ライフサイエンスコーパス: PIP2

1 esting more direct modulation of channels by PIP2 .

2 e produced PI-4,5-bisphosphate (PI(4,5)P2 or PIP2).

3 to phosphatidylinositol (4,5) bis-phosphate (PIP2).

4 ger phosphatidylinositol (4,5)-bisphosphate (PIP2).

5 on in phosphatidylinositol 4,5-bisphosphate (PIP2).

6 -alpha-phosphatidylinositol 4,5-diphosphate (PIP2).

7 lipid phosphatidylinositol 4,5-bisphosphate (PIP2).

8 s were dependent on intracellular Ca(2+) and PIP2.

9 delineate time- or region-specific roles of PIP2.

10 lular side) with the aid of the phospholipid PIP2.

11 protein kinase C (PKC) substrate that binds PIP2.

12 ular dialysis of a nonhydrolysable analog of PIP2.

13 and receptor complex formation through PIP5K-PIP2.

14 SDs) in response to voltage, retigabine, and PIP2.

15 ding ability of different PLCzeta mutants to PIP2.

16 uced cortical actin density and phospholipid PIP2.

17 s and affects carbachol-induced depletion of PIP2.

18 NBCe1 activity paralleled changes in surface PIP2.

19 ltage sensor from the pore in the absence of PIP2.

20 e, through OST1-dependent phosphorylation of PIP2;1 at Ser-121.

21 t not a phosphodeficient form (Ser121Ala) of PIP2;1 constitutively enhanced the Pf of guard cell prot

22 aling, was able to phosphorylate a cytosolic PIP2;1 peptide at Ser-121.

23 Upon expression in pip2;1 plants, a phosphomimetic form (Ser121Asp) but not

24 in guard cells, which were both abrogated in pip2;1 plants.

25 OST1 enhanced PIP2;1 water transport activity when coexpressed in Xeno

26 g the Plasma membrane Intrinsic Protein 2;1 (PIP2;1) aquaporin have a defect in stomatal closure, spe

27 to restore ABA-dependent stomatal closure in pip2;1.

28 in regulating the cell-surface expression of PIP2;7 during abiotic stress conditions through protein-

29 O and PIP2;7 resulted in decreased levels of PIP2;7 in the plasma membrane and abolished the membrane

30 stitutive expression of fluorescently tagged PIP2;7 in TSPO-overexpressing transgenic lines resulted

31 meter (HPFM) revealed that overexpression of PIP2;7 induced a sixfold increase in root hydraulic cond

32 moter activity and a significant decrease in PIP2;7 mRNA abundance within 2 h.

33 Exposure to salt led to a repression of PIP2;7 promoter activity and a significant decrease in P

34 apid internalization of fluorescently-tagged PIP2;7 proteins was observed but removal from the cell m

35 Coexpression of TSPO and PIP2;7 resulted in decreased levels of PIP2;7 in the pla

36 (Col-0) and transgenic lines overexpressing PIP2;7 were used to investigate and compare their respon

37 tners uncovered a plasma membrane aquaporin, PIP2;7.

38 ne water permeability mediated by transgenic PIP2;7.

39 ls is controlled by cellular availability of PIP2, a membrane phospholipid.

40 ulated exocytosis, as depletion of membranal PIP2 abolishes CDO.

41 lthough the specific molecular mechanism for PIP2 action remains to be uncovered, data support a hypo

42 be disrupted by PIP2, consequently reducing PIP2 activation of KATP channels.

43 These results taken together indicate that PIP2 affects islet beta-cell KATP channels not only by i

44 PIP2 also increased the spontaneous solubilization of ph

45 g ligand, phosphatidylinositol bisphosphate (PIP2), although these exhibit opposite coupling to openi

46 d stimulation, but opened in the presence of PIP2, although with only a low open-probability profile.

47 d prevented by intracellular dialysis with a PIP2 analog.

48 r tested this by introducing a water-soluble PIP2 analogue (diC8 -PIP2 ) into neurons, which in OT ne

49 gered by naturally occurring polyphosphates (PIP2 and ATP) and magnesium ions (Mg(2+)).

50 e-sensitive phosphatase (VSP) that decreases PIP2 and bypasses the InsP3/Ca(2+) pathway.

51 Data indicate that both PIP2 and Ca(2+)-CaM perform the same function on IKS cha

52 s of feedback based on the consumption of PM PIP2 and function at ER-PM junctions to mediate nonvesic

53 and pore opening require the membrane lipid PIP2 and intracellular ATP, respectively, as cofactors,

54 membranes and effects of Galpha, Gbetagamma, PIP2 and Na(+) analyzed.

55 By directly responding to G proteins, PIP2 and Na(+), GIRK is under the control of multiple si

56 -directed mutagenesis, we found that ABCA1's PIP2 and phosphatidylserine translocase activities are i

57 , SF-1) ligand binding domain (LBD) bound to PIP2 and PIP3 show the lipid hydrophobic tails sequester

58 Here, we reveal the competition of PIP2 and the calcified CaM N lobe to a previously uniden

59 r results establish the relationship between PIP2 and the voltage dependence of cortical KCNQ channel

60 cation module, the MARCKS peptide sequesters PIP2 and thereby inhibits PI3K binding to the membrane.

61 se to phosphatidylinositol-4,5-bisphosphate (PIP2) and cargo binding at multiple sites.

62 nt on phosphatidylinositol 4,5-bisphosphate (PIP2) and is related to SNARE complex formation.

63 aptic phosphatidylinositol 4,5-bisphosphate (PIP2) and that alterations in PIP2 at the immunological

64 abolite), phosphatidylinositol bisphosphate (PIP2), and H(+) as possible channel activators.

65 brane phosphatidylinositol 4,5-bisphosphate (PIP2), and these interactions provide a molecular explan

66 sensors with a closed pore in the absence of PIP2, and reveals a regulatory interaction between CaM a

67 ls that contributes to VSD-pore coupling via PIP2, and thereby influences the unique gating effects o

68 PIP2 appears to influence AHPs in OT neurons by reducing

69 aromyces cerevisiae, Adr1-Cat8 and Adr1-Oaf1/Pip2 are pairs of activators that act together to regula

70 t the levels of phosphoinositol biphosphate (PIP2) are reduced in postmortem human brain tissues of A

71 Bilayers doped with either PIP2 as the natural receptor lipid of ezrin or a Ni-nitr

72 about the direct physiological functions of PIP2 at postsynaptic as opposed to presynaptic sites.

73 -bisphosphate (PIP2) and that alterations in PIP2 at the immunological synapse regulate cortical acti

74 Phosphatidylinositol (PI) 4,5-bisphosphate (PIP2) at the plasma membrane (PM) constitutively control

75 ce of phosphatidylinositol-4,5-bisphosphate (PIP2) availability on SGN electrophysiology.

76 sis and identify a rapidly recruited dynamin/PIP2/BAR assembly that regulates the exocytic fusion por

77 following TMD0, and Kir6.2 near the proposed PIP2 binding site, and where ATP density is observed, su

78 Although one of the two PIP2 binding sites is preserved, the symmetric MV dimer

79 rved, suggest SUR1 may contribute to ATP and PIP2 binding to enhance Kir6.2 sensitivity to both.

80 in by phosphatidylinositol-4,5-bisphosphate (PIP2) binding and a threonine phosphorylation at positio

81 demonstrate that together Ca(2+)-PKC and the PIP2-binding peptide of MARCKS modulate the level of fre

82 -1; CADPS/UNC31) and ubMunc13-2 (UNC13B) are PIP2-binding proteins required for Ca(2+)-triggered vesi

83 l regulate the membrane association of other PIP2-binding proteins, and the findings illustrate the p

84 cing clustering of anionic lipids, including PIP2, both in simple asymmetric bilayers, and in more co

85 activators require the membrane phospholipid PIP2 but appear to interact independently with different

86 ) and phosphatidylinositol-4,5-bisphosphate (PIP2), but the role of CaM in channel function is still

87 We confirmed its direct gating by PS and PIP2, but found a lack of the strong intrinsic temperatu

88 suggests that PLCzeta binds significantly to PIP2, but not to phosphatidic acid or phosphatidylserine

89 ave similar affinities for membranes lacking PIP2, but the C2B domain dominates binding to PIP2-conta

90 e of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-

91 antly decrease sensitivity of the channel to PIP2 (by 5-30-fold).

92 in-3A C2 domains operate in cooperation with PIP2/Ca(2+) and SNAP25 to bind the plasma membrane, adop

93 Phosphoinositol-4,5-bisphosphate (PIP2) can directly or indirectly modify ion-channel prop

94 Activated Vn harbored on PIP2 clusters may form small oligomeric interaction plat

95 d C2B-phosphatidylinositol 4,5-bisphosphate (PIP2) complexes, revealing how Rabphilin-3A C2 domains o

96 xperiments demonstrating that an increase in PIP2 concentration recruits more ezrin to the apical pla

97 es GIRK2 to respond to natural variations of PIP2 concentration.

98 xposure to locally high myo-inositol-derived PIP2 concentrations.

99 ntial role in maintaining the sAHP under low PIP2 conditions.

100 sor fluorescence closely overlap under basal PIP2 conditions.

101 complex with SUR1 could not be disrupted by PIP2, consequently reducing PIP2 activation of KATP chan

102 ex with a phosphatidylinositol bisphosphate (PIP2) -containing lipid bilayer, using coarse-grained mo

103 only the ezrin T567D mutant, upon binding to PIP2-containing bilayers, undergoes a remarkable conform

104 IP2, but the C2B domain dominates binding to PIP2-containing membranes.

105 In addition, PIP2 controls the apical and lateral localization of Cra

106 ults show that, although putative Syt1-SNARE/PIP2 coupling through the polybasic region of the C2B do

107 associated with reduction in expression of a PIP2 degrading enzyme, synaptojanin 1 (synj1).

108 s are secondary to increased expression of a PIP2-degrading enzyme, the phosphoinositol phosphatase s

109 energy greatly increases in the presence of PIP2 demonstrating that a larger number of bonds between

110 brane undulations and bending rigidity, in a PIP2-dependent manner.

111 esults suggest that, after receptor-mediated PIP2 depletion and increased cytosolic Ca(2+), calcified

112 PIP2 depletion evokes a C-terminal conformational change

113 PIP2 depletion reduced spike-evoked Ca(2+) entry and vol

114 nt and gate opening, either by a mutation or PIP2 depletion, we show that KCNE3 directly affects the

115 stimulation is attributed to robust membrane PIP2 depletion, whereas the rapid desensitization of alp

116 effect of phosphoinositol-4,5-bisphosphate (PIP2) depletion on MET current amplitude and adaptation,

117 tion, phosphatidylinositol 4,5-bisphosphate (PIP2) depletion, and diacylglycerol production.

118 ed by phosphatidylinositol 4,5-bisphosphate (PIP2) depletion.

119 be uncovered, data support a hypothesis for PIP2 directly regulating channel conformation to alter c

120 lipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) directly stimulates heterologously expressed elec

121 lipid phosphatidylinositol 4,5-bisphosphate (PIP2) directly stimulates NBCe1-A in an excised macropat

122 Thus, through oligomerization, PIP2 directs a transient vinculin sequestration at FAs t

123 Cytoskeletal disruption, which speeds PIP2 dispersion, attenuated potentiation of KCNQ2/3 curr

124 These additional data attribute PIP2 effects to actions on MET-channel properties and no

125 Conversely, depletion of endogenous PIP2 either by serotonin-induced phospholipase C (PLC) a

126 rough specific interactions with clusters of PIP2 embedded in lipid membranes.

127 lipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) enabled the slow AHP component (sAHP) in cortical

128 tation on the membrane, resulting in a local PIP2 enrichment, which has the potential to signal towar

129 direct regulation via membrane potential and PIP2, especially within the specialized architecture of

130 domains away from the central axis and that PIP2 essentially induces opposite motions of the major b

131 logical membrane potentials, suggesting that PIP2 exerts a tonic inhibitory influence.

132 ABCA1 has PIP2 floppase activity, which increases cell surface PIP

133 rotein Nir2 is essential for replenishing PM PIP2 following receptor-induced hydrolysis, but key mech

134 conformation corresponds to an "uncoupled," PIP2-free state of KCNQ1, with activated voltage sensors

135 This study elucidates the mechanism by which PIP2-generating enzyme controls Akt activation upstream

136 suggested that distinct isoforms of the main PIP2-generating enzyme, phosphatidylinositol 4-phosphate

137 is ablated, a condition that likely impairs PIP2 generation.

138 equent phosphatidylinositol 4,5 biphosphate (PIP2) generation.

139 and its homolog Nir3 differentially regulate PIP2 homeostasis in cells during intense receptor stimul

140 plasma membrane doubles the contribution of PIP2 homotetramers.

141 ciates with the membrane by interacting with PIP2 However, the interaction with PIP2 is not required

142 ant proteins were purified, and the in vitro PIP2 hydrolysis and binding properties were monitored.

143 Nir2 detects PIP2 hydrolysis and translocates to ER-PM junctions via

144 Moreover, pilocarpine blocked CCh-stimulated PIP2 hydrolysis in M3R-overexpressing cells, thus, it ac

145 , we also show that phospholipase C-mediated PIP2 hydrolysis is necessary and sufficient to trigger t

146 In contrast to CCh, pilocarpine stimulated PIP2 hydrolysis only in cells overexpressing M1R but not

147 PIP2 hydrolysis only occurs under strong Ca(2+) influx c

148 s apparently opened by membrane force due to PIP2 hydrolysis-induced changes in bilayer strain.

149 l via phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis.

150 These findings reveal an important role for PIP2 in coupling retigabine binding to altered VSD funct

151 Modulating the amount of free PIP2 in inner hair-cell stereocilia resulted in the foll

152 egulates focal adhesions in conjunction with PIP2 in lipid membranes and other cytoskeletal component

153 rrently unknown which lipid kinases generate PIP2 in nociceptive dorsal root ganglia (DRG) neurons an

154 and the DCM/HCM-associated R975W mutant bind PIP2 in their inactive conformations, and R975W MV fails

155 lipid, phosphatidylinositol 4,5-bisphophate (PIP2), in the inner leaflet.

156 sitol 4,5-bisphosphate (PIP2), we found that PIP2 increases alpha-helical propensity in the N terminu

157 PIP2 increases the macroscopic current amplitude by stab

158 examined the effect of the R165A mutation on PIP2-induced changes in channel function and conformatio

159 PIP2 inhibits the channel activity by directly binding t

160 First, we showed that PIP2-insensitive Syn-1A-5RK/A mutant complex with SUR1 c

161 can be triggered by the vesicle docking C2B-PIP2 interaction and raise the possibility that Syt1 rin

162 on Syt1 mutants that might impair Syt1-SNARE/PIP2 interaction, Ca(2+)-binding, or membrane penetratio

163 Interestingly, these cargo and PIP2 interactions are not conserved in yeast.

164 ts are attenuated upon disruption of channel:PIP2 interactions.

165 oducing a water-soluble PIP2 analogue (diC8 -PIP2 ) into neurons, which in OT neurons not only preven

166 Indeed, PIP2 is a pivotal source for second messenger generation

167 Although PIP2 is also concentrated at the dendritic spines, littl

168 Collectively, PIP2 is critically required for induction of LTD whereas

169 Furthermore, we discovered that PIP2 is effluxed from cells to apoA1, where it is associ

170 h membrane domains in live cells and whether PIP2 is metabolized during Ca(2+)-triggered fusion were

171 ting with PIP2 However, the interaction with PIP2 is not required for polar localization and the func

172 l unclear, and its possible interaction with PIP2 is unknown.

173 Phosphatidylinositol 4,5-biphosphate (PIP2) is a cell membrane phosphoinositide crucial for ce

174 lipid phosphatidylinositol 4,5-bisphosphate (PIP2) is a potent inhibitory gating modifier of hEAG1 ch

175 Phosphatidylinositol 4,5-biphosphate (PIP2) is critical for T lymphocyte activation serving as

176 brane phosphatidylinositol 4,5-bisphosphate (PIP2) is required for Ca(2+)-triggered vesicle exocytosi

177 IPKIgamma), a phospholipid kinase generating PIP2, is positively expressed in breast cancer tissues,

178 regulatory pathway for NBCe1 involving both PIP2 itself and generated InsP3/Ca(2+).

179 This study is a quantitative assessment of PIP2 itself as a regulator of NBCe1-B and -C in the inta

180 We found that PIP2 itself is effluxed to apoA1 and it circulates on pl

181 amatically reduces the binding of PLCzeta to PIP2, leading to complete abolishment of its Ca(2+) osci

182 We examined how changes in PIP2 levels affected AHPs, somatic [Ca(2+) ]i , and whol

183 Manipulations of PIP2 levels affected both medium and slow AHP currents i

184 n of synj1 in ApoE4 KI mouse models restores PIP2 levels and, more important, rescues AD-related cogn

185 Mouse plasma PIP2 levels are apoA1 gene dosage-dependent and are >1 m

186 Here, we examined whether changes in PIP2 levels could shift the voltage-activation range of

187 Manipulations of PIP2 levels did not modulate AHPs by influencing Ca(2+)

188 In contrast, hippocampal PIP2 levels in ApoE4 mice did not increase after blast T

189 UNC3230 lowered PIP2 levels in DRG neurons and attenuated hypersensitivi

190 ppase activity, which increases cell surface PIP2 levels that mediate apoA1 binding and lipid efflux

191 In two animal models of cardiac hypertrophy, PIP2 levels were significantly reduced in hypertrophic h

192 A decrease of PIP2 levels, in particular through mutations in Phosphat

193 gical methods to modulate enzymes that alter PIP2 levels, making it difficult to delineate time- or r

194 kinase PIPKIgamma90, which increases global PIP2 levels, shifted the KCNQ voltage activation to with

195 as shown that the sAHP is gated by increased PIP2 levels, which are generated downstream of calcium b

196 roBDNF-dependent p75NTR activation regulates PIP2 levels.

197 st-induced TBI, phosphoinositol biphosphate (PIP2) levels in hippocampal regions of young ApoE3 mice

198 ll in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the primary cultured cardiomyocytes from

199 raction with the membrane, in which multiple PIP2 lipids bind the canonical lipid-binding site and un

200 lipid- and ion-specific manner for POPA and PIP2 lipids; and 6) the monovalent anion type has little

201 ells of rats (Sprague Dawley) of either sex, PIP2 localizes within stereocilia, near stereocilia tips

202 nary edema, this binding stabilizes the ENaC-PIP2-MARCKS complex, which is necessary for the open pro

203 ith a phosphatidylinositol 4,5-bisphosphate (PIP2) marker in pollen tubes.

204 dy, we expand on a previous observation that PIP2 may also directly stimulate NBCe1 in the intact ooc

205 y, the Ca(2+)-PKC-stimulated release of free PIP2 may well regulate the membrane association of other

206 s required for the rapid replenishment of PM PIP2 mediated by Nir2.

207 ate that NBCe1-B and -C are regulated by two PIP2-mediated signalling pathways.

208 s its phosphatidylinositol 4,5-bisphosphate (PIP2) membrane substrate.

209 The results indicate that PIP2 modulates both the ImAHP and IsAHP in OT neurons, m

210 acylglycerol (DAG) or IP3 availability, i.e. PIP2 modulation of AHPs is not likely to involve downstr

211 of Gbetagamma, GIRK2 opens as a function of PIP2 mole fraction with Hill coefficient 2.5 and an affi

212 ometry dependent on the quantity of PIP1 and PIP2 molecules available.

213 ved, the symmetric MV dimer that bridges two PIP2 molecules differs from the asymmetric vinculin dime

214 P2 sequestration, thereby releasing multiple PIP2 molecules that recruit multiple active PI3K molecul

215 plasma membrane aquaporins (PIPs), PIP1 and PIP2 monomers interact to form heterotetramers.

216 o coexpressed PIP2-PIP1 dimers with PIP1 and PIP2 monomers to experimentally investigate the localiza

217 ening phosphatidylinositol 4,5-bisphosphate (PIP2)-negative charges with poly-l-lysine and prevented

218 t is associated with HDL in plasma, and that PIP2 on HDL is taken up by target cells in a scavenger r

219 Phosphatidylinositol-4,5-bisphosphate (PIP2), one of the key phospholipids, directly interacts

220 ested that phosphoinositol-4,5-bisphosphate (PIP2) only induces vinculin homodimers, which are asymme

221 Enzymatic cleavage of cell surface PIP2 or decreased cellular PIP2 by knockdown of phosphat

222 fferent PH domains with membranes containing PIP2 or PIP3, allowing us to obtain a detailed molecular

223 that phosphatidylinositol-4,5-bisphosphate (PIP2) or clotrimazole is necessary for channel opening b

224 Specifically, a decrease in PIP2 per se can inhibit NBCe1, whereas hydrolysis of PIP

225 monstrates for the first time that depleting PIP2 per se inhibits NBCe1 activity.

226 ipids in the surrounding membrane, including PIP2 (phosphatidylinositol-4,5-bisphosphate) in the inne

227 stigated this hypothesized Ca(2+)-PKC-MARCKS-PIP2-PI3K-PIP3 amplification module and tested its key p

228 findings 1) show that the Ca(2+)-PKC-MARCKS-PIP2-PI3K-PIP3 system functions as an activation module

229 Upon coexpression of tandem PIP2-PIP1 dimers in Xenopus oocytes, we can address, for

230 We have also coexpressed PIP2-PIP1 dimers with PIP1 and PIP2 monomers to experime

231 All PIP2-PIP1 heterotetrameric species localize at the plasm

232 Our results show that PIP2-PIP1 heterotetramers can assemble with 3:1, 1:3, or

233 , and phosphatidylinositol 4,5-bisphosphate (PIP2)) PLs containing palmitoyl-oleoyl and dimyristoyl f

234 a(2+) stores and by helping to replenish the PIP2 pool accessible to leukotriene receptors, ostensibl

235 and P2Y receptors utilize distinct membrane PIP2 pools.

236 PIP2-PP also inhibited heterologously expressed Kv1.1/Kv

237 PIP2-PP specifically inhibited the LVA current in SGNs,

238 ation of PIP2 using a palmitoylated peptide (PIP2-PP), slowed adaptation rate in SGN populations.

239 Reducing PIP2 production using wortmannin, or sequestration of PI

240 inding assays demonstrated that ABCA1 led to PIP2 redistribution from the inner to the outer leaflet

241 over, we show that fusion pore formation and PIP2 redistribution precedes actin and myosin recruitmen

242 rapid desensitization of alpha1B-AR delimits PIP2 reduction and augments current activation by protei

243 long QT syndrome mutants suggested impaired PIP2 regulation as the cause for channel dysfunction.

244 tion with previous findings implicate a dual PIP2 regulatory pathway for NBCe1 involving both PIP2 it

245 or 2:2 stoichiometry, depending on PIP1 and PIP2 relative expression in the cell.

246 Flow cytometry and PIP2 reporter-binding assays demonstrated that ABCA1 led

247 h an exponential time course that paralleled PIP2 resynthesis as measured with a PIP2-sensitive fluor

248 r of inositol monophosphatases that prevents PIP2 resynthesis.

249 sm is associated with an active transport of PIP2 rich organelles from the cell perinuclear area to t

250 e exocytosis, but whether vesicles fuse into PIP2-rich membrane domains in live cells and whether PIP

251 ptation but relatively little is known about PIP2 's control of these AHPs.

252 Together this shows PIP2's pivotal role in auditory MET, likely as a direct

253 Further findings support PIP2's role in modulating a fast, myosin-independent, an

254 Phosphatidylinositol 4,5-bisphosphate (PIP2)-sensitive transient receptor potential canonical c

255 ralleled PIP2 resynthesis as measured with a PIP2-sensitive fluorophore and confocal imaging.

256 nts the first use of VSP to characterize the PIP2 sensitivity of a transporter.

257 alt bridge residues (R204A) reduces apparent PIP2 sensitivity of channel activity, and here we show t

258 of plasma membrane PIP2 to characterize the PIP2 sensitivity of NBCe1-B and -C in whole oocytes by c

259 orylation of the MARCKS peptide reverses the PIP2 sequestration, thereby releasing multiple PIP2 mole

260 ipids and suggests that manipulations of the PIP2 signaling pathway may represent a strategy to treat

261 molecular switch," binding to and regulating PIP2 signaling to regulate processes like proplatelet ex

262 isms involving inositol-derived increases in PIP2, SMIT1, and likely other related sodium-dependent s

263 tetrameric configurations formed by PIP1 and PIP2 subunits have not been addressed yet.

264 sal relationship between changes in pTau and PIP2/synj1 levels after TBI, we tested if down-regulatio

265 Spatiotemporal analysis of PIP2 synthesis in T lymphocytes suggested that distinct

266 ale rats, we demonstrated that inhibition of PIP2 synthesis with wortmannin robustly blocked both the

267 ion of phosphatidylinositol 4,5-biphosphate (PIP2), synthesized by phosphatidylinositol 4-phosphate 5

268 of how tumor cells recruit and organize the PIP2-synthesizing enzymes with PI3K in the plasma membra

269 wn of phosphatidylinositol 4,5-bisphosphate (PIP2), the mechanism by which the PLC pathway activates

270 rived phosphatidylinositol 4,5-bisphosphate (PIP2), the mechanisms and functional consequences of the

271 lipid phosphatidylinositol 4,5-bisphosphate (PIP2), the source of the Ca(2+)-releasing second messeng

272 lease phosphatidylinositol-4,5-bisphosphate (PIP2), thereby stimulating production of the signaling l

273 Reducing PIP2 through phosphatases abolished the biphasic kinetic

274 We propose that PIP2, through the control of Crag's subcellular localiza

275 ocal fluorescence imaging of plasma membrane PIP2 to characterize the PIP2 sensitivity of NBCe1-B and

276 Binding of PIP2 to ezrin induces a conformational change permitting

277 ent binding and phosphorylation of substrate PIP2 to generate product PIP3.

278 se can inhibit NBCe1, whereas hydrolysis of PIP2 to inositol 1,4,5-trisphosphate/Ca(2+) can stimulat

279 aM N lobe interacts with helix B in place of PIP2 to limit excessive IKS current inhibition.

280 It phosphorylates PIP2 to produce PIP3, to which Akt binds.

281 form a critical site where CaM competes with PIP2 to stabilize the channel open state.

282 d two anionic lipids (phosphatidylserine and PIP2) to make PI3Kalpha competent for bilayer docking, a

283 lipid phosphatidylinositol-4,5-bisphosphate (PIP2) to produce the signaling lipid phosphatidylinosito

284 lipid phosphatidylinositol 4,5-bisphosphate (PIP2) to propagate diverse intracellular responses that

285 imulatory receptor is crucial for regulating PIP2 turnover by allowing the recruitment and activation

286 ivation, the molecular mechanisms regulating PIP2 turnover remain largely unknown.

287 ds on phosphatidylinositol 4,5-bisphosphate (PIP2), underlies the effects of 2-AG.

288 mmetric vinculin dimer that bridges only one PIP2 Unlike vinculin, wild-type MV and the DCM/HCM-assoc

289 uction using wortmannin, or sequestration of PIP2 using a palmitoylated peptide (PIP2-PP), slowed ada

290 ce of phosphatidylinositol 4,5-bisphosphate (PIP2), we found that PIP2 increases alpha-helical propen

291 Elevated relative levels of PIP and PIP2 were directly confirmed using mass spectrometry.

292 sive behavior of proteins and lipids such as PIP2 which interact tightly with Kir channels.

293 brane phosphatidylinositol 4,5-bisphosphate (PIP2), which is fundamental for maintaining regulated ex

294 vo by phosphatidylinositol 4,5-bisphosphate (PIP2), which is generated from myo-inositol, an osmolyte

295 mins, amphiphysin, syndapin, endophilin, and PIP2, which are rapidly and transiently recruited to the

296 Src, resulting in the spatial generation of PIP2, which is the substrate PI3K required for PIP3 gene

297 peptide of MARCKS modulate the level of free PIP2, which serves as both a docking target and substrat

298 region are involved in the interactions with PIP2, whilst residues within the distal JM region exhibi

299 ucing activity and in vitro interaction with PIP2 without affecting its Ca(2+) sensitivity.

300 -sensitive phosphatase (VSP), which depletes PIP2 without changing inositol 1,4,5-trisphosphate, and