ライフサイエンスコーパス: phosphatidylinositol

1 hannels established a Ca(2+)-dependent local phosphatidylinositol 1,4,5-trisphosphate gradient, which

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

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

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

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

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

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

8 I3K/AKT pathway as the lipid phosphatase for phosphatidylinositol 3,4,5-triphosphate.

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

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

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

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

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

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

15 ositol 3,4,5-trisphosphate (PI(3,4,5)P3) and phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2), sugge

16 erentially with maturing macropinosomes in a phosphatidylinositol 3,5-bisphosphate-dependent manner a

17 C2 is a Na(+)-selective channel activated by phosphatidylinositol 3,5-bisphosphate.

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

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

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

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

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

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

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

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

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

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

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

29 Phosphatidylinositol 3-kinase (PI3K) pathway activation

30 Phosphatidylinositol 3-kinase (PI3K) pathway activation

31 Phosphatidylinositol 3-kinase (PI3K) pathway activity wa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 Phosphatidylinositol 3-kinase alpha is an attractive tar

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

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

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

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

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

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

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

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

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

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

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

68 The phosphatidylinositol 3-kinase delta (PI3Kdelta) pathway

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

70 Phosphatidylinositol 3-kinase p110delta isoform (PI3K p1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 In MKs, the level of phosphatidylinositol 3-monophosphate (PI3P) was signific

94 osphoinositide species with a preference for phosphatidylinositol 3-monophosphate and phosphatidylino

95 dentified the phosphoinositide lipids (PIPs) phosphatidylinositol 3-phosphate (PI(3)P) and phosphatid

96 erminal PX domain of Vam7 binds to the lipid phosphatidylinositol 3-phosphate (PI3P) and the tetherin

97 the process, specifically for Vps34-mediated phosphatidylinositol 3-phosphate (PI3P) deposition.

98 nramp4 Our results indicate that AtPH1 binds phosphatidylinositol 3-phosphate (PI3P) in vivo and acts

99 w that Vps13 binds phospholipids, especially phosphatidylinositol 3-phosphate (PI3P), via its SHR_BD

100 of Cb binds phosphoinositides, specifically phosphatidylinositol 3-phosphate (PI3P).

101 g and by amino acid-stimulated production of phosphatidylinositol 3-phosphate (PtdIns3P) by the lipid

102 The activated Akt acted through phosphatidylinositol 3-phosphate 5-kinase and Rab11 to f

103 tophagy pathways, which are characterized by phosphatidylinositol 3-phosphate [PI(3)P]-positive membr

104 ylinositol 3-kinase) complex and its product phosphatidylinositol 3-phosphate [PtdIns(3)P] play key r

105 actin immobilized by the local enrichment of phosphatidylinositol (3,4,5)-triphosphate (PIP3) within

106 nked scaffold that facilitates nucleation of phosphatidylinositol (3,4,5)-triphosphate at the plasma

107 This in turn increased the level of phosphatidylinositol (3,4,5)-triphosphate, which transac

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

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

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

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

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

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

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

115 The PPI phosphatidylinositol (3,5)-bisphosphate (PI(3,5)P2) is e

116 onal marker) and its upstream molecule FIG4 (phosphatidylinositol (3,5)-bisphosphate 5-phosphatase) a

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

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

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

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

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

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

123 nositol-3-phosphate pool in early endosomes; phosphatidylinositol-3,4-biphosphate and the GTPase Rab5

124 tivity, we determined that whereas levels of phosphatidylinositol-3,4-bisphosphate and phosphatidylin

125 plasma membrane, intracellular clathrin and phosphatidylinositol-3,4-bisphosphate predict the excita

126 analysis, the TRPML1 structure reveals that phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2) bi

127 -abundance and LEL-enriched signalling lipid phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2), w

128 PIKfyve is a lipid kinase that generates phosphatidylinositol-3,5-bisphosphate and, directly or i

129 Kfyve modulates phagosome maturation through phosphatidylinositol-3,5-bisphosphate-dependent activati

130 ylating phosphatidylinositol-3-phosphate and phosphatidylinositol-3,5-bisphosphate.

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

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

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

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

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

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

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

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

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

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

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

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

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

144 4 PI3K is thought to be the main producer of phosphatidylinositol-3-monophosphate, a lipid that contr

145 hough signaling via the lipid kinase PI(3)K (phosphatidylinositol-3-OH kinase), the serine-threonine

146 5-trisphosphate were below detection limits, phosphatidylinositol-3-phosphate (PI(3)P) levels in rod

147 s nanomolar affinity for bilayers containing phosphatidylinositol-3-phosphate (PI[3]P).

148 singly, the regulatory early endosomal lipid phosphatidylinositol-3-phosphate (PtdIns(3)P) persists o

149 5-biphosphate marks the plasma membrane, and phosphatidylinositol-3-phosphate and phosphatidylinosito

150 in, an enzyme specifically dephosphorylating phosphatidylinositol-3-phosphate and phosphatidylinosito

151 , distinct from any later encounter with the phosphatidylinositol-3-phosphate pool in early endosomes

152 tely after budding coincides with a burst of phosphatidylinositol-3-phosphate, distinct from any late

153 s involved in autophagy initiation, and bind phosphatidylinositol-3-phosphate.

154 Phosphatidylinositol 4,5-biphosphate (PIP2) is critical

155 sociated adaptors, and leads to reduction of phosphatidylinositol 4,5-biphosphate from the plasma mem

156 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is a m

157 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is a n

158 study the direct interaction of Ca(2+) with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the m

159 Moreover, steady-state PM phosphatidylinositol 4,5-bisphosphate (PI[4,5]P2) levels

160 Previous work demonstrated that the lipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) enabled th

161 is conformational transition is dependent on phosphatidylinositol 4,5-bisphosphate (PIP2) and is rela

162 arance and recovery correlated with synaptic phosphatidylinositol 4,5-bisphosphate (PIP2) and that al

163 analyses of Rabphilin-3A C2B-SNAP25 and C2B-phosphatidylinositol 4,5-bisphosphate (PIP2) complexes,

164 s TRPC4/5 channel activity is potentiated by phosphatidylinositol 4,5-bisphosphate (PIP2) depletion.

165 hoinositides in vitro and colocalized with a phosphatidylinositol 4,5-bisphosphate (PIP2) marker in p

166 Cgamma, enzymes that deplete plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2), and these

167 on by SMIT-transported, myo-inositol-derived phosphatidylinositol 4,5-bisphosphate (PIP2), the mechan

168 , we show that CDO is contingent on membrane phosphatidylinositol 4,5-bisphosphate (PIP2), which is f

169 2/3 channel activity is augmented in vivo by phosphatidylinositol 4,5-bisphosphate (PIP2), which is g

170 with CCh resulted in a similar reduction in phosphatidylinositol 4,5-bisphosphate (PIP2).

171 cific interactions with the regulatory lipid phosphatidylinositol 4,5-bisphosphate (PIP2).

172 ,5-trisphosphate (Ins(1,4,5)P3) 3-kinase and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) 3-

173 Phosphatidylserine (PtdSer) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) ha

174 holipase requiring the cellular host factors phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and ub

175 ipid-binding module in TMEM24 transports the phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] precur

176 Membrane phosphoinositides, especially phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], regul

177 itol 4-phosphate 5-kinase that Mcp5 binds to phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2].

178 main enriched in the regulatory phospholipid phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] is

179 er by the presence of phospholipid vesicles, phosphatidylinositol 4,5-bisphosphate and Ca(2+), or by

180 NCX inactivation occurs in the absence of phosphatidylinositol 4,5-bisphosphate and is facilitated

181 kers for the anionic signaling phospholipids phosphatidylinositol 4,5-bisphosphate and phosphatidic a

182 otentiated by cold temperature involving the phosphatidylinositol 4,5-bisphosphate binding residue (L

183 S4 movement and gate opening by mutations or phosphatidylinositol 4,5-bisphosphate depletion, we show

184 intact F-actin architecture is required for phosphatidylinositol 4,5-bisphosphate homeostasis mediat

185 ion displaces ciliary Inpp5e and accumulates phosphatidylinositol 4,5-bisphosphate in distal cilia.

186 phospholipase C (PLC) isozymes to hydrolyze phosphatidylinositol 4,5-bisphosphate into the second me

187 Specific binding of ENTH to phosphatidylinositol 4,5-bisphosphate leads to a substan

188 olipase C-beta (PLC-beta) isoforms hydrolyze phosphatidylinositol 4,5-bisphosphate to the second mess

189 haq Therefore, XY-69 can replace radioactive phosphatidylinositol 4,5-bisphosphate used in convention

190 Although phosphatidylinositol 4,5-bisphosphate, 3-phosphate, and

191 odomains, which are enriched in cholesterol, phosphatidylinositol 4,5-bisphosphate, and gangliosidic

192 dhesion of a pleckstrin homology domain with phosphatidylinositol 4,5-bisphosphate.

193 sence and presence of phosphatidylserine and phosphatidylinositol 4,5-bisphosphate.

194 t increases substantially in the presence of phosphatidylinositol 4,5-bisphosphate.

195 beta1 activity measured with the fluorescent phosphatidylinositol 4,5-bisphosphate/inositol 1,4,5-tri

196 o Syt7 in the presence or absence of l-alpha-phosphatidylinositol 4,5-diphosphate (PIP2).

197 which is associated with the recruitment of phosphatidylinositol 4-kinase 2A.

198 Phosphatidylinositol 4-kinase beta (PI4KB) is one of fou

199 onserved role for Gga proteins in regulating phosphatidylinositol 4-kinase function at the TGN.

200 cluding oxysterol binding protein (OSBP) and phosphatidylinositol 4-kinase III beta (PI4KB).

201 tes the activity of a cellular lipid kinase, phosphatidylinositol 4-kinase IIIalpha (PI4KA).

202 teroviruses, enterovirus 71 (EV71) relies on phosphatidylinositol 4-kinase IIIbeta (PI4KB) for genome

203 The lipid kinase phosphatidylinositol 4-kinase IIIbeta (PI4KB) is an esse

204 Phosphatidylinositol 4-kinase IIIbeta (PI4KB) is indispe

205 rotein of enterovirus 71 recruits an enzyme, phosphatidylinositol 4-kinase IIIbeta, by interacting wi

206 We identify two motifs in the yeast phosphatidylinositol 4-kinase, Pik1, which are required

207 trongest temporal change is seen at a SNP in phosphatidylinositol 4-kinase, which is involved in a pa

208 for phosphatidylinositol 3-monophosphate and phosphatidylinositol 4-monophosphate.

209 hosphatidylinositol 3-phosphate (PI(3)P) and phosphatidylinositol 4-phosphate (PI(4)P) as regulators

210 udy, we found that Hh elevates production of phosphatidylinositol 4-phosphate (PI(4)P).

211 ing protein (OSBP) exchanges cholesterol and phosphatidylinositol 4-phosphate (PI-4P) at contact site

212 eracts with actin and regulates the level of phosphatidylinositol 4-phosphate (PI4P) in the membranes

213 one of four human PI4K enzymes that generate phosphatidylinositol 4-phosphate (PI4P), a minor but ess

214 ATPase activity, which remains dependent on phosphatidylinositol 4-phosphate (PI4P), a regulator of

215 domain targets it to the Golgi by binding to phosphatidylinositol 4-phosphate (PtdIns(4)P) in the Gol

216 e distribution, fate, and functional role of phosphatidylinositol 4-phosphate (PtdIns4P) during phago

217 PM depletion of either phosphatidylinositol 4-phosphate (PtdIns4P) or PtdIns(4,

218 At the trans-Golgi network (TGN), phosphatidylinositol 4-phosphate (PtdIns4P) plays import

219 lipid localization, as overexpression of the phosphatidylinositol 4-phosphate 5-kinase alpha [PtdIns(

220 on yeast zygotes and show by perturbation of phosphatidylinositol 4-phosphate 5-kinase that Mcp5 bind

221 wn to be necessary for the export of Mss4, a phosphatidylinositol 4-phosphate 5-kinase, and required

222 How the biosynthesis of PtdIns(4,5)P2 by phosphatidylinositol 4-phosphate 5-kinases (PI4P 5-kinas

223 We measured dynamic changes of PI(4,5)P2, phosphatidylinositol 4-phosphate, diacylglycerol, inosit

224 the Golgi apparatus by controlling levels of phosphatidylinositol 4-phosphate, which facilitates carg

225 phatase activity toward the phosphoinositide phosphatidylinositol (4,5)-bisphosphate or altered the s

226 move laterally across the plasma membrane to phosphatidylinositol (4,5)-bisphosphate-enriched domains

227 hich encodes a conserved PM scaffold for the phosphatidylinositol-4 kinase Stt4, build CRs that can s

228 th the surrounding plasma membrane, contains phosphatidylinositol-4,5-biphosphate and a smaller amoun

229 In endocytic traffic, phosphatidylinositol-4,5-biphosphate marks the plasma me

230 ted by conformational changes in response to phosphatidylinositol-4,5-bisphosphate (PIP2) and cargo b

231 kinases phosphorylate the constitutive lipid phosphatidylinositol-4,5-bisphosphate (PIP2) to produce

232 1 C terminus (CT) binds calmodulin (CaM) and phosphatidylinositol-4,5-bisphosphate (PIP2), but the ro

233 Phosphatidylinositol-4,5-bisphosphate (PIP2), one of the

234 TRPM4 is a calcium-activated, phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) -m

235 he affinity of the polybasic lysine patch to phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2).

236 Phosphatidylinositol-4,5-bisphosphate 3-kinase 1A, activ

237 ivation of canonical nuclear factor kappa B, phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt, and

238 The phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt/ mamm

239 Phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] is ess

240 dynamins bind the plasma membrane-localized phosphatidylinositol-4,5-bisphosphate using the pleckstr

241 ed in all LPS responses, but a single lipid (phosphatidylinositol-4,5-bisphosphate) regulates many LP

242 converts phosphatidylinositol-5-phosphate to phosphatidylinositol-4,5-bisphosphate.

243 antimalarial drugs, including the Plasmodium phosphatidylinositol-4-OH kinase (PI4K)-specific inhibit

244 hat the Cryptosporidium lipid kinase PI(4)K (phosphatidylinositol-4-OH kinase) is a target for pyrazo

245 ly, EV71 infection induces the production of phosphatidylinositol-4-phosphate (PI4P).

246 rough direct phosphorylation of FA-localized phosphatidylinositol-4-phosphate 5-kinase type-l gamma (

247 and found that mainly phosphatidic acid and phosphatidylinositol-4-phosphate enhance association of

248 A substantial burst of phosphatidylinositol-4-phosphate immediately after buddi

249 ne, and phosphatidylinositol-3-phosphate and phosphatidylinositol-4-phosphate mark distinct endosomal

250 itol-4,5-biphosphate and a smaller amount of phosphatidylinositol-4-phosphate.

251 Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-leve

252 ompartments and perturbs the activity of the phosphatidylinositol 5-kinase PIKfyve to manipulate PI(3

253 Type 2 phosphatidylinositol-5-phosphate 4-kinase (PI5P4K) conve

254 w that mice with germline deletion of type 2 phosphatidylinositol-5-phosphate 4-kinase gamma (Pip4k2c

255 2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1

256 ,5-bisphosphate and, directly or indirectly, phosphatidylinositol-5-phosphate [PtdIns(5)P].

257 sitol-5-phosphate 4-kinase (PI5P4K) converts phosphatidylinositol-5-phosphate to phosphatidylinositol

258 Phosphatidylinositol and its phosphorylated derivatives

259 rast, tumor tissues displayed an increase in phosphatidylinositols and arachidonate-containing phosph

260 atidylethanolamine, phosphatidylcholine, and phosphatidylinositol, and found all three similarly inhi

261 sitol 4,5-bisphosphate [PI(4,5)P2] precursor phosphatidylinositol between bilayers, allowing replenis

262 alpha (PITPalpha), a protein which shuttles phosphatidylinositol between organelles, is essential fo

263 the myristoylated Arf1/Brag2 complex with a phosphatidylinositol bisphosphate (PIP2) -containing lip

264 rearrangements to the common gating ligand, phosphatidylinositol bisphosphate (PIP2), although these

265 monstrate that the vesicular signaling lipid phosphatidylinositol bisphosphate PI(3,5)P2 modulates TP

266 es showed that total phosphatidylcholine and phosphatidylinositol (but not diacylglycerol or sphingom

267 ) are downstream of IRK and are activated by phosphatidylinositol-dependent kinase 1 (PDK1) phosphory

268 rdin reductase with Akt/protein kinase B and phosphatidylinositol-dependent kinase 1 regulates glycog

269 mplex along with PIGK, PIGS, PIGT, and PIGU (phosphatidylinositol-glycan biosynthesis classes K, S, T

270 creased expression of the odr-2 glycosylated phosphatidylinositol (GPI)-linked signaling gene in the

271 ular mechanisms that mediate localization of phosphatidylinositol kinases responsible for synthesis o

272 59 polar phospholipids (phosphatidylserines, phosphatidylinositols, lysophosphatidylinositols, and ph

273 e-resident phospholipids with preference for phosphatidylinositol monophosphates and forms oligomers.

274 The cellular mass of phosphatidylinositol monophosphates and Golgi PI-4P meas

275 rapamycin-inducible system in which various phosphatidylinositol phosphatases were recruited to the

276 protein-membrane interactions by binding to phosphatidylinositol phosphate (PIP) molecules.

277 Type Igamma phosphatidylinositol phosphate kinase (PIPKIgamma), a ph

278 l G protein and upstream regulator of type I phosphatidylinositol phosphate kinases (PIP5Ks) and PM P

279 of Dok7 associates with membranes containing phosphatidylinositol phosphates (PIPs) via interactions

280 ctor, whereas the PH domain binds to various phosphatidylinositol-phosphates.

281 Phosphatidylinositol, phosphatidylserine and phosphatidy

282 nce of Naa60 toward membranes containing the phosphatidylinositol PI(4)P, thus possibly explaining th

283 Depletion of phosphatidylinositol (PI) by targeting bacterial PI-spec

284 the cooperation of 14-3-3zeta with specific phosphatidylinositol (PI) enzymes.

285 monstrate that PI(4)P, the predominant Golgi phosphatidylinositol (PI) species, directly interacts wi

286 sphoinositide synthesis is the conversion of phosphatidylinositol (PI) to PI4P, the precursor of PI(4

287 n obtained by both WDLC and EDLC was rich in phosphatidylinositol (PI), and contents were 37.8 and 25

288 tidylserine (PS), phosphatidylglycerol (PG), phosphatidylinositol (PI), and sulfatides (ST).

289 ne (PC), phosphatidylethanolamines (PE), and phosphatidylinositol (PI), in newly fertilized individua

290 endosomal trafficking regulator, the class 3 phosphatidylinositol (PtdIns) 3-kinase vacuolar protein

291 eature of PITPs is their ability to exchange phosphatidylinositol (PtdIns) molecules between membrane

292 and metabolome analyses both identified the phosphatidylinositol signaling pathway as a target of in

293 in phospholipids, and several phosphorylated phosphatidylinositol species are known to regulate key a

294 were increased in normoxic pellets, whereas phosphatidylinositol species were the most prominent lip

295 by nonessential fatty acids and a variety of phosphatidylinositol species with further in-tumor varie

296 Enzymatic treatment with phosphatidylinositol-specific phospholipase C, a phospho

297 he autophagy-initiation complex localizes to phosphatidylinositol synthase (PIS)-enriched ER subdomai

298 VPS34 activity by increasing the binding of phosphatidylinositol to VPS34.

299 the phosphoinositide signaling modulated by phosphatidylinositol transfer protein type alpha (PITPal

300 Phosphatidylinositol-transfer proteins (PITPs) regulate