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1 ic binding to acidic phospholipids including phosphoinositides.
2 macological targeting of membrane-associated phosphoinositides.
3           CB is tethered to the membrane via phosphoinositides.
4 ion of its headgroup produces seven distinct phosphoinositides.
5                                              Phosphoinositide 3 kinase (PI3K) is a direct upstream ac
6 requires the multimodular B-cell adaptor for phosphoinositide 3-kinase (BCAP).
7 oughput virtual screening (HTVS) study using phosphoinositide 3-kinase (both PI3Kgamma and PI3Kdelta)
8                                              Phosphoinositide 3-kinase (PI3-K) is involved in both In
9 rain neuroblasts (NBs) in Drosophila utilize Phosphoinositide 3-kinase (PI3-kinase) and DE-cadherin t
10                       RAS signalling through phosphoinositide 3-kinase (PI3-Kinase) has been shown to
11 led that platelet DREAM positively regulates phosphoinositide 3-kinase (PI3K) activity during platele
12                                              Phosphoinositide 3-kinase (PI3K) activity is stimulated
13 evels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased
14  (PTEN), a tumor suppressor that counteracts phosphoinositide 3-kinase (PI3K) activity, is one of the
15 fication or ligand overexpression maintained phosphoinositide 3-kinase (PI3K) and MEK/ERK signaling e
16 )/LYN complexes, which allows recruitment of phosphoinositide 3-kinase (PI3K) and phosphorylation of
17                                              Phosphoinositide 3-kinase (PI3K) and the proteasome path
18                                              Phosphoinositide 3-kinase (PI3K) beta signaling is requi
19 ficient of SHP2 binding (PDGFRalpha-F720) or phosphoinositide 3-kinase (PI3K) binding (PDGFRalpha-F73
20                                              Phosphoinositide 3-kinase (PI3K) generation of PI(3,4,5)
21 120 (Buparlisib) is one of the most advanced phosphoinositide 3-kinase (PI3K) inhibitors for the trea
22                                              Phosphoinositide 3-kinase (PI3K) is deregulated in a wid
23                    Inhibitors of the class I phosphoinositide 3-kinase (PI3K) isoform PI3Kalpha have
24  to the functions of the ubiquitous class IA phosphoinositide 3-kinase (PI3K) isoforms, p110alpha and
25  but not by AG1478, indicating that Gi/o and phosphoinositide 3-kinase (PI3K) mediate the increase in
26                    Because regulation of the phosphoinositide 3-kinase (PI3K) pathway is critical for
27                            Activation of the phosphoinositide 3-kinase (PI3K) pathway occurs widely i
28                                          The phosphoinositide 3-kinase (PI3K) pathway plays an integr
29                                          The phosphoinositide 3-kinase (PI3K) pathway regulates multi
30 ubtype frequently harbors aberrations in the phosphoinositide 3-kinase (PI3K) pathway, raising the po
31                             Effectors of the phosphoinositide 3-kinase (PI3K) signal transduction pat
32                  Activating mutations in the phosphoinositide 3-kinase (PI3K) signaling pathway are f
33 hanisms such as tyrosine phosphorylation and phosphoinositide 3-kinase (PI3K) signaling.
34 of insulin-like growth factor-1R/INSR-driven phosphoinositide 3-kinase (PI3K) signaling.
35 Ralpha), produced in tumour cells, activates phosphoinositide 3-kinase (PI3K) signalling by binding t
36 d mGluR I subsequently induces activation of phosphoinositide 3-kinase (PI3K) through phosphorylation
37                           Both myosin II and phosphoinositide 3-kinase (PI3K) were found to hold stri
38 tic signaling by the pre-TCR/Notch effector, phosphoinositide 3-kinase (PI3K), and by inositol-trisph
39  of mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and interferon regulat
40 ncover the role of Vps34, the sole class III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs
41                                          The phosphoinositide 3-kinase (PI3K), which phosphorylates p
42 inase 1 (PDK1) is a pivotal regulator in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway t
43 bly, nearly all KRAS deficient cells exhibit phosphoinositide 3-kinase (PI3K)-dependent mitogen-activ
44                       We hypothesized that a phosphoinositide 3-kinase (PI3K)-dependent signaling pat
45 iphosphate at the plasma membrane to enhance phosphoinositide 3-kinase (PI3K)-dependent tumor cell in
46 red systolic contractility and activated the phosphoinositide 3-kinase (PI3K)-pathway in the heart.
47                                 Genes in the phosphoinositide 3-kinase (PI3K)/AKT pathway are the mos
48 tly contributes to activating the consequent phosphoinositide 3-kinase (PI3K)/Akt signaling pathway.
49 w that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K)/Akt-dependent manner, r
50 n the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rap
51 activities of bone morphogenetic protein and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)
52                                  Moreover, a Phosphoinositide 3-kinase (PI3K)alpha inhibitor disrupte
53                         Classically Class IB phosphoinositide 3-kinase (PI3Kgamma) plays a role in ex
54 rmacologic targeting of the gamma isoform of phosphoinositide 3-kinase (PI3Kgamma), highly expressed
55        Mutations in the catalytic subunit of phosphoinositide 3-kinase (PIK3CA) and other PI3K-AKT pa
56                    Our findings suggest that phosphoinositide 3-kinase activation promotes PKM2 phosp
57 subtype that showed increased sensitivity to phosphoinositide 3-kinase and fibroblast growth factor r
58 ifloxacin, an IKr blocker with no effects on phosphoinositide 3-kinase and INa-L prolonged APD acutel
59 ics of chemoattractant-induced activation of phosphoinositide 3-kinase and Rac effectors.
60                          Also, inhibition of phosphoinositide 3-kinase but not NF-kappaB had a simila
61                    The protein expression of phosphoinositide 3-kinase catalytic subunit PI3K(p110alp
62                        Aberrant signaling of phosphoinositide 3-kinase delta (PI3Kdelta) has been imp
63                                Inhibition of phosphoinositide 3-kinase delta (PI3Kdelta) is an appeal
64 n-of-function variants in the genes encoding phosphoinositide 3-kinase delta (PI3Kdelta) lead to accu
65                                              Phosphoinositide 3-kinase enhancer (PIKE) is a group of
66                                              Phosphoinositide 3-kinase gamma (PI3Kgamma) is an attrac
67                  Using an established enzyme phosphoinositide 3-kinase gamma, we discuss the insights
68 as independent of the regulatory function of phosphoinositide 3-kinase in mediating the metabolic act
69 cted findings cast doubt over the utility of phosphoinositide 3-kinase inhibition in acute respirator
70  to include time and INa-L in evaluating the phosphoinositide 3-kinase inhibition-derived proarrhythm
71  phenotype of patient cells was resistant to phosphoinositide 3-kinase inhibition.
72 nal phenotype, and this could be reversed by phosphoinositide 3-kinase inhibitors.
73 location biosensor for signaling through the phosphoinositide 3-kinase pathway, along with a cytosoli
74  either mitogen-activated protein kinases or phosphoinositide 3-kinase prevented the MP-induced endot
75 sely to sepsis and burns datasets but not to phosphoinositide 3-kinase signatures.
76                       For example, the PI3K (phosphoinositide 3-kinase) pathway connected to the prod
77                                        PI3K (phosphoinositide 3-kinase)/AKT and RAS/MAPK (mitogen-act
78 e findings further support engagement of the phosphoinositide 3-kinase-AKT signaling axis by H-Ras.
79 is response was mediated in part through the phosphoinositide 3-kinase-AKT signaling pathway.
80    Here, we studied the function of class II phosphoinositide 3-kinase-C2alpha (PI3K-C2alpha) in rena
81       Duvelisib is an oral dual inhibitor of phosphoinositide 3-kinase-delta (PI3K-delta) and PI3K-ga
82 estin-1 to the plasma membrane, and promoted phosphoinositide 3-kinase-dependent activation of protei
83           The enhanced respiratory burst was phosphoinositide 3-kinase-dependent but delayed apoptosi
84  enhances the glycine-activated current in a phosphoinositide 3-kinase-dependent manner, a positive f
85 tion of the 5' to 3' exonuclease EXO1 by the phosphoinositide 3-kinase-like kinases ATM (ataxia telan
86 ghly conserved 3744-residue protein from the Phosphoinositide 3-Kinase-related kinase (PIKK) family a
87 pression of insulin receptor substrate 1 and phosphoinositide 3-kinase.
88 utation in p110alpha, a catalytic subunit of phosphoinositide 3-kinase.
89 ate sodium current (INa-L) via inhibition of phosphoinositide 3-kinase.
90 ity, but this was not mediated by inhibiting phosphoinositide 3-kinase.
91 s/extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/AKT and signal transducer and
92 ha (HIF-1alpha) stabilization, including the phosphoinositide 3-kinase/Akt pathway, Siah1, and Siah2,
93                                       First, phosphoinositide 3-kinase/Akt signaling is hyperactivate
94 n through phosphatase and tensin homolog and phosphoinositide 3-kinase/Akt signaling pathways.
95  of HCK reduced survival and attenuated BTK, phosphoinositide 3-kinase/AKT, and mitogen-activated pro
96  Rac1 and downregulating p22(phox) through a phosphoinositide 3-kinase/Akt-mediated mechanism.
97 ion of mitogen-activated protein kinases and phosphoinositide 3-kinase/Akt.
98    In this study, we tested whether the dual phosphoinositide 3-kinase/mechanistic target of rapamyci
99 resulted in dose-dependent inhibition of the phosphoinositide 3-kinase/mechanistic target of rapamyci
100                                              Phosphoinositide 3-kinase/PI3K functioned as an essentia
101    Furthermore, LMP1 activated and triggered phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pa
102 ion, and invasion of Huh-7 cells through the phosphoinositide 3-kinase/protein kinase B pathway and i
103 through the aberrant expression of the TYRO3/phosphoinositide 3-kinase/protein kinase B signal transd
104 everal signal transduction pathways, such as phosphoinositide 3-kinase/protein kinase B, which are cr
105 inflammatory molecules and the activation of phosphoinositide 3-kinases (PI3K) in a process that requ
106 e elucidation of the biological functions of phosphoinositide 3-kinases (PI3K) was realized years ago
107        The physiologic roles of the class II phosphoinositide 3-kinases (PI3Ks) and their contributio
108                                              Phosphoinositide 3-kinases (PI3Ks) are a family of lipid
109                                          The phosphoinositide 3-kinases (PI3Ks) are a family of lipid
110                                              Phosphoinositide 3-kinases (PI3Ks) are ubiquitous lipid
111                                              Phosphoinositide 3-kinases (PI3Ks) regulate several cell
112 lpha regulatory (PIK3R1) subunit of class IA phosphoinositide 3-kinases (PI3Ks).
113 implications for cancer treatments targeting phosphoinositide 3-kinases and Akt because they may impa
114                                Inhibition of phosphoinositide 3-kinases, responsible for the synthesi
115 fy a kinase-independent function of class II phosphoinositide 3-OH kinase alpha (PI3K-C2alpha) acting
116           Mutations in the gene encoding the phosphoinositide 3-phosphatase myotubularin (MTM1) are r
117 e expansion phenotypes, and mutations in the phosphoinositide (3) phosphate kinase Fab1 that performs
118                 In PC12 cells, inhibition of phosphoinositide-3 kinase (PI3K) activity blocked export
119                                              Phosphoinositide-3 kinase (PI3K) generates PtdIns(3,4,5)
120                                   SMG-1 is a phosphoinositide-3 kinase (PI3K) involved in mediating n
121 f activated AKT owing to the deregulation of phosphoinositide-3 kinase (PI3K) signaling, and depletio
122                        Depletion of class II phosphoinositide-3 kinase alpha (PI3K C2A), but not inhi
123 racellular signal-regulated kinase 1/2, p38, phosphoinositide-3 kinase signaling pathways.
124 lated GRP78 then bound to VPS34, a class III phosphoinositide-3 kinase, consequently preventing the s
125 3-RAF1 aberrantly activate both the MAPK and phosphoinositide-3 kinase/mammalian target of rapamycin
126 tracellular signal-regulated kinase/RSK1 and phosphoinositide-3 kinase/mTOR pathway, which synergizes
127                                Specifically, phosphoinositide-3 kinases (class I PI3Ks, beta and gamm
128                             Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha
129  a fly-human cross-species comparison of the phosphoinositide-3-kinase (PI3K) interactome in a drosop
130 a clear degenerating axons slowly due to low phosphoinositide-3-kinase (PI3K) signalling and, subsequ
131 holipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kinase (PI3K), and subsequently to ph
132 4,5-trisphosphate (PIP3) by the lipid kinase phosphoinositide-3-kinase (PI3K).
133 s in PIK3R1 encoding a regulatory subunit of phosphoinositide-3-kinase (PI3K).
134 lls from patients treated with idelalisib, a phosphoinositide-3-kinase delta inhibitor recently appro
135 adding idelalisib, a first-in-class targeted phosphoinositide-3-kinase delta inhibitor, to bendamusti
136                    Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mT
137 on of the essential NMD effector UPF1 by the phosphoinositide-3-kinase-like kinase (PIKK) SMG-1 is a
138 ve been proposed, such as activations of the phosphoinositide-3-kinase/Akt pathway and p38 mitogen-ac
139 ating mutations in PIK3CA, the gene encoding phosphoinositide-(3)-kinase alpha (PI3Kalpha), are frequ
140  allografts (Fib-MCs) demonstrated increased phosphoinositide-3kinase (PI3K) dependent activation of
141 erse membrane cargo by the tubby domain in a phosphoinositide 4,5-bisphosphate (PI(4,5)P2)-dependent
142 congenital muscular dystrophies to defective phosphoinositide 5-phosphatase activity that is becoming
143 ynamics is established by the cilia-enriched phosphoinositide 5-phosphatase, Inpp5e.
144 distribution is created by Inpp5e, a ciliary phosphoinositide 5-phosphatase.
145 ivity that phosphorylates the 3'-hydroxyl of phosphoinositides and a protein-kinase activity that inc
146 regulate the localization of PIP3 and PI(3)P phosphoinositides and Akt activation.
147 latelets have reduced intracellular pools of phosphoinositides and an 80% reduction in IP3 generation
148          The cleaved N-terminal domain binds phosphoinositides and cardiolipin, forms membrane-disrup
149              The orchestrated recognition of phosphoinositides and concomitant intracellular release
150                Two important identifiers are phosphoinositides and GTP-bound GTPases, which provide w
151                                              Phosphoinositides and phosphoinositide binding proteins
152                                              Phosphoinositides and phosphoinositide binding proteins
153 ors to obtain complexes of ion channels with phosphoinositides and to use computational and experimen
154                                              Phosphoinositides are small phospholipids that control d
155 demonstrate that phospholipids, specifically phosphoinositides, are important regulators of TRPV1 and
156 ion of the primary cilium and maintenance of phosphoinositide balance in nondividing cells.
157                       Our study highlights a phosphoinositide-based mechanism for control of choleste
158                        Phosphoinositides and phosphoinositide binding proteins play a critical role i
159                        Phosphoinositides and phosphoinositide binding proteins play critical roles in
160 rates that VACV H7 displays a novel fold for phosphoinositide binding, which is essential for poxviru
161 pamycin-resistant mutants, we identify Pib2 (PhosphoInositide-Binding 2) as a master regulator of TOR
162 t P4-ATPase Drs2, ATP8A2 is not regulated by phosphoinositides but undergoes phosphorylation on the s
163  Although Ca(2+) is known to directly impact phosphoinositide clustering, little is known about the m
164 tecting' sensors that selectively report the phosphoinositide composition of clathrin-associated stru
165 s a coordinated change in the Rab GTPase and phosphoinositide composition of the endosomal membrane.
166 senger myo-inositol 1,4,5-trisphosphate, and phosphoinositides comprises a huge field of biology.
167  demonstrate the possibility that switchable phosphoinositide conformational states can serve as lipi
168                               Luminal pH and phosphoinositide content are fundamental features of org
169                                       Direct phosphoinositide control of the activity of ion channels
170 e of these sensors to follow the dynamics of phosphoinositide conversion during endocytosis.
171 ol 4,5-biphosphate (PIP2) is a cell membrane phosphoinositide crucial for cell signaling and activati
172              In summary, ebselen affects the phosphoinositide cycle and has CNS effects on surrogate
173 f membrane interactions and in the ranges of phosphoinositide densities that they sense.
174 ey do not require high "stimulus-responsive" phosphoinositide density for membrane binding.
175  of sphingolipids, which in turn activates 3-phosphoinositide dependent protein kinase-1 (Pdk1) and m
176 olipid synthesis and ectopically activates 3-phosphoinositide dependent protein kinase-1 (Pdk1) and m
177 rturb multiple signalling pathways including phosphoinositide-dependent cytosolic calcium ([Ca(2+) ]i
178                                     The PI3K/phosphoinositide-dependent kinase (PDK) 1 pathway repres
179 and the phosphatidylinositol 3-kinase (PI3K)/phosphoinositide-dependent kinase 1 (PDK1) pathway.
180 Src signaling, leading to PI3K activation of phosphoinositide-dependent kinase 1 (PDK1).
181        We found that mice lacking the kinase phosphoinositide-dependent kinase 1 selectively lack LC.
182 5 min of training, in which phosphorylated 3-phosphoinositide-dependent kinase-1 (p-PDK1) is increase
183            Key steps of this process are (i) phosphoinositide-dependent membrane recruitment, (ii) FG
184 n of PIK3CA-driven HNSCC is facilitated by 3-phosphoinositide-dependent protein kinase (PDK1) and enh
185              In this manner, we identified 3-phosphoinositide-dependent protein kinase 1 (PDK1) as a
186                                            3-Phosphoinositide-dependent protein kinase 1 (PDK1) is a
187 volves formation of a protein complex with 3-phosphoinositide-dependent protein kinase 1 (PDK1).
188 sis or transfection of active Akt1 or Pdpk1 (phosphoinositide-dependent protein kinase 1 ) augmented
189 ith alpha2M*, CS-GRP78 signaling activates 3-phosphoinositide-dependent protein kinase-1 (PDK1) to in
190      TIPE2 functioned as a local enhancer of phosphoinositide-dependent signaling and cytoskeleton re
191                                     Membrane phosphoinositides, especially phosphatidylinositol 4,5-b
192  comparison, CID spectra of {LGa2}(5+)-bound phosphoinositides generally resulted in fragment ions co
193        This demonstrates a mechanism where a phosphoinositide-generating enzyme PIPKIgamma couples wi
194                           Here, we show that phosphoinositide-generating enzyme, PIPKIgamma, expressi
195 sed of kinases, GTPases, and lipids, such as phosphoinositides, helps to coordinate all of these proc
196                   Here, Sac1 participates in phosphoinositide homeostasis by limiting PM phosphatidyl
197 nthesis as a major regulatory junction in PM phosphoinositide homeostasis.
198 AR1 expression also enhanced agonist-induced phosphoinositide hydrolysis and endothelial barrier perm
199 4,5-bisphosphate, mimicking presence of this phosphoinositide in the prospore membrane.
200        In agreement, SEC3a-N interacted with phosphoinositides in vitro and colocalized with a phosph
201 keratinocytes depleted from WD repeat domain phosphoinositide interacting 1 or Unc-51 like autophagy
202        Genetic ablation of WD repeat domain, phosphoinositide-interacting protein 2 in B cells alone
203             Myo-inositol is the precursor of phosphoinositides, key signaling lipids including phosph
204            Here we report that PI5P4Kbeta, a phosphoinositide kinase that regulates PI(5)P levels, de
205 so caused a dramatic generalized decrease in phosphoinositide levels that was rescued by inositol sup
206 is gain-of-function activity shifts cellular phosphoinositide levels, hyperactivates the PI3K/Akt cel
207   Phosphatase and tensin homolog (PTEN) is a phosphoinositide lipid phosphatase and one of the most f
208 y of enzymes constituting a junction between phosphoinositide lipid signaling and the trans-membrane
209 cell-free system, we recently identified the phosphoinositide lipids (PIPs) phosphatidylinositol 3-ph
210                                              Phosphoinositide lipids (PPIs) are enriched in the nucle
211                               Phosphorylated phosphoinositide lipids (PPIs) are low-abundance signali
212 ne trafficking requires coordination between phosphoinositide lipids, Rab GTPases, and microtubule-ba
213                     However, the dynamics of phosphoinositide metabolism have not been analyzed in ne
214                   We studied the dynamics of phosphoinositide metabolism in sympathetic neurons upon
215 velop a quantitative description of neuronal phosphoinositide metabolism.
216 velop a quantitative description of neuronal phosphoinositide metabolism.
217 hosphocholine membranes doped with different phosphoinositides on silicon/silicon dioxide substrates
218 to nitrocellulose membranes immobilized with phosphoinositides or sulfatide, but not with cardiolipin
219 ng a new perspective on the function of this phosphoinositide phosphatase in health and development.
220                                    FIG4 is a phosphoinositide phosphatase that is mutated in several
221                       Synaptojanin (Synj), a phosphoinositide phosphatase, is known to play an import
222    The biological relevance of most of these phosphoinositide phosphatases in acute myeloid leukemia
223                              Three different phosphoinositide phosphates (mono-, di-, and triphosphor
224 intensities obtained in positive ion-mode of phosphoinositide phosphates and phosphatidic acid bound
225 ons impaired phosphatase activity toward the phosphoinositide phosphatidylinositol (4,5)-bisphosphate
226                                 The membrane phosphoinositide phosphatidylinositol (PI) 4,5-bisphosph
227 naling that functions to dephosphorylate the phosphoinositide phosphatidylinositol 3,4,5-trisphosphat
228 es the integral membrane protein ATP1A1, the phosphoinositide phosphatidylinositol-4,5-bisphosphate (
229 teracts with a plasma membrane (PM)-specific phosphoinositide, phosphatidylinositol-(4,5)-bisphosphat
230 i trigger a signaling cascade culminating in phosphoinositide-phospholipase C (PLC) activation, which
231 mobile G-actin pool in spines depends on the phosphoinositide PI(3,4,5)P3 and involves the actin mono
232    Thus, a neuronal program dependent on the phosphoinositide PI(3,4,5)P3 is sufficient to trigger al
233  functionally regulated by hydrolysis of the phosphoinositide PI(4,5)P2 and changes in the level of p
234 mpared to serotonin in both calcium flux and phosphoinositide (PI) hydrolysis assays.
235                                 We find that phosphoinositide (PI) kinase signaling controls a conser
236 rane recruitment of TIRAP is mediated by its phosphoinositide (PI)-binding motif (PBM).
237                       By phosphorylating the phosphoinositide- (PI) binding domain of Daple, Akt abol
238 astating pediatric neuromuscular disorder of phosphoinositide (PIP) metabolism resulting from mutatio
239                             Although various phosphoinositides (PIPs) have been detected on phagosome
240                                              Phosphoinositides (PIs) are phospholipids that perform c
241                         Plasma membrane (PM) phosphoinositides play essential roles in cell physiolog
242                                              Phosphoinositides play important roles in numerous intra
243 s4P during phagocytosis and suggest that the phosphoinositide plays important roles during the matura
244      SopE and SopB target MYO6 to coordinate phosphoinositide production at invasion foci, facilitati
245                                     Limiting phosphoinositide production leads to a blockage of the a
246 eclin 1-Vps34 complex and thereby inhibiting phosphoinositide production.
247 pids (mainly phosphatidylserine (PtdSer) and phosphoinositides (PtdIns)) but the molecular details of
248 tic variation affects expression of VAC14, a phosphoinositide-regulating protein, to influence suscep
249 rther exploring the mechanisms underlying PM phosphoinositide regulation.
250 n assembly factors Dia2 and N-WASP reside on phosphoinositide-rich membranes for longer periods to pe
251 ay transient, low-affinity interactions with phosphoinositide-rich membranes, whereas F-actin assembl
252 cular principles by which ABPs interact with phosphoinositide-rich membranes.
253         Studies have also shown that nuclear phosphoinositide(s) regulates processes such as mRNA exp
254 tion are currently known: (i) binding of the phosphoinositide second messenger PIP3, (ii) binding of
255 by TIPE2 (TNFAIP8L2), a transfer protein for phosphoinositide second messengers.
256                                              Phosphoinositides serve as key membrane determinants for
257 nally, in eukaryotes, the negatively charged phosphoinositides serve as key signals not only through
258 al point of convergence between Hedgehog and phosphoinositide signaling at cilia that maintains TZ fu
259  and PIP kinases serve as a proximal node in phosphoinositide signaling axis and how its interaction
260 des (e.g. mTORC1) dominates the landscape of phosphoinositide signaling axis in cancer research.
261                          Here, we review the phosphoinositide signaling axis in cancer, giving due we
262                     The partially understood phosphoinositide signaling cascade regulates multiple as
263 d PI(4,5)P2, a technical issue hindering the phosphoinositide signaling field.
264                                              Phosphoinositide signaling has been implicated in the re
265 linositol-transfer proteins (PITPs) regulate phosphoinositide signaling in eukaryotic cells.
266 demonstrate that platelet PITPalpha-mediated phosphoinositide signaling is inconsequential for in viv
267 data suggest a general principle for how the phosphoinositide signaling landscape is physically bit m
268                       Here, we show that the phosphoinositide signaling modulated by phosphatidylinos
269                                  Calcium and phosphoinositide signaling regulate cell division in mod
270  and talin together control the adhesion and phosphoinositide signaling that regulates conversion to
271  that hijack the host actin cytoskeleton and phosphoinositide signaling to drive pathogen invasion.
272 microtubule and actin cytoskeletal dynamics, phosphoinositide signaling, clathrin-mediated endocytosi
273                Lipid signaling, particularly phosphoinositide signaling, plays a key role in regulati
274 duction is a model system for the ubiquitous phosphoinositide signaling.
275 eta cells in pulses regulated by calcium and phosphoinositide signaling.
276 w that FplA binds with high affinity to host phosphoinositide-signaling lipids, revealing a potential
277  to and from the plasma membrane, as well as phosphoinositide signalling and cholesterol homeostasis.
278 l(-) regulates the organization of the major phosphoinositide species PtdIns(4,5)P2 into microdomains
279 ain to properly bind lipids depending on the phosphoinositide species with a preference for phosphati
280                            The activation of phosphoinositide-specific phospholipase C (PI-PLC) is on
281  when spheroplast lysates are incubated with phosphoinositide-specific phospholipase C (PI-PLC).
282                                              Phosphoinositide-specific phospholipase C (PLC) is an im
283 V120027 promotes the recruitment of TRPC3 or phosphoinositide-specific phospholipase C (PLCgamma) to
284 ng differentiation in the cellular levels of phosphoinositide-specific phospholipase Cbeta (PLCbeta)
285 , the pleckstrin homology domain of Cb binds phosphoinositides, specifically phosphatidylinositol 3-p
286 nd plasma membrane lipids and many have high phosphoinositide specificity.
287                                     INPP5E's phosphoinositide substrates PI(4,5)P2 and PI(3,4,5)P3 ac
288 -bisphosphate (PtdIns(3,5)P2), whereas other phosphoinositides such as PtdIns(4,5)P2, which is enrich
289                         The first step in PM phosphoinositide synthesis is the conversion of phosphat
290 odia typically harbor higher densities of 3' phosphoinositides than adjacent regions at the cell peri
291                   There are seven species of phosphoinositides that are interconverted by lipid kinas
292 mino acid residues and acidic lipids such as phosphoinositides that play a primary role in these inte
293 E complex formation and its interaction with phosphoinositides, the function of Syx's polybasic juxta
294 ct as a cellular sensor and controller of PM phosphoinositides, thereby influencing many PM processes
295 on the membrane phospholipids, including the phosphoinositides, to form the proinflammatory arachidon
296 Thus, the leukocyte polarizer is a dual-role phosphoinositide-transfer protein and represents a poten
297 ar3 silencing causes apoptosis, triggered by phosphoinositide trisphosphate depletion and decreased A
298 bition by muscarinic receptors that increase phosphoinositide turnover in neurons is enhanced in Kcnq
299                                          The phosphoinositide, which is present in the plasmalemma be
300                              They generate 3-phosphoinositides, which are known to function as import

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