ライフサイエンスコーパス: PtdIns

1 in the activation of the phosphorylation of PtdIns.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 4-fold and 4-fold toward PtdIns(3,5)P(2) and PtdIns(3)P, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 4,5)P2 By binding with NEDD4-1 and producing PtdIns(4,5)P2, PIPKIgammai5 perturbs NEDD4-1-mediated Mi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 Sec14 action as a PtdIns-presentation scaffold requires heterotypic exchan

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

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

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

292 Expression of a PtdIns-specific bacterial PLC generates diacylglycerol a

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

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

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

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

297 indispensable role in phosphatidylinositol (PtdIns) synthesis.

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

299 lix have specific functional involvements in PtdIns transfer activity.

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

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