ライフサイエンスコーパス: PIP2

1 esting more direct modulation of channels by PIP2 .

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

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

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

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

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

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

8 H domain all preferred to interact with free PIP2.

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

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

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

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

13 d MA strongly preferred binding to clustered PIP2.

14 ular dialysis of a nonhydrolysable analog of PIP2.

15 and receptor complex formation through PIP5K-PIP2.

16 opening is regulated by the signaling lipid PIP2.

17 ding ability of different PLCzeta mutants to PIP2.

18 vesicles containing either clustered or free PIP2.

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

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

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

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

26 Here, we investigated how deregulation of PIP2;5 expression affects water relations and growth usi

27 At the leaf level, where the PIP2;5 gene is weakly expressed in wild-type plants, the

28 The plasma membrane intrinsic protein PIP2;5 is the most highly expressed aquaporin in maize (

29 nically was higher in PIP2;5 OE and lower in pip2;5 KO lines compared with the corresponding wild-typ

30 s, whereas no difference was observed in the pip2;5 KO lines.

31 f the cells is not radially uniform but that PIP2;5 may be saturated in cell layers with apoplastic b

32 well-watered conditions, demonstrating that PIP2;5 may play a beneficial role in plant growth under

33 of roots grown hydroponically was higher in PIP2;5 OE and lower in pip2;5 KO lines compared with the

34 the hydraulic conductance was higher in the PIP2;5 OE lines compared with the wild-type plants, wher

35 that of xylem water potential, was faster in PIP2;5 OE plants upon mild stress, but not in well-water

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

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

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

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

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

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

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

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

44 It is likely that this mechanism of PIP2 activation is conserved among Kv7 channels.

45 PIP2 also increased the spontaneous solubilization of ph

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

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

48 d prevented by intracellular dialysis with a PIP2 analog.

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

50 lipid phosphatase activity converts PIP3 to PIP2 and antagonizes the PI3K-Akt pathway.

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

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

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

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

55 lices 4 and 5 of the GTPase G-domain bind to PIP2 and identified the specific residues in these struc

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

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

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

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

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

67 PIP2 appears to influence AHPs in OT neurons by reducing

68 The measured clustering and dynamics of PIP2 are inconsistent with the unmodified forms of the r

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

70 that Gag multimerization can further enrich PIP2 at assembly sites.

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

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

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

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

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

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

77 dge, dynamic mechanism: a radial gradient of PIP2 binding sites that are themselves mobile.

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

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

80 d the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding protein, myristoylated alanine-rich C-kina

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

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

83 PI(4,5)P2's binding affinity or mutation of PIP2-binding sites on TAK1 abolish its activation and th

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 Local production of PIP2 by PIP5K then recruited TIRAP to the preassembled c

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

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

94 We showed previously that in model membranes PIP2 can form nanoscopic clusters bridged by multivalent

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

96 Protein-induced PIP2 clustering and multivalent cation-induced PIP2 clus

97 P2 clustering and multivalent cation-induced PIP2 clustering are additive.

98 interface mutation led to a loss of induced PIP2 clustering in MACA, indicating the importance of pr

99 rotein-protein interactions are required for PIP2 clustering, formation of a regular lattice is not.

100 ound that HIV-1 Gag multimerization promotes PIP2 clustering.

101 However, HIV-1 MA itself did not induce PIP2 clustering.

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

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

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

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

106 sor fluorescence closely overlap under basal PIP2 conditions.

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

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

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

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

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

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

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

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

115 PIP2 depletion evokes a C-terminal conformational change

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

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

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

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

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

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

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

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

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

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

126 Rather, we found that the spatial PIP2 distributions and how they change in time are expla

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

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

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

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

131 IV-1 Gag can selectively target pre-existing PIP2-enriched domains of the plasma membrane for viral a

132 These effects could explain the observed PIP2 enrichment in HIV-1.

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

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

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

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

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

138 Within and near clusters, HA and PIP2 follow a similar spatial dependence, which can be d

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

140 lipid phosphatidylinositol 4,5-bisphosphate (PIP2) forms nanoscopic clusters in cell plasma membranes

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

142 incorporation, we studied the desorption of PIP2 from biomimetic giant unilamellar vesicles by means

143 on of phosphatidylinositol 4,5-bisphosphate (PIP2) from the plasma membrane to actin rich regions in

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

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

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

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

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

149 plasma membrane doubles the contribution of PIP2 homotetramers.

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

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

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

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

154 Given that the local concentration of PIP2 in biological membranes is variable, spontaneous cu

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

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

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

158 -quenching of acyl chain-labeled fluorescent PIP2 in liposomes, implying clustering.

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

160 to elucidate the mechanical consequences of PIP2 incorporation, we studied the desorption of PIP2 fr

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

162 PIP2 inhibits the channel activity by directly binding t

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

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

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

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

167 Incorporation of PIP2 into biomimetic membranes, however, has at times re

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

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

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

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

172 PIP2, we showed that the fast desorption of PIP2 is facilitated by presence of an arachidonic lipid

173 The headgroup of PIP2 is highly negatively charged, and this lipid displa

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

175 lution imaging of living cells, we find that PIP2 is tightly colocalized with and modulated by overex

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

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

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

179 Phosphatidylinositol-4,5-bisphosphate (PIP2) is an important signaling lipid in eukaryotic cell

180 Phosphatidylinositol 4,5-bisphosphate (PIP2) is critical for HIV-1 virus assembly.

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

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

183 Given the crucial role of PIP2, it is imperative to study its localization, intera

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 roBDNF-dependent p75NTR activation regulates PIP2 levels.

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

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

201 with the age of the vesicles suggested that PIP2 lipids were being desorbed from the outer leaflet o

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

203 iating interactions with membrane-associated PIP2 lipids; these insights that may inform the future d

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

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

206 variable, spontaneous curvature generated by PIP2 may affect the formation of highly curved structure

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

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

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

210 y externally increasing the concentration of PIP2 micelles.

211 embranes; however, the processes determining PIP2 mobility and thus its spatial patterns are not full

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

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

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

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

216 ribed by an HA-dependent potential gradient; PIP2 molecules move as if they are attracted to the cent

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

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

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

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

221 Upon addition, PIP2 occupies a site on KCNQ1 within the inner membrane

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

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

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

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

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

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

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

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

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

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

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

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

234 All PIP2-PIP1 heterotetrameric species localize at the plasm

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

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

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

238 and P2Y receptors utilize distinct membrane PIP2 pools.

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

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

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

242 Reducing PIP2 production using wortmannin, or sequestration of PI

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

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

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

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

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

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

249 ing phosphatidylinositol-(4,5)-bisphosphate (PIP2), resulting in VEGF-exacerbated defects in angiogen

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

251 r of inositol monophosphatases that prevents PIP2 resynthesis.

252 PIP2, suggesting that the virus assembles at PIP2-rich microdomains.

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

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

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

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

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

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

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

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

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

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

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

264 Lipid binding may occur through PIP3/PIP2-specific PH domains or nonspecific ionic interactio

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

266 The viral membrane is enriched in PIP2, suggesting that the virus assembles at PIP2-rich m

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

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

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

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

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

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

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

274 Without PIP2, the pore remains closed.

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

276 Reducing PIP2 through phosphatases abolished the biphasic kinetic

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

278 Binding of PIP2 to ezrin induces a conformational change permitting

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

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

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

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

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

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

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

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

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

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

289 By means of a saturated chain homolog of PIP2, we showed that the fast desorption of PIP2 is faci

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

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

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

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

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

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

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

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

298 peptide binds to phospholipids, particularly PIP2, with a dissociation constant of 17.64 nM.

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