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

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

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

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

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

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

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

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

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

19 c fibroblasts resulted in elevated levels of phosphatidylinositol 3,4,5,-trisphosphate, a product of

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 Our studies suggest that PTEN regulates the phosphatidylinositol 3,4, 5,-trisphosphate and Akt signa

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

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

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

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

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

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

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

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

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

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

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

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

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 ily and Syk tyrosine kinases, and perhaps by phosphatidylinositol 3,4,5-trisphosphate, BCR-coupled si

59 Recent cloning of a rat brain phosphatidylinositol 3,4, 5-trisphosphate binding protei

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

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

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

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

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

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

66 tion of Ypk1 and SGK by Pkh1 did not require phosphatidylinositol 3,4,5-trisphosphate, consistent wit

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

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

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

72 ably expressing ectopic wild-type and mutant 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 Intriguingly, in plants, phosphatidylinositol (3,4,5)-trisphosphate has not been

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

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

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

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

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

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

84 d by a rapid increase in the accumulation of phosphatidylinositol 3,4,5-trisphosphate in vivo, and ad

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

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

104 Phosphatidylinositol 3,4, 5-trisphosphate-mediated membr

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 onsistent with the notion that DAF-18 acts a phosphatidylinositol 3,4,5-trisphosphate phosphatase in

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

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

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

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

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

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

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

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

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

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

122 t increased abundance of membrane-associated 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 icroscopy data showed that H(2)O(2) elevated phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3))

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

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

129 ineating the regulatory mechanism underlying phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) m

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

131 is a lipid phosphatase with activity against 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 (PI3K), tensin homology protein (PTEN), and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 L did not induce the in vivo accumulation of phosphatidylinositol-3,4,5-trisphosphate (PIP(3)), where

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 the phosphoinositide 3-kinase (PI3K) product phosphatidylinositol 3,4, 5-trisphosphate (PIP3) into ph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 P1), which has 3-phosphatase activity toward phosphatidylinositol 3,4,5-trisphosphate (PIP3).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 Resultant phosphatidylinositol 3,4,5-trisphosphate probably functi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 3-kinase and its second messenger products, phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

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

253 P(2)), whereas osmotic stress increased both phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P

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

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

256 ly demonstrated that the D3-phosphoinositide phosphatidylinositol 3,4,5-trisphosphate (PtdIns-3,4,5-P

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

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

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

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

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

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

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

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

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

266 ed for chemoattractant-induced production of phosphatidylinositol 3,4,5-trisphosphate [PtdIns (3,4,5)

267 as been suggested that PTEN dephosphorylates phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3, 4,5)

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

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

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

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

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

273 -2, but not IQGAP3, binds preferentially to phosphatidylinositol 3,4,5-trisphosphate (PtdInsP(3)).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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