5Pase substrate phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P3],

148 The role of phosphatidylinositol 3,4,5-trisphosphate (PI3,4,5P(3)) a

149 and results in the sequential generation of phosphatidylinositol-3,4,5-trisphosphate (PI3,4,5P(3)).

150 and GST pull-down assays demonstrated strong phosphatidylinositol 3,4,5-trisphosphate-PI3K interactio

151 Phosphatidylinositol (3,4,5) trisphosphate (PIP(3))-depe

152 tide exchange factor, is dually activated by phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)) and

153 to mediate delivery of the second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)) to t

154 In other systems, phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)), a m

155 The second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)), for

156 Phosphatidylinositol (3,4,5)-trisphosphate (PIP(3))-depe

157 ally direct the synthesis and degradation of phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)).

158 t regulatory signaling pathways, mediated by phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) and ta

159 Phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) and th

160 many target proteins have been shown to bind phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) and/or

161 atidylinositol 4,5-bisphosphate (PIP(2)) and phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) are no

162 RGS GAP activity is inhibited by phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) but no

163 We also examined the regulation of phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) during

164 s to promote membrane ruffling by regulating phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) dynami

165 and epidermal growth factor (EGF)-stimulated phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) genera

166 The role of the lipid phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) has be

167 Phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) produc

168 Binding of the membrane phospholipid phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) to the

169 We previously reported that phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), a lip

170 Phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), a pri

171 sphatidylinositol 4,5-bisphosphate (PIP(2)), phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), and p

172 racts with the product of the PI3K reaction, phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), in th

173 The major lipid product of PI 3-kinase, phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), was a

174 directly to PIs, and with highest potency to phosphatidylinositol 3,4,5-trisphosphate (PIP(3)).

175 ettes back-filled with a solution containing phosphatidylinositol 3,4,5-trisphosphate (PIP(3)).

176 hat continuous synthesis and availability of phosphatidylinositol-(3,4,5)-trisphosphate (PIP(3)) at t

177 T1/2 translocate to the membrane and bind to phosphatidylinositol-(3,4,5)-trisphosphate (PIP(3)) thro

178 atidylinositol-4,5-bisphosphate (PIP(2)) and phosphatidylinositol-3,4,5-trisphosphate (PIP(3)) activa

179 duced conductance, while pipette infusion of phosphatidylinositol-3,4,5-trisphosphate (PIP(3)) does n

180 t activation relies on the binding of Akt to phosphatidylinositol-3,4,5-trisphosphate (PIP(3)) in the

181 Synthesis of phosphatidylinositol (3,4,5) trisphosphate (PIP3) by pho

182 ls were able to couple receptor occupancy to phosphatidylinositol (3,4,5) trisphosphate (PIP3) produc

183 sional (3D) cell migration using imaging for phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and ac

184 This prevented the increase in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and th

185 atidylinositol (4,5)-bisphosphate (PIP2) and phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in 1-p

186 ells expressing the mutant failed to elevate phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in mut

187 The signaling lipid phosphatidylinositol (3,4,5)-trisphosphate (PIP3) is a k

188 tol 4,5-bisphosphate (PI(4,5)P2) and reduced phosphatidylinositol (3,4,5)-trisphosphate (PIP3) levels

189 re necessary and sufficient for accumulating phosphatidylinositol (3,4,5)-trisphosphate (PIP3) on B c

190 find that persistent, optogenetically driven phosphatidylinositol (3,4,5)-trisphosphate (PIP3) produc

191 TEN), which negatively regulates tumorigenic phosphatidylinositol (3,4,5)-trisphosphate (PIP3) signal

192 PTEN has a central role in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) signal

193 Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), an IP

194 f the CTL phosphoproteome, the production of phosphatidylinositol (3,4,5)-trisphosphate (PIP3), and t

195 ntal measurements of Aktp308, total Akt, and phosphatidylinositol (3,4,5)-trisphosphate (PIP3), from

196 vely binds to a rare signaling phospholipid, phosphatidylinositol (3,4,5)-trisphosphate (PIP3), in th

197 ase 5 and 6 activity that depends on ciliary phosphatidylinositol (3,4,5)-trisphosphate (PIP3), not s

198 The P-Rex (phosphatidylinositol (3,4,5)-trisphosphate (PIP3)-depend

199 naling in the liver leads to accumulation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3).

200 Because SHIP dephosphorylates phosphatidylinositol 3,4,5-trisphosphate (PIP3) and acti

201 e (fMLP) induce neutrophils to polarize with phosphatidylinositol 3,4,5-trisphosphate (PIP3) and prot

202 tion, growth and proliferation by generating phosphatidylinositol 3,4,5-trisphosphate (PIP3) in the i

203 last differentiation from deletion of RGS10; phosphatidylinositol 3,4,5-trisphosphate (PIP3) is essen

204 apical (AP) surface and that AP addition of phosphatidylinositol 3,4,5-trisphosphate (PIP3) is suffi

205 ide growth factors induces the production of phosphatidylinositol 3,4,5-trisphosphate (PIP3) through

206 n foci interact with signals such as Ras and phosphatidylinositol 3,4,5-trisphosphate (PIP3) to form

207 Direct application of phosphatidylinositol 3,4,5-trisphosphate (PIP3) to the i

208 Phosphatidylinositol 3,4,5-trisphosphate (PIP3) was pref

209 ctivity is based on the dephosphorylation of phosphatidylinositol 3,4,5-trisphosphate (PIP3), an esse

210 neration of the key lipid signaling molecule phosphatidylinositol 3,4,5-trisphosphate (PIP3), and ina

211 lizes the phosphoinositide second messenger, phosphatidylinositol 3,4,5-trisphosphate (PIP3), as its

212 Phosphatidylinositol 3,4,5-trisphosphate (PIP3), the pri

213 ely active PI3K or intracellular infusion of phosphatidylinositol 3,4,5-trisphosphate (PIP3), the sec

214 This results in a localized accumulation of phosphatidylinositol 3,4,5-trisphosphate (PIP3), which p

215 ein-coupled receptor (GPCR) stimulation, the phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependen

216 Phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependen

217 ckstrin homology (PH) domain that recognizes phosphatidylinositol 3,4,5-trisphosphate (PIP3).

218 phatidylinositol 4,5-bisphosphate (PIP2) and phosphatidylinositol 3,4,5-trisphosphate (PIP3).

219 ction and turnover of their membrane ligand, phosphatidylinositol 3,4,5-trisphosphate (PIP3).

220 PH) domains, which bind the second messenger phosphatidylinositol 3,4,5-trisphosphate (PIP3).

221 lucose homeostasis through the production of phosphatidylinositol 3,4,5-trisphosphate (PIP3).

222 phoinositide 3-kinase (PI3K) and its product phosphatidylinositol(3,4,5)-trisphosphate (PIP3) control

223 Phosphatidylinositol-(3,4,5)-trisphosphate (PIP3), a pro

224 nce the recruitment of Grb2 was dependent on phosphatidylinositol-(3,4,5)-trisphosphate (PIP3), we ex

225 survival by generating the second messenger phosphatidylinositol-(3,4,5)-trisphosphate (PIP3).

226 C and H(2)S treatments caused an increase in phosphatidylinositol-3,4,5 trisphosphate (PIP3), AKT pho

227 N tumor suppressor acts as a phosphatase for phosphatidylinositol-3,4,5-trisphosphate (PIP3) [1, 2].

228 previously the development of small-molecule phosphatidylinositol-3,4,5-trisphosphate (PIP3) antagoni

229 timulating production of the signaling lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3) by the l

230 Phosphatidylinositol-3,4,5-trisphosphate (PIP3) has been

231 Phosphatidylinositol-3,4,5-trisphosphate (PIP3), the pro

232 membrane through Gi signaling pathways by a phosphatidylinositol-3,4,5-trisphosphate (PIP3)-dependen

233 sphate (PIP2) to produce the signaling lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3).

234 ubunits, resulting in enhanced generation of phosphatidylinositol-3,4,5-trisphosphate (PIP3).

235 As expected, a decrease of phosphatidylinositol (3,4,5)-trisphosphate pools and AKT

236 back loop for sustained PI3K recruitment and phosphatidylinositol-3,4,5-trisphosphate production, req

237 -p110 dimer, and these foci are not sites of phosphatidylinositol-3,4,5-trisphosphate production.

238 Furthermore, phosphatidylinositol (3,4, 5)-trisphosphate (PtdIns (3,4

239 ated the activation of proteins that require phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5

240 pecific membrane compartment where levels of phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5

241 h activation leads to hydrolyzation of PIP3 (Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5

242 al for negative control of the production of phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5

243 h promotes Tec membrane localization through phosphatidylinositol 3,4,5-trisphosphate (PtdIns 3,4,5-P

244 Although phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

245 ARAP1 is a phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

246 ar to be a substrate for calpain 2; however, phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

247 itol 4,5-bisphosphate (PtdIns(4,5)P(2)), and phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

248 nositol 3,4-bisphosphate (PtdIns(3,4)P2) and phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

249 is a central feature of eukaryotic cells and phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

250 Motile nonmuscle cells concentrate phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

251 Signaling by the second messenger phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

252 tide 3-OH kinase (PI3K), PtdIns(3,4)P(2) and phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

253 CSF, which increased PI3K activity and total phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

254 gy 2 domain containing protein that can bind phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

255 3-kinase and its second messenger products, phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

256 of KATP channels by the PI 3-kinase product phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

257 have high phosphoinositide specificity, i.e. phosphatidylinositol 3,4,5-trisphosphate (PtdIns-(3,4,5)

258 generate the intracellular signaling lipid, phosphatidylinositol(3,4,5)trisphosphate (PtdIns(3,4,5)P

259 osphate (InsP6) to InsP7, conferred enhanced phosphatidylinositol-(3,4,5)-trisphosphate (PtdIns(3,4,5

260 Phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P

261 Many neutrophil functions are regulated by phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P

262 protein tyrosine phosphatase PTP-MEG2 binds phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P

263 In contrast, phosphatidylinositol-3,4,5-trisphosphate (PtdIns-3,4,5-P

264 e generation of two major second messengers, phosphatidylinositol-3,4,5-trisphosphate (PtdIns-3,4,5-P

265 Bruton's tyrosine kinase (Btk) binds to phosphatidylinositol-3,4,5-trisphosphate (PtdIns-3,4,5-P

266 f phosphoinositide 3-kinase (PI3K)-dependent phosphatidylinositol (3,4,5)-trisphosphate [PtdIns(3,4,5

267 Addition of the PI3K product phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P

268 cation and subsequent immunocytochemistry of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P

269 crophage that lead to transient formation of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P

270 ss IB PI3K results in the rapid synthesis of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P

271 K)-dependent signalling by dephosphorylating phosphatidylinositol 3,4,5-trisphosphate (PtdInsP(3)).

272 -2, but not IQGAP3, binds preferentially to phosphatidylinositol 3,4,5-trisphosphate (PtdInsP(3)).

273 We identified phosphatidylinositol 3,4,5-trisphosphate RAC exchanger 2

274 After induction with insulin, phosphatidylinositol 3,4,5-trisphosphate recruits OGT fr

275 Phosphatidylinositol 3,4,5-trisphosphate shows an extrao

276 edback system that maintains and amplifies a phosphatidylinositol-3,4,5-trisphosphate signal at the l

277 icantly increased by elevating intracellular phosphatidylinositol (3,4,5)-trisphosphate signaling wit

278 some ten (PTEN) is an important regulator of phosphatidylinositol-(3,4,5,)-trisphosphate signalling,

279 tic cleft of PTEN, a structure essential for phosphatidylinositol 3,4,5-trisphosphate specificity.

280 tibodies directed against mTOR or RICTOR had phosphatidylinositol 3,4,5-trisphosphate-stimulated Ser-

281 ractions of 3T3-L1 adipocytes, revealed that phosphatidylinositol 3,4,5-trisphosphate-stimulated Ser-

282 s, loss of PTEN leads to increased levels of phosphatidylinositol (3,4,5)-trisphosphate, stimulation

283 cks the E17K Akt1 interaction with its PIP3 (phosphatidylinositol (3,4,5)-trisphosphate) substrate.

284 the mobilization of Ca(2+), the synthesis of phosphatidylinositol 3,4,5-trisphosphate, the activation

285 lso dependent on the interaction of Btk with phosphatidylinositol 3,4,5-trisphosphate, the product of

286 tase that can dephosphorylate position D3 of phosphatidylinositol-3,4,5 trisphosphate, the site that

287 cells by binding the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate through the ple

288 ol 5'-phosphatase 1 (SHIP1) dephosphorylates phosphatidylinositol 3,4,5-trisphosphate to phophatidyli

289 t left the concentration of the anchor lipid phosphatidylinositol-3,4,5-trisphosphate unchanged.

290 can be spatially regulated independently of phosphatidylinositol (3,4,5)-trisphosphate via phosphory

291 Finally, concurrent production of phosphatidylinositol 3,4,5-trisphosphate was found to co

292 ity in the absence of Ca2+ when PI-4,5-P2 or phosphatidylinositol 3,4,5-trisphosphate were present.

293 of phosphatidylinositol-3,4-bisphosphate and phosphatidylinositol-3,4,5-trisphosphate were below dete

294 tment appeared to bypass the requirement for phosphatidylinositol 3,4,5-trisphosphate when Akt was us

295 y and accompanied by localized production of phosphatidylinositol 3,4,5-trisphosphate, whereas MAPK a

296 of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate, which are clea

297 Mechanistically, the interaction of phosphatidylinositol (3,4,5)-trisphosphate with AKT faci

298 ge factor for Arf GTPases, selectively binds phosphatidylinositol 3,4,5-trisphosphate with high affin

299 sphatidylinositol 3-kinase and production of phosphatidylinositol 3,4,5-trisphosphate with the phosph

300 INa-L was also increased, and inhibitable by phosphatidylinositol 3,4,5-trisphosphate, with hours of