ライフサイエンスコーパス: PtdIns

1 PtdIns is a poor substrate for PIP5K, but it also shows

2 PtdIns(3)P production was not observed in the protrusion

3 PtdIns(3,4,5)P3-dependent Rac exchanger 1 (PREX1) is a R

4 PtdIns(3,5)P2 deficiency causes neurodegeneration in mic

5 PtdIns(4)P binding to TTBK2 and the distal appendage pro

6 PtdIns(4,5)P(2) binding promotes the interaction between

7 PtdIns(4,5)P2 and SNX5 function together to protect Hrs

8 PtdIns(4,5)P2 binding to the ATG14-BATS domain regulates

9 PtdIns(4,5)P2 generation at these sites requires PIPKIga

10 PtdIns(4,5)P2 is an important signaling lipid with conse

11 nvasion and metastasis 1), Vav and P-Rex1/2 (PtdIns(3,4,5)P3 (phosphatidylinositol (3,4,5)-triphospha

12 d messenger phosphatidylinositol(3,4,5)P(3) (PtdIns(3,4,5)P(3)) is formed by stimulation of various r

13 way can compensate for depletion of dOCRL, a PtdIns(4,5)P(2) phosphatase.

14 t phospholipid phosphatase in establishing a PtdIns(3,4,5)P(3) compass.

15 lpha-helix that penetrates the membrane in a PtdIns(4,5)P(2)-independent manner.

16 I2b to plasma membrane show that WIPI2b is a PtdIns(3)P effector upstream of Atg16L1 and is required

17 , namely the Sec14p homolog PstB2p/Pdr17p; a PtdIns 4-kinase, Stt4p; and a C2 domain of Psd2p.

18 remature actin assembly during CME through a PtdIns(4,5)P2-dependent mechanism.

19 In addition, PtdIns(3,4)P2 is able to bind to Dlg1.

20 phatidylinositol 4-phosphate 5-kinase alpha [PtdIns(4)P5K] activator Arf6 or PtdIns(4)P5K alone, or t

21 sulting in distinct regions with alternating PtdIns(4)P depletion and enrichment.

22 SPR experiments identify PtdIns(4,5)P(2) and PtdIns(3,4,5)P(3) as preferred targets of NOXO1beta PX.

23 paratus that probably houses the Ca(2+)- and PtdIns(4,5)P2-binding sites.

24 ell activation by altering PI3K activity and PtdIns levels.

25 d interactions among TECPR1, Atg12-Atg5, and PtdIns(3)P provide the fusion specificity between autoph

26 et genes, the binding event between ING2 and PtdIns(5)P is required for ING2 promoter occupancy and I

27 the TIPE3 protein enhances PtdIns(4,5)P2 and PtdIns(3,4,5)P3, is overexpressed in certain cancers, an

28 kinase (PI3K) generates PtdIns(3,4,5)P3 and PtdIns(3,4)P2, leading to the activation of proliferativ

29 ionalize phosphorylation of Ins(1,4,5)P3 and PtdIns(4,5)P2 by HsIPMK.

30 PIKfyve perturbation and PtdIns(3,5)P2 reduction result in massive membrane vacuo

31 n nonleukocytes that showed that PIKfyve and PtdIns(5)P control Rac and cell migration.

32 ophagosomes have associated PIPKIgammai5 and PtdIns(4,5)P2 that are colocalized with late endosomes a

33 fold the polyphosphoinositides PtdIns3P and PtdIns(3,5)P(2) using a conserved FRRG motif.

34 bind polyphosphoinositides) are PtdIns3P and PtdIns(3,5)P2 binding autophagy related proteins.

35 In yeast and mammals, PtdIns3P and PtdIns(3,5)P2 play crucial roles in trafficking toward t

36 ers Atg18, Atg21, and Hsv2 bind PtdIns3P and PtdIns(3,5)P2 with high affinities in the nanomolar to l

37 sphatidylinositol 3-phosphate (PtdIns3P) and PtdIns(3,5)P2, lipids which regulate endo-lysosomal memb

38 phoinositides) are a family of PtdIns3P- and PtdIns(3,5)P2-binding proteins that play an important ro

39 gulates PIP5K transcription and PtdIns4P and PtdIns(4,5)P2 levels, in particular their association wi

40 dIns(3,4,5)P3 5-phosphatases (eg, SHIP), and PtdIns(3,4)P2 4-phosphatases (eg, INPP4B).

41 idylinositol-4,5-bisphosphate (also known as PtdIns(4,5)P2) rearrange locally at endoplasmic reticulu

42 P2), whereas other phosphoinositides such as PtdIns(4,5)P2, which is enriched in plasma membranes, in

43 ridge Wnt-induced and Dishevelled-associated PtdIns(4,5)P2 production to the phosphorylation of Lrp6.

44 PtdIns lipid homeostasis via VAP-associated PtdIns transfer proteins.

45 inked myotubular myopathy (XLMTM)-associated PtdIns(3)P phosphatase myotubularin (MTM1).

46 The BATS domain also strongly binds PtdIns(4,5)P2, but the functional significance has been

47 g to phosphatidylinositol (4,5)bisphosphate (PtdIns(4,5)P(2)) production, signalosome formation, and

48 of phosphatidylinositol (4,5)-bisphosphate (PtdIns(4,5)P(2)) from their cytoplasmic leaflet.

49 into phosphatidylinositol 4,5-bisphosphate (PtdIns(3,4)P2).

50 that phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2) binds to the N terminus of the channel-di

51 Phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2) helps control various endolysosome functi

52 Phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2), a master architect of endolysosome and v

53 lipid phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2), whereas other phosphoinositides such as

54 ining phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)) and whether they function by a universa

55 oduct phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).

56 ) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).

57 ated, phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) -modulated, non-selective cation channel

58 e and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) 3-kinase activities.

59 ) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) have been implicated in the maintenance o

60 on of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) landmarks for polarized membrane morphoge

61 ucing phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), stabilizes Mig6 expression.

62 with phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-binding protein Amer1/WTX/Fam123b.

63 d its phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-binding tail domain.

64 ch to phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2).

65 and phosphatidylinositol-(4,5)-bisphosphate [PtdIns(4,5)P2].

66 ] and phosphatidylinositol 3,5-bisphosphate [PtdIns(3,5)P(2)] at the D-3 position.

67 is of phosphatidylinositol-3,5-bisphosphate [PtdIns(3,5)P2] and for the regulation of endolysosomal m

68 ly to phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P(2)] via a pleckstrin homology domain locate

69 ) and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] as well as PtdIns4P 5-kinases mediating t

70 lipid phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2] during vegetative plant growth remain obs

71 lipid phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] is critical for polar tip growth of polle

72 Phosphatidylinositol-4,5-bisphosphate, PtdIns(4,5)P(2), is an essential signalling lipid that r

73 mediately after the PH domain decreases both PtdIns(4)P binding and ceramide transfer by CERT.

74 pting the PH-START interaction increase both PtdIns(4)P-binding affinity and ceramide transfer activi

75 the channel are important for activation by PtdIns(3,5)P2 and inhibition by PtdIns(4,5)P2.

76 steady-state vacuolar pH is not affected by PtdIns(3,5)P2 depletion, it may have a role in stabilizi

77 ctivation by PtdIns(3,5)P2 and inhibition by PtdIns(4,5)P2.

78 whereas chemotaxis and ROS are regulated by PtdIns(5)P-dependent activation of Rac.

79 tify a role for IPIP27 in mediating cellular PtdIns(4,5)P(2) homeostasis.

80 tified IPIP27 as a key modulator of cellular PtdIns(4,5)P(2) homeostasis required for normal cytokine

81 We show that the conserved PtdIns(4)P 5-kinase, Mss4, forms dynamic, oligomeric str

82 ole for the Vac14 homocomplex in controlling PtdIns(3,5)P2 levels.

83 Our data indicate that MPK6 controls PtdIns(4,5)P2 production and membrane trafficking in pol

84 fy a novel PTEN/dPLCXD pathway that controls PtdIns(4,5)P(2) levels on endosomes.

85 in a ubiquitous ternary complex that couples PtdIns(3,5)P2 synthesis with turnover at endosomal membr

86 mediates and reveal a mechanism for coupling PtdIns(4,5)P2 hydrolysis with carrier biogenesis on endo

87 id phosphatase consistently causes decreased PtdIns(3,5)P(2) levels, cell-specific sensitivity to par

88 n homolog on chromosome 10) dephosphorylates PtdIns(3,4,5)P3 and negatively regulates the AKT pathway

89 The tumor suppressor PTEN dephosphorylates PtdIns(3,4,5)P(3) into PtdIns(4,5)P(2) Here, we make the

90 Analysis of an Rbd2 mutant with diminished PtdIns(4,5)P2-binding capacity indicates that this inter

91 de that SHIP1 prevents formation of top-down PtdIns(3,4,5)P(3) polarity to facilitate proper cell att

92 substrate for the Vps34 downstream effector PtdIns 3-phosphate 5-kinase (PIKfyve), which phosphoryla

93 Effector-PtdIns-3-P binding appears to mediate cell entry via lip

94 TEN abundance and thereby promoting elevated PtdIns(4,5)P2 levels in response to TGFbetaR signaling.

95 RT inside the cell, consistent with enhanced PtdIns(4)P binding of the mutant.

96 demonstrate that the TIPE3 protein enhances PtdIns(4,5)P2 and PtdIns(3,4,5)P3, is overexpressed in c

97 strongly with STEEP, leading to increased ER PtdIns(3)P levels and membrane curvature.

98 cterial phagosomes, indicating that extended PtdIns(3)P signaling on phagosomes in the Mtmr4-knockdow

99 rons and Schwann cells, and how loss of FIG4/PtdIns(3,5)P(2)-mediated functions contribute to the pat

100 plasma membrane association of a fluorescent PtdIns(4,5)P2 reporter and decreased endocytosis without

101 lglycerol in the PM, has to reach the ER for PtdIns resynthesis.

102 n rearrangement at junctions is required for PtdIns(4,5)P2 reorganization and efficient STIM1-ORAI1 c

103 that the mucolipin domain is responsible for PtdIns(3,5)P2 binding and subsequent channel activation,

104 Here we demonstrate a role for PtdIns 4-kinases and PtdIns4P 5-kinases in selective and

105 Understanding the direct role for PtdIns(3,4,5)P(3) and other anionic phospholipids in the

106 her, the data indicate an important role for PtdIns(4,5)P2 in the control of clathrin dynamics and in

107 k2 double mutant, consistent with a role for PtdIns(4,5)P2 in the regulation of clathrin-mediated end

108 This study identifies an unexpected role for PtdIns(4,5)P2 signaling in the regulation of ATG14 compl

109 binds to the PH domain at the same site for PtdIns(4)P-binding, suggesting that the START domain com

110 Tubules emerged from PtdIns(4)P-rich regions, where ADP-ribosylation factor-l

111 Kfyve), which phosphorylates Vps34-generated PtdIns(3)P to produce PtdIns (3,5)P2.

112 Phosphoinositide-3 kinase (PI3K) generates PtdIns(3,4,5)P3 and PtdIns(3,4)P2, leading to the activa

113 SGK3 is controlled by hVps34 that generates PtdIns(3)P, which binds to the PX domain of SGK3 promoti

114 m 5 (PIPKIgammai5), an enzyme that generates PtdIns(4,5)P2 in mammalian cells.

115 ion of LAPTM4B in EGFR sorting by generating PtdIns(4,5)P2 and recruiting SNX5.

116 SPR experiments identify PtdIns(4,5)P(2) and PtdIns(3,4,5)P(3) as preferred targe

117 Further highlighting its importance, PtdIns(3,5)P2 misregulation leads to the development of

118 lix have specific functional involvements in PtdIns transfer activity.

119 ly assessed the lysosomal and vacuolar pH in PtdIns(3,5)P2-depleted cells.

120 zed to areas of the plasma membranes rich in PtdIns, suggesting a role for the PH domain in the biolo

121 ion following cell adhesion due to increased PtdIns(3,4,5)P(3) production.

122 its association with the C2 domain inhibits PtdIns(3)P binding.

123 PTEN dephosphorylates PtdIns(3,4,5)P(3) into PtdIns(4,5)P(2) Here, we make the unexpected discovery t

124 lipid kinase phosphorylates PtdIns(3)P into PtdIns(3,5)P2 whereas the Fig4/Sac3 lipid phosphatase an

125 inhibition of phosphatidylinositol 3-kinase (PtdIns 3-kinase) activity rescues the Ca(2+) release def

126 er of EGFR trafficking regulated by LAPTM4B, PtdIns(4,5)P2 signaling, and the ESCRT complex and defin

127 mics simulations of the mammalian StART-like PtdIns/phosphatidylcholine (PtdCho) transfer protein PIT

128 Interaction with PtdInsPs, likely PtdIns(3)P, plays a role in localizing IDE to endosomes,

129 d in Nir2-depleted cells, leading to limited PtdIns synthesis and ultimately to loss of signaling fro

130 lecule in this process is the inositol lipid PtdIns(4,5)P(2), which recruits numerous factors to the

131 -dependent production of the signaling lipid PtdIns(3)P in the protrusion membrane, which relies on t

132 tively, these studies suggest that the local PtdIns(4,5)P(2) concentration in the plasma membrane may

133 e ER to the plasma membrane (PM) to maintain PtdIns(4,5)P2 levels.

134 phatase activity is critical for maintaining PtdIns(4,5)P(2) homeostasis and highlight a critical rol

135 tion of Vps34 could be at the center of many PtdIns(3)P-dependent cellular processes.

136 This was enhanced by muscarinic-mediated PtdIns(4,5)P(2) hydrolysis, leading to dynamic recruitme

137 PIK3C2A-mediated PtdIns(3)P production in S. flexneri protrusions was reg

138 cytoplasmic tail of Rbd2 appears to modulate PtdIns(4,5)P2 distribution on the cell cortex.

139 We report here that a myotubularin PtdIns(3)P 3-phosphatase, myotubularin-related protein-4

140 olipid transport to the trans-Golgi network, PtdIns(4)P consumption interrupts this transport in resp

141 hosphate (PtdIns4P) or PtdIns(4,5)P2 but not PtdIns(3,4,5)P3 was sufficient to evoke K-Ras translocat

142 Loss of IPIP27 causes accumulation of PtdIns(4,5)P(2) on aberrant endomembrane vacuoles, mislo

143 s have been shown to promote accumulation of PtdIns(4,5)P(2) on endosomes and cytokinesis defects.

144 de 5-phosphatase OCRL causes accumulation of PtdIns(4,5)P(2) on membranes and, ultimately, Lowe syndr

145 gest that localized membrane accumulation of PtdIns(4,5)P(2) or PtdIns(3,4,5)P(2) may serve to recrui

146 ring phosphate groups through the actions of PtdIns(3,4,5)P3 3-phosphatase (PTEN), PtdIns(3,4,5)P3 5-

147 e kinase, likely by increasing the amount of PtdIns(4,5)P(2) available to generate phosphatidylinosit

148 ascent phagosomes prior to the appearance of PtdIns(3)P in a manner dependent on the large GTPase dyn

149 sulting in the production and association of PtdIns(4,5)P(2) with p53.

150 How the biosynthesis of PtdIns(4,5)P2 by phosphatidylinositol 4-phosphate 5-kina

151 2.1-knockout mice had altered composition of PtdIns lipids, suggesting a crucial role for native Kv2.

152 composed of physiological concentrations of PtdIns(4,5)P(2) and that this motility is inhibited by h

153 e (BATS) domain that senses the curvature of PtdIns(3)P-containing membrane.

154 hat coordinates synthesis and degradation of PtdIns(3,5)P2 by a poorly understood process.

155 Depletion of PtdIns(4,5)P(2) from the plasma membrane of HEK293 cells

156 Moreover, depletion of PtdIns(5)P attenuates ING2-mediated regulation of these

157 c siRNA expression increased the duration of PtdIns(3)P on phagosomal membranes.

158 interplay of antagonistic binding effects of PtdIns(3,4,5)P(3) and other anionic phospholipids, regul

159 Elimination of PtdIns(4,5)P(2), which is required for actin remodeling

160 PtdIns(4,5)P2 The Ins(1,4,5)P3 headgroup of PtdIns(4,5)P2 binds in precisely the same orientation as

161 Accordingly, premature hydrolysis of PtdIns(4)P impaired SKIP recruitment and phagosome resol

162 Despite the importance of PtdIns(4,5)P(2) in cytokinesis, the regulation of this l

163 n significant differences in the kinetics of PtdIns(4,5)P(2) recovery following repetitive muscarinic

164 The level of PtdIns(3)P on phagosomes oscillates in two waves during

165 and loss-of-function mutants, the levels of PtdIns monophosphates and bisphosphates were changed, wi

166 meostasis in controlling the organization of PtdIns(4,5)P2 microdomains and membrane remodeling.

167 trate that the proper oscillation pattern of PtdIns(3)P on phagosomes, programmed by the coordinated

168 in sequence to provide overlapping pools of PtdIns(3)P on phagosomes.

169 the two-ligand mechanism for potentiation of PtdIns 4-OH kinase activity is a broadly conserved featu

170 with phagosomes and prolongs the presence of PtdIns(4,5)P(2) and actin on their membranes.

171 detachment of Vps34 stops the production of PtdIns(3)P, allowing for the turnover of this lipid by P

172 but surprisingly only a modest reduction of PtdIns(4,5)P(2) because of robust up-regulation of PtdIn

173 rvival factor PKB, through the regulation of PtdIns(3,4,5)P(3) synthesis.

174 vity, as needed, for localized regulation of PtdIns(4,5)P(2) synthesis.

175 neration in mice and humans, but the role of PtdIns(3,5)P2 in non-neural tissues is poorly understood

176 Atg12-5-16L1 recruitment and significance of PtdIns(3)P synthesis at autophagosome formation sites ar

177 lecule and PITPalpha; (iv) the trajectory of PtdIns or PtdCho into and through the lipid-binding pock

178 n that coordinates synthesis and turnover of PtdIns(3,5)P2.

179 homolog (PTEN), resulting in upregulation of PtdIns(3,4,5)P3 signaling in BM myeloid progenitors.

180 e, providing proof of concept for the use of PtdIns 3-kinase inhibitors in myotubular myopathy and su

181 e role of PTEN lipid-phosphatase activity on PtdIns(3,4,5)P3 and inhibition of PI3K pathway is well c

182 mation, exerts lipid phosphatase activity on PtdIns(3,4,5)P3.

183 and AP2 in the LRP6 signalosomes depended on PtdIns(4,5)P(2), and both clathrin and AP2 were required

184 membrane accumulation of PtdIns(4,5)P(2) or PtdIns(3,4,5)P(2) may serve to recruit NOXO1beta and act

185 pparent impact on resting PtdIns(4,5)P(2) or PtdIns(4)P levels.

186 Moreover, inhibition of PIPKI-alpha or PtdIns(4,5)P(2) association results in p53 destabilizati

187 inase alpha [PtdIns(4)P5K] activator Arf6 or PtdIns(4)P5K alone, or treatment with the phosphatidylin

188 sIPMK in complex with either Ins(1,4,5)P3 or PtdIns(4,5)P2 The Ins(1,4,5)P3 headgroup of PtdIns(4,5)P

189 of AnkB or of its linkages to either p62 or PtdIns(3)P or loss of PIK3C3 all impaired organelle tran

190 osphatidylinositol 4-phosphate (PtdIns4P) or PtdIns(4,5)P2 but not PtdIns(3,4,5)P3 was sufficient to

191 t regulates autophagy, but the role of other PtdIns kinases has not been examined.

192 (dynamin activator) and clathrin, and PBP10 (PtdIns 4,5-P2-binding peptide) inhibited agonist-induced

193 used, in part, by transfer of phagolysosomal PtdIns(4)P to the endoplasmic reticulum, a process media

194 etely abolishes the production of phagosomal PtdIns(3)P and disables phagosomes from recruiting multi

195 arkably, persistent appearance of phagosomal PtdIns(3)P, as a result of inactivating mtm-1, blocks ph

196 eration of phosphatidylinositol-3-phosphate (PtdIns(3)P) and recruitment of the PtdIns(3)P-binding pr

197 Phosphatidylinositol 3-phosphate (PtdIns(3)P) is a phosphoinositide that is rapidly synthe

198 Phosphatidylinositol 3-phosphate (PtdIns(3)P) is a signaling molecule important for many m

199 it p62 and phosphatidylinositol 3-phosphate (PtdIns(3)P) lipids generated by PIK3C3.

200 omal lipid phosphatidylinositol-3-phosphate (PtdIns(3)P) persists on tPCs as long as their luminal pH

201 ulation of phosphatidylinositol-3-phosphate (PtdIns(3)P) production and ER membrane curvature formati

202 dence that Phosphatidylinositol 3-Phosphate (PtdIns(3)P) regulates vacuole fusion in vti11 mutants, a

203 -localized phosphatidylinositol 3-phosphate (PtdIns(3)P) synthesis.

204 ally binds phosphatidylinositol 3-phosphate (PtdIns(3)P) via its C2 domain, an association that may b

205 ecifically phosphatidylinositol-3-phosphate (PtdIns-3-P).

206 ype Igamma phosphatidylinositol 4-phosphate (PtdIns(4)P) 5-kinase (PIPKIgamma) and inositol polyphosp

207 c pools of phosphatidylinositol 4-phosphate (PtdIns(4)P) dedicated to specific biological outcomes.

208 binding to phosphatidylinositol 4-phosphate (PtdIns(4)P) in the Golgi membrane, whereas its C-termina

209 Phosphatidylinositol-4-phosphate (PtdIns(4)P), which is abundant in maturing phagolysosome

210 oinositide phosphatidylinositol-5-phosphate (PtdIns(5)P) regulates a subset of ING2 targets in respon

211 horylating phosphatidylinositol 3-phosphate [PtdIns(3)P] and phosphatidylinositol 3,5-bisphosphate [P

212 duction of phosphatidylinositol 3-phosphate [PtdIns(3)P] at the plasma membrane surrounding protrusio

213 irectly to phosphatidylinositol 3-phosphate [PtdIns(3)P] in vitro and colocalized with the PtdIns(3)P

214 generates phosphatidylinositol 3-phosphate [PtdIns(3)P] on the forming autophagosomal membrane.

215 ts product phosphatidylinositol 3-phosphate [PtdIns(3)P] play key roles in autophagy initiation.

216 properties to stimulate PtdIns-4-phosphate [PtdIns(4)P] synthesis.

217 ndirectly, phosphatidylinositol-5-phosphate [PtdIns(5)P].

218 Phosphatidylinositol (PtdIns) is a structural phospholipid that can be phospho

219 regulator, the class 3 phosphatidylinositol (PtdIns) 3-kinase vacuolar protein sorting 34 (Vps34), in

220 osphate (PtdIns4P) and phosphatidylinositol (PtdIns) although to different extents, with isoform gamm

221 ng membrane-associated phosphatidylinositol (PtdIns) transfer proteins PYK2 N-terminal domain-interac

222 ir ability to exchange phosphatidylinositol (PtdIns) molecules between membranes, and this property i

223 main requires both its phosphatidylinositol (PtdIns)- and phosphatidylcholine (PtdCho)-binding proper

224 Multiple phosphatidylinositol (PtdIns) 3-kinases (PI3Ks) can produce PtdIns3P to contro

225 iate the activities of phosphatidylinositol (PtdIns) 4-OH kinases and help channel production of spec

226 res steady delivery of phosphatidylinositol (PtdIns) from its site of synthesis in the ER to the plas

227 The phosphatidylinositol (PtdIns) 3-kinase Vps34 is a lipid kinase that regulates

228 atidylserine (PtdSer) and phosphoinositides (PtdIns)) but the molecular details of this process are n

229 s, and the plant enzyme cannot phosphorylate PtdIns(4,5)P2 Therefore, crystallographic analysis of th

230 The Fab1/PIKfyve lipid kinase phosphorylates PtdIns(3)P into PtdIns(3,5)P2 whereas the Fig4/Sac3 lipi

231 roduction of the lipid second messenger PIP3/PtdIns(3,4,5)P3 (phosphatidylinositol (3,4,5)-trisphosph

232 description of key aspects of the PITPalpha PtdIns/PtdCho exchange cycle and offer a rationale for t

233 engine by which Sec14-like PITPs potentiate PtdIns kinase activities is a heterotypic lipid-exchange

234 ) as substrate; the MTMR8/R9 complex prefers PtdIns(3)P.

235 ficity, wherein the MTMR6/R9 complex prefers PtdIns(3,5)P(2) as substrate; the MTMR8/R9 complex prefe

236 he Drosophila RdgB homolog, Nir2, a presumed PtdIns transfer protein, not only transfers PtdIns from

237 ylates Vps34-generated PtdIns(3)P to produce PtdIns (3,5)P2.

238 is regarded as the only kinase that produces PtdIns(3)P in phagosomal membranes.

239 4,5)P2 By binding with NEDD4-1 and producing PtdIns(4,5)P2, PIPKIgammai5 perturbs NEDD4-1-mediated Mi

240 Interestingly, INPP5E and its product--PtdIns(4)P--accumulate at the centrosome/basal body in n

241 ons of PtdIns(3,4,5)P3 3-phosphatase (PTEN), PtdIns(3,4,5)P3 5-phosphatases (eg, SHIP), and PtdIns(3,

242 However, rapid PtdIns(4,5)P(2) hydrolysis induced artificially after WN

243 mechanism by which TRPML channels recognize PtdIns(3,5)P2 and increase their Ca(2+) conductance rema

244 A pip5k1 pip5k2 double mutant with reduced PtdIns(4,5)P2 levels showed dwarf stature and phenotypes

245 that in Drosophila melanogaster PTEN reduces PtdIns(4,5)P(2) levels on endosomes, independently of it

246 s formed by Kv2 channel-VAP pairing regulate PtdIns lipid homeostasis via VAP-associated PtdIns trans

247 ever, the molecular mechanisms that regulate PtdIns(3)P removal from the phagosome have remained uncl

248 , our findings indicate that MTMR4 regulates PtdIns(3)P degradation in macrophages and thereby contro

249 2.1-containing ER-PM junctions in regulating PtdIns lipid metabolism in brain neurons.

250 ing interacting partners of WIPIs, WD-repeat PtdIns(3)P effector proteins, we found that Atg16L1 dire

251 mTORC1 repressed PtdIns(3,4,5)P3 production and determined the requiremen

252 mulation, with no apparent impact on resting PtdIns(4,5)P(2) or PtdIns(4)P levels.

253 Since PtdIns(4)P is required for cholesterol and sphingolipid

254 zation of the major phosphoinositide species PtdIns(4,5)P2 into microdomains on the plasma membrane,

255 ine (PtdCho)-binding properties to stimulate PtdIns-4-phosphate [PtdIns(4)P] synthesis.

256 Ins/PtdCho-exchange mechanism for stimulated PtdIns(4)P synthesis either arose independently during e

257 ould be blocked by sequestering cell surface PtdIns-3-P or by utilizing inositides that competitively

258 he lipid kinase responsible for synthesizing PtdIns(3,5)P2.

259 with greater affinity to PtdIns(4,5)P2 than PtdIns(3,4,5)P3, and Cnk1 localized to areas of the plas

260 Therefore, we conclude that PtdIns(4,5)P(2) promotes the assembly of LRP6 signalosom

261 manipulating cellular pH, we determined that PtdIns(3)P behaves similarly in canonical phagosomes as

262 localized lipid exchanger that ensures that PtdIns synthesis is matched with PtdIns(4,5)P2 utilizati

263 There is also evidence that PtdIns(3,5)P2 may play a role in lysosomal acidification

264 Given that PtdIns(3)P-dependent signaling is important for multiple

265 ter hyperosmotic shock, which indicates that PtdIns(3,5)P2 levels are greatly abated.

266 Here we report that PtdIns(4,5)P(2) specifically induces partial membrane pe

267 Our results reveal that PtdIns(4)P homoeostasis, coordinated by PIPKIgamma and I

268 ive fluorescence imaging analysis shows that PtdIns(4,5)P(2)-dependent membrane penetration of H(0) i

269 The PtdIns 4-kinase Pik1 is involved in Atg9 trafficking thr

270 This patterning activity requires both the PtdIns(4,5)P2 binding and homo-oligomerization activitie

271 ubiquitin ligase complex, components of the PtdIns 3-kinase complex, and the ESCRT machinery.

272 hosphate (PtdIns(3)P) and recruitment of the PtdIns(3)P-binding protein WIPI2 to virion-containing en

273 In these cells, however, much of the PtdIns(4,5)P(2) was localized intracellularly, rather th

274 Taken together, the data indicate that the PtdIns/PtdCho-exchange mechanism for stimulated PtdIns(4

275 tdIns(3)P] in vitro and colocalized with the PtdIns(3)P markers FYVE and SetA in cotransfected cells.

276 omain of Cnk1 bound with greater affinity to PtdIns(4,5)P2 than PtdIns(3,4,5)P3, and Cnk1 localized t

277 at competitively inhibit effector binding to PtdIns-3-P.

278 and expressed in Escherichia coli) binds to PtdIns(4,5)P2 via a polybasic lysine patch in the C2B do

279 While it is known that Myo1c bound to PtdIns(4,5)P2 in fluid-lipid bilayers can propel actin f

280 e cytoplasmic tail of Rbd2 binds directly to PtdIns(4,5)P2 and is sufficient for Rbd2's role in actin

281 TGN triggers a signalling pathway leading to PtdIns(4)P dephosphorylation.

282 importance of the conversion of PI(4,5)P2 to PtdIns during endocytosis is demonstrated by the presenc

283 er 30-fold, and enhanced the activity toward PtdIns(3)P by only 2-fold.

284 eased the enzymatic activity of MTMR6 toward PtdIns(3,5)P(2) by over 30-fold, and enhanced the activi

285 PtdIns transfer protein, not only transfers PtdIns from the ER to the PM but also transfers PtdOH to

286 phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) by mTORC1 in CTLs.

287 phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) for their activation.

288 (Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3, leading to the inhibition of calcium mo

289 ular myopathy and suggesting that unbalanced PtdIns 3-kinase activity plays a critical role in the pa

290 is a heterotypic lipid-exchange cycle where PtdIns is a common exchange substrate among the Sec14-li

291 However, the mechanism by which PtdIns(4,5)P(2) regulates the signalosome formation rema

292 Overall, we propose a model in which PtdIns(3,5)P2 does not govern the steady-state pH of vac

293 her, these findings support a model in which PtdIns(5)P functions as a sub-nuclear trafficking factor

294 nophosphorylated phosphoinositides, of which PtdIns(4)P is most abundant in phagolysosomes, contribut

295 ggesting that the START domain competes with PtdIns(4)P for association with the PH domain.

296 NEDD4-1 is required for its interaction with PtdIns(4,5)P2 By binding with NEDD4-1 and producing PtdI

297 g function facilitate Amer1 interaction with PtdIns(4,5)P2, which is produced locally upon Wnt3a stim

298 y, we show that beta-arrestin interacts with PtdIns kinases PI4KIIalpha and PIP5KIbeta.

299 nsures that PtdIns synthesis is matched with PtdIns(4,5)P2 utilization so that cells maintain their s

300 imicked by treating wild-type seedlings with PtdIns(3,5)P2, corroborating that this PPI is important