ライフサイエンスコーパス: PtdIns

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 4,5)P2 By binding with NEDD4-1 and producing PtdIns(4,5)P2, PIPKIgammai5 perturbs NEDD4-1-mediated Mi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 ell activation by altering PI3K activity and PtdIns levels.

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

285 2.1-containing ER-PM junctions in regulating PtdIns lipid metabolism in brain neurons.

286 2.1-knockout mice had altered composition of PtdIns lipids, suggesting a crucial role for native Kv2.

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

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

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

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

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

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

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

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

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

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

297 lix have specific functional involvements in PtdIns transfer activity.

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

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

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