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)P, the precursor of PtdIns(4,5)P(2), did not in

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 Sec14 action as a PtdIns-presentation scaffold requires heterotypic exchan

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 Expression of a PtdIns-specific bacterial PLC generates diacylglycerol a

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

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

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

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

22 4-fold and 4-fold toward PtdIns(3,5)P(2) and PtdIns(3)P, respectively.

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

24 PtdIns(4)P, PtdIns(5)P, PtdIns(3,5)P(2), and PtdIns(3,4,5)P(3) with high affinity.

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

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

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

28 detector of the Mss4 PtdIns(4)P 5-kinase and PtdIns(4,5)P(2) and serves as a negative regulator of Pt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 ace plasmon resonance and enables it to bind PtdIns(3,5)P(2) on a dot-blot.

48 Bacterially expressed rat PSP binds PtdIns(3,4)P(2) with a K(d) of 2.4 x 10(-11) M.

49 NTH domain, a protein that selectively binds PtdIns(4,5)P(2).

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

51 h the Atg12-Atg5 conjugate, and TECPR1 binds PtdIns(3)P upon association with the Atg12-Atg5 conjugat

52 P] and phosphatidylinositol 4,5-biphosphate [PtdIns(4,5)P2].

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

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

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

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

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

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

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

60 metabolic conversion to PI 4,5-bisphosphate (PtdIns(4,5)P(2)) and other downstream metabolites.

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

62 r for phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P(2))--a key signalling lipid in diverse cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 P1 toward the TGN membranes enriched in both PtdIns(4)P and GTP-bound ARF1.

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

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

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

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

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

87 hereas the MTMR8/R9 complex reduces cellular PtdIns(3)P levels.

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

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

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

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

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

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

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

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

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

97 the kinase Akt and thus augmented downstream PtdIns(3,4,5)P3 signaling in mouse neutrophils.

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

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

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

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

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

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

104 /KO) mice is able to support the demands for PtdIns(3,5)P(2)/PtdIns5P synthesis during life.

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

106 exchange of phosphatidylcholine (PtdCho) for PtdIns, or vice versa, in a poorly understood progressio

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

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

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

110 HT(2A) receptors and point to a key role for PtdIns(4,5)P(2) in the gating of this current.

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

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

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

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

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

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

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

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

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

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

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

122 lix have specific functional involvements in PtdIns transfer activity.

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

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

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

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

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

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

129 xible functional engineering of a Sec14-like PtdIns transfer protein-an engineering invisible to stan

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

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

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

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

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

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

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

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 ctions as a coincidence detector of the Mss4 PtdIns(4)P 5-kinase and PtdIns(4,5)P(2) and serves as a

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 isruption in hi559 mutants abrogates de novo PtdIns synthesis, resulting in hepatomegaly at 5 days po

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

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

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

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

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

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

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

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

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

152 PLC-independent depletion of PtdIns(4,5)P(2) using a voltage-sensitive phosphatase (c

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

154 Intracellular dialysis of PtdIns(4,5)P(2) inhibited desensitization both in native

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

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

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

158 HIP1 are critical in regulating the level of PtdIns(3,4,5)P(3) during chemotaxis.

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

160 Maintaining proper levels of PtdIns(4,5)P(2) at the plasma membrane (PM) is crucial f

161 gnificantly increases the cellular levels of PtdIns(5)P, the product of PI(3,5)P(2) dephosphorylation

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

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

164 in the activation of the phosphorylation of PtdIns.

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

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

167 PtdIns(4)P, the precursor of PtdIns(4,5)P(2), did not inhibit desensitization, consis

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

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

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

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

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

173 5)P(2) and serves as a negative regulator of PtdIns(4,5)P(2) synthesis at the PM.

174 r lipid kinases, allowing the resynthesis of PtdIns(4,5)P(2).

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 y mobile membrane compartment as the site of PtdIns synthesis and a likely source of PtdIns of all me

178 e of PtdIns synthesis and a likely source of PtdIns of all membranes.

179 d to quantify multiple fatty-acyl species of PtdIns(3,4,5)P(3) in unstimulated mouse and human cells

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

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

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

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

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

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

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

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 to complex the phosphoinositides PtdIns(3)P, PtdIns(4)P, PtdIns(5)P, PtdIns(3,5)P(2), and PtdIns(3,4,

193 he phosphoinositides PtdIns(3)P, PtdIns(4)P, PtdIns(5)P, PtdIns(3,5)P(2), and PtdIns(3,4,5)P(3) with

194 ositides PtdIns(3)P, PtdIns(4)P, PtdIns(5)P, PtdIns(3,5)P(2), and PtdIns(3,4,5)P(3) with high affinit

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

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

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

198 vel and crucial role in producing phagosomal PtdIns(3)P.

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

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

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

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 jugate and phosphatidylinositol 3-phosphate (PtdIns[3]P) to promote autophagosome-lysosome fusion.

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

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

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

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

211 omposed of phosphatidylinositol 3-phosphate [PtdIns(3)P] and phosphatidylinositol 4,5-biphosphate [Pt

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

222 indispensable role in phosphatidylinositol (PtdIns) synthesis.

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

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

227 le CD3 zeta to complex the phosphoinositides PtdIns(3)P, PtdIns(4)P, PtdIns(5)P, PtdIns(3,5)P(2), and

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

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

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

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

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

238 4,5)P2 By binding with NEDD4-1 and producing PtdIns(4,5)P2, PIPKIgammai5 perturbs NEDD4-1-mediated Mi

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

240 steady-state levels of the PIKfyve products PtdIns(3,5)P(2) and PtdIns5P selectively decreased, but

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 In this study, we show that SHIP1 regulates PtdIns(3,4,5)P(3) production in response to cell adhesio

246 over efferocytosis potentially by regulating PtdIns(3,4,5)P(3) levels that modulate Rac GTPase and F-

247 ties of PIKI-1 and VPS-34 by down-regulating PtdIns(3)P on phagosomes.

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

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

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

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

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

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

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

255 In mammals, PIKfyve synthesizes PtdIns(3,5)P(2) and PtdIns5P lipids that regulate endoso

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

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

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

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

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

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

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

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

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

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

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

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

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

269 n and detail the molecular mechanisms of the PtdIns(4)P and ARF1 recognition.

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

271 We show that the PtdIns-synthesizing enzyme PIS associates with a rapidly

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

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

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

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

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

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

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

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

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

281 ivity of MTMR8 by 1.4-fold and 4-fold toward PtdIns(3,5)P(2) and PtdIns(3)P, respectively.

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

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

284 d, phosphatidylinositol(3,4,5)trisphosphate (PtdIns(3,4,5)P(3)).

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

286 phosphatidylinositol-(3,4,5)-trisphosphate (PtdIns(3,4,5)P3)-mediated membrane translocation of the

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

288 gh phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) is known to regulate the phosphorylat

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

290 It is poorly understood where PtdIns is located within cells and how it moves around b

291 HM) site, by mTORC2, it is not clear whether PtdIns(3,4,5)P(3) can directly regulate mTORC2 kinase ac

292 To determine whether PtdIns(4,5)P(2) is a direct activator of TRPV6, we purif

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

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

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

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

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

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

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

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

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