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1 sence and presence of phosphatidylserine and phosphatidylinositol 4,5-bisphosphate.
2 igh curvature strictly depends on binding to phosphatidylinositol 4,5-bisphosphate.
3 hosphatidic acid and boosts the synthesis of phosphatidylinositol 4,5-bisphosphate.
4 rn repeated for C2F domain interactions with phosphatidylinositol 4,5-bisphosphate.
5 2 phosphorylation and impaired metabolism of phosphatidylinositol 4,5-bisphosphate.
6 pids, capsaicin-induced activity depended on phosphatidylinositol 4,5-bisphosphate.
7 the membrane phospholipid signaling molecule phosphatidylinositol 4,5-bisphosphate.
8 lipase C, and it increased the hydrolysis of phosphatidylinositol 4,5-bisphosphate.
9 in, and treatment with neomycin to sequester phosphatidylinositol 4,5-bisphosphate.
10 ivity is promoted by G proteins that deplete phosphatidylinositol 4,5-bisphosphate.
11 dhesion of a pleckstrin homology domain with phosphatidylinositol 4,5-bisphosphate.
12 t increases substantially in the presence of phosphatidylinositol 4,5-bisphosphate.
13 converts phosphatidylinositol-5-phosphate to phosphatidylinositol-4,5-bisphosphate.
14 es the interactions with the signaling lipid phosphatidylinositol-4,5-bisphosphate.
15 a specific structure upon binding its ligand phosphatidylinositol-(4,5)-bisphosphate.
16 Gag through interaction with an acidic lipid phosphatidylinositol-(4,5)-bisphosphate.
17 ced YAP nuclear accumulation via the FAK-Src-phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K) si
18 rms that one important physiological signal, phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) ac
19 ound to be mediated at least in part through phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) ac
20 h encodes the catalytic subunit alpha of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) fr
21 tivation of spleen tyrosine kinase (Syk) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K).
22 the list of genes encoding components of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AK
25 ential methylation of two replicated PIK3CD (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic
26 sequencing found a missense mutation in the Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic
28 ncers (CRCs) with oncogenic mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic
29 intact signaling through the Janus Kinase 2/phosphatidylinositol-4,5-bisphosphate 3-kinase pathway.
30 Itk(-/-)Btk(-/-) mast cells, and blockage of phosphatidylinositol-4,5-bisphosphate 3-kinase, Akt, or
31 breast cancer bearing an activating PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalyti
32 r receptor 2 (HER2; ERBB2) amplification and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalyti
33 e included an activating mutation in PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalyti
35 ivation of canonical nuclear factor kappa B, phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt, and
38 Postzygotic somatic mutations activating the phosphatidylinositol-4,5-bisphosphate-3-kinase (PI3K)-pr
42 r reorientation, while depleting the pool of phosphatidylinositol-4,5-bisphosphate, an activator of m
43 er by the presence of phospholipid vesicles, phosphatidylinositol 4,5-bisphosphate and Ca(2+), or by
44 iven by the plasma membrane phosphoinositide phosphatidylinositol 4,5-bisphosphate and cargo relieves
45 NCX inactivation occurs in the absence of phosphatidylinositol 4,5-bisphosphate and is facilitated
46 kers for the anionic signaling phospholipids phosphatidylinositol 4,5-bisphosphate and phosphatidic a
47 this regard, phosphoinositides, particularly phosphatidylinositol 4,5-bisphosphate and phosphatidylin
48 shuttles two lipid second messengers, i.e., phosphatidylinositol 4,5-bisphosphate and phosphatidylin
49 ortical granule exocytosis, the elevation of phosphatidylinositol 4,5-bisphosphate and the large, lat
50 ne and occurs following its interaction with phosphatidylinositol-(4,5)-bisphosphate and its subseque
51 taining 2 mol % 1,2-dipalmitoyl-sn-glycero-3-phosphatidylinositol-4,5-bisphosphate and Atto488-1,2-di
52 branes containing the annexin binding lipids phosphatidylinositol-4,5-bisphosphate and phosphatidylse
53 odomains, which are enriched in cholesterol, phosphatidylinositol 4,5-bisphosphate, and gangliosidic
55 d protein kinase, the signaling phospholipid phosphatidylinositol-(4, 5)-bisphosphate, and the c-Abl-
56 sphate (PIP3) signaling and converts PIP3 to phosphatidylinositol (4,5)-bisphosphate at the plasma me
57 otentiated by cold temperature involving the phosphatidylinositol 4,5-bisphosphate binding residue (L
58 ge-sensing domain, and about cold sensor and phosphatidylinositol 4,5-bisphosphate binding sites, whi
59 ) input, including motifs for calmodulin and phosphatidylinositol 4,5-bisphosphate binding, protein k
62 rotein (GFP)-Myo1c mutants revealed that the phosphatidylinositol-4,5-bisphosphate-binding site is ne
63 ale reorganization of phosphatidylserine and phosphatidylinositol 4,5-bisphosphate but not other anio
64 yoblast fusion depended on dynamin activity, phosphatidylinositol(4,5)bisphosphate content, and cell
66 nventional secretory mechanism that involves phosphatidylinositol 4,5-bisphosphate-dependent insertio
67 leaflet of plasma membranes that may control phosphatidylinositol 4,5-bisphosphate-dependent membrane
69 ivates p75NTR to induce a Rac1-dependent and phosphatidylinositol 4,5-bisphosphate-dependent signalin
70 orrelating with the drug's ability to induce phosphatidylinositol 4,5-bisphosphate depletion after ag
71 nding to KCNQ2 channel, caused resistance to phosphatidylinositol 4,5-bisphosphate depletion, and inc
72 S4 movement and gate opening by mutations or phosphatidylinositol 4,5-bisphosphate depletion, we show
74 , an endosome-localized enzyme that produces phosphatidylinositol 4,5-bisphosphate, directly interact
76 move laterally across the plasma membrane to phosphatidylinositol (4,5)-bisphosphate-enriched domains
77 penetrate in trans to a membrane containing phosphatidylinositol 4,5 bisphosphate, even if phosphati
78 intact F-actin architecture is required for phosphatidylinositol 4,5-bisphosphate homeostasis mediat
79 increases phospholipase C activity, causing phosphatidylinositol 4,5-bisphosphate hydrolysis and ino
81 ion displaces ciliary Inpp5e and accumulates phosphatidylinositol 4,5-bisphosphate in distal cilia.
82 in the surrounding membrane, including PIP2 (phosphatidylinositol-4,5-bisphosphate) in the inner leaf
83 beta1 activity measured with the fluorescent phosphatidylinositol 4,5-bisphosphate/inositol 1,4,5-tri
85 phospholipase C (PLC) isozymes to hydrolyze phosphatidylinositol 4,5-bisphosphate into the second me
87 membrane, where receptors are activated and phosphatidylinositol-4,5-bisphosphate is concentrated.
89 PIPKIgamma activity and, thereby, modulates phosphatidylinositol (4,5)-bisphosphate levels and adhes
90 ds of an I-BAR domain, we find clustering of phosphatidylinositol 4,5-bisphosphate-like lipids that i
93 uration to membranes containing PS even if a phosphatidylinositol 4,5 bisphosphate membrane is presen
94 Neurites induce formation of plasma membrane phosphatidylinositol 4,5-bisphosphate microdomains at na
95 rings were initiated by a circular array of phosphatidylinositol(4,5)bisphosphate microdomains, and
96 red filaments on lipid monolayers containing phosphatidylinositol-4,5-bisphosphate, mimicking presenc
98 Each GABA(A) receptor pentamer contains two phosphatidylinositol-4,5-bisphosphate molecules, the hea
99 phatase activity toward the phosphoinositide phosphatidylinositol (4,5)-bisphosphate or altered the s
102 interaction of ExoU with soluble analogs of phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P(2)).
103 (3,4,5)-trisphosphate (PI(3,4,5)P3) to form phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P2).
105 yn with the acidic phosphoinositides (PIPs), phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) and
106 Many actin-regulatory proteins interact with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) and
107 we show that Flower Ca(2+) channel-dependent phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) comp
108 utative second messengers, change in pH, and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) depl
109 the effects of Ca(2+), calmodulin (CaM), and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) in e
110 phate-mediated Ca(2+) release by hydrolyzing phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) in t
111 osphoinositides and the other explaining how phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) infl
113 by the Galphaq/phospholipase Cbeta (PLCbeta)/phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) sign
115 lysosomes, whereas PI 4-phosphates, such as phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)), are
116 terminal myristoylated matrix (MA) domain to phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)).
117 to the plasma membrane (PM), where it binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and di
125 s recently found to bind to the phospholipid phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a mar
126 study the direct interaction of Ca(2+) with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the m
127 demonstrated to be secreted from cells in a phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2)-depend
128 nexin A2 (AnxA2), to induce the formation of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2)-rich d
131 occur through interactions of proteins with phosphatidylinositol(4,5)-bisphosphate (PI(4,5)P2), whic
134 virtue of its affinity to the phospholipid, phosphatidylinositol-4,5-bisphosphate (PI(4,5)P(2)).
135 embrane protein ATP1A1, the phosphoinositide phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2), and T
136 by bradykinin led to a moderate decrease in phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2), but n
138 e proteins are critical for the synthesis of phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P(2)], a
139 on the ability of PI5P4Kalpha to synthesize phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P2] rath
140 M8 requires the plasma membrane phospholipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2) or PI
141 ) enzyme and to lead to a robust decrease in phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)] leve
142 for both cooling agonists and membrane lipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].
143 evation of cytosolic Ca(2+) and modulated by phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].
144 pase C pathway, leading to the hydrolysis of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].
145 holipase requiring the cellular host factors phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and ub
152 ipid-binding module in TMEM24 transports the phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] precur
154 idylinositol 3-phosphate [PI(3)P] along with phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] to sti
155 ubule cell survival through interaction with phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], but p
161 erminal myristoylated matrix (MA) domain and phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P(2)].
162 ion is stimulated by physiological levels of phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2] and
163 highly basic region (MA-HBR) interacts with phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2], a P
164 to PM sites is facilitated by its binding to phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2], and
165 sma membrane (PM)-specific phosphoinositide, phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2].
166 binding to the plasma membrane phospholipid phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2].
173 le interactions with plasma membrane lipids: Phosphatidylinositol (4, 5)-bisphosphate (PIP(2)) activa
174 have previously shown that the phospholipid, phosphatidylinositol (4, 5)-bisphosphate (PIP(2)), direc
179 i/o) activation of TRPC4 through hydrolysing phosphatidylinositol 4,5-bisphosphate (PIP(2) ) to produ
180 ally dependent on and bimodally regulated by phosphatidylinositol 4,5-bisphosphate (PIP(2) ), the sub
183 ted mechanisms, namely depletion of membrane phosphatidylinositol 4,5-bisphosphate (PIP(2)) and a ris
184 is mediated by its role in the generation of phosphatidylinositol 4,5-bisphosphate (PIP(2)) and in in
185 oform SGK1.1 interacts with phosphoinositide-phosphatidylinositol 4,5-bisphosphate (PIP(2)) and is di
188 ransition of this region that is promoted by phosphatidylinositol 4,5-bisphosphate (PIP(2)) is also p
189 h mutant forms of Merlin that cannot bind to phosphatidylinositol 4,5-bisphosphate (PIP(2)) or that c
191 nsporter (hSERT), in which direct binding of phosphatidylinositol 4,5-bisphosphate (PIP(2)) stabilize
193 n of G(q/11)-coupled receptors both consumes phosphatidylinositol 4,5-bisphosphate (PIP(2)) via phosp
194 s disrupt current potentiation by increasing phosphatidylinositol 4,5-bisphosphate (PIP(2)), and our
195 dynamically regulated plasma membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP(2)), but it i
196 steric actions of agonist and membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP(2)), but lack
198 persistence in bulk membranes, in particular phosphatidylinositol 4,5-bisphosphate (PIP(2)), initiall
203 utyrate (PDBu), a PKC catalytic subunit, and phosphatidylinositol-4,5-bisphosphate (PIP(2)) and phosp
204 ds in DRG neurons and injection of exogenous phosphatidylinositol-4,5-bisphosphate (PIP(2)) fully rev
205 he Syt-7 C2AB tandem binds liposomes lacking phosphatidylinositol-4,5-bisphosphate (PIP(2)) with grea
206 e capsaicin receptor, TRPV1, is regulated by phosphatidylinositol-4,5-bisphosphate (PIP(2)), although
210 We previously reported that the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) directly s
211 Previous work demonstrated that the lipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) enabled th
213 is conformational transition is dependent on phosphatidylinositol 4,5-bisphosphate (PIP2) and is rela
214 a process that involves binding of ezrin to phosphatidylinositol 4,5-bisphosphate (PIP2) and phospho
215 arance and recovery correlated with synaptic phosphatidylinositol 4,5-bisphosphate (PIP2) and that al
216 lly investigated the close interplay between Phosphatidylinositol 4,5-bisphosphate (PIP2) and the F-a
218 analyses of Rabphilin-3A C2B-SNAP25 and C2B-phosphatidylinositol 4,5-bisphosphate (PIP2) complexes,
219 evident at the level of Galphaq activation, phosphatidylinositol 4,5-bisphosphate (PIP2) depletion,
220 s TRPC4/5 channel activity is potentiated by phosphatidylinositol 4,5-bisphosphate (PIP2) depletion.
221 ve previously reported that the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) directly st
223 from the cell-surface, and redistribution of phosphatidylinositol 4,5-bisphosphate (PIP2) from the pl
224 ducing (pronociceptive) receptors signal via phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis.
228 used an initial increase and a later fall in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in t
229 hoinositides in vitro and colocalized with a phosphatidylinositol 4,5-bisphosphate (PIP2) marker in p
230 d it remains unclear how PLCzeta targets its phosphatidylinositol 4,5-bisphosphate (PIP2) membrane su
231 6R associated weakly but preferentially with phosphatidylinositol 4,5-bisphosphate (PIP2) through the
232 -beta) isozymes hydrolyze the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) to propagat
233 lserine, phosphatidic acid, cardiolipin, and phosphatidylinositol 4,5-bisphosphate (PIP2)) PLs contai
234 Cgamma, enzymes that deplete plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2), and these
235 on by SMIT-transported, myo-inositol-derived phosphatidylinositol 4,5-bisphosphate (PIP2), the mechan
236 diacylglycerols produced by PLC breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2), the mechan
237 e replenishment of the membrane phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2), the source
238 permissive role in myogenesis and depends on phosphatidylinositol 4,5-bisphosphate (PIP2), underlies
239 the N termini in the presence and absence of phosphatidylinositol 4,5-bisphosphate (PIP2), we found t
240 , we show that CDO is contingent on membrane phosphatidylinositol 4,5-bisphosphate (PIP2), which is f
241 2/3 channel activity is augmented in vivo by phosphatidylinositol 4,5-bisphosphate (PIP2), which is g
242 ctivation of IPF fibroblasts, we noticed the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding pro
243 Oxo-M inhibition is occluded by screening phosphatidylinositol 4,5-bisphosphate (PIP2)-negative ch
252 only in an 84-residue sequence that binds to phosphatidylinositol(4,5)bisphosphate (PIP2), the substr
253 o re-synthesize phosphoinositides, including phosphatidylinositol-(4,5)-bisphosphate (PIP2), resultin
254 ted by conformational changes in response to phosphatidylinositol-4,5-bisphosphate (PIP2) and cargo b
255 al understanding of how the signalling lipid phosphatidylinositol-4,5-bisphosphate (PIP2) and intrace
256 inositides, we investigated the influence of phosphatidylinositol-4,5-bisphosphate (PIP2) availabilit
257 f this linkage is the activation of ezrin by phosphatidylinositol-4,5-bisphosphate (PIP2) binding and
261 kinases phosphorylate the constitutive lipid phosphatidylinositol-4,5-bisphosphate (PIP2) to produce
262 the GIRK1 subunit in a manner that requires phosphatidylinositol-4,5-bisphosphate (PIP2), but is oth
263 1 C terminus (CT) binds calmodulin (CaM) and phosphatidylinositol-4,5-bisphosphate (PIP2), but the ro
265 rich C kinase substrate (MARCKS) and release phosphatidylinositol-4,5-bisphosphate (PIP2), thereby st
266 catalyze the final step in the synthesis of phosphatidylinositol-4,5-bisphosphate (PIP2), which in t
267 channels exhibit spontaneous activity via a phosphatidylinositol-4,5-bisphosphate (PIP2)-dependent g
268 ntial for the maintenance of plasma membrane phosphatidylinositol 4,5-bisphosphate pools but only dur
270 6 (LRP5/6) and frizzled proteins, leading to phosphatidylinositol (4,5)bisphosphate (PtdIns(4,5)P(2))
271 hosphatidylinositol 3,4,5-trisphosphate into phosphatidylinositol 4,5-bisphosphate (PtdIns(3,4)P2).
272 sphatidylinositol-5-phosphate (PtsIns5P) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).
273 pha (also known as PIP5K1A)) and its product phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).
274 ,5-trisphosphate (Ins(1,4,5)P3) 3-kinase and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) 3-
276 eins controlling the lateral organization of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) la
277 inase i5 (PIPKIgammai5), an enzyme producing phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), s
278 n via its actin-binding motor domain and its phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-bi
279 phosphorylation via a novel interaction with phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-bi
281 he affinity of the polybasic lysine patch to phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2).
282 sphatidylinositol 4-phosphate (PtdIns4P) and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] as
283 main enriched in the regulatory phospholipid phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] is
284 phoinositide second messengers, PtdIns5P and phosphatidylinositol-(4,5)-bisphosphate [PtdIns(4,5)P2].
285 The functions of the minor phospholipid phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2] du
287 domains that exhibit specificity for binding phosphatidylinositol-4,5-bisphosphate (PtdIns4,5P2).
288 ed in all LPS responses, but a single lipid (phosphatidylinositol-4,5-bisphosphate) regulates many LP
289 for promoting the spatially highly organized phosphatidylinositol-4,5-bisphosphate signaling program
290 e 1alpha (PIP5K), the enzyme responsible for phosphatidylinositol 4,5-bisphosphate synthesis, is modi
292 ning cholesterol, phosphatidylserine, and/or phosphatidylinositol-4,5-bisphosphate, thus providing a
293 embrane and electrostatically interacts with phosphatidylinositol 4,5-bisphosphate to stabilize MA or
294 olipase C-beta (PLC-beta) isoforms hydrolyze phosphatidylinositol 4,5-bisphosphate to the second mess
296 haq Therefore, XY-69 can replace radioactive phosphatidylinositol 4,5-bisphosphate used in convention
297 dynamins bind the plasma membrane-localized phosphatidylinositol-4,5-bisphosphate using the pleckstr
298 ain probe revealed that the regulatory lipid phosphatidylinositol 4,5-bisphosphate was enriched at si
299 arly in IS formation, in parallel to a local phosphatidylinositol (4,5)-bisphosphate wave, and requir
300 bicans IRS4 encodes a protein that regulates phosphatidylinositol-(4,5)-bisphosphate, which was shown