ライフサイエンスコーパス: phosphoinositide

1 n of VSG genes may entail control of nuclear phosphoinositides.

2 tidylethanolamines, phosphatidylserines, and phosphoinositides.

3 entration of lipids, such as cholesterol and phosphoinositides.

4 ion of its headgroup produces seven distinct phosphoinositides.

5 the plasma membrane by recognizing specific phosphoinositides.

6 by a conserved C-terminal domain that binds phosphoinositides.

7 very few reports on the impact of elevating phosphoinositides.

8 An ARF GEF known as General receptor for 3-phosphoinositides 1 (Grp1) is recruited to the plasma me

9 he WIPI2 (WD-repeat protein interacting with phosphoinositide 2) gene at position 5265458 (c.G745A;pV

10 FR1 on alcohol drinking are mediated via the phosphoinositide 3 kinase (PI3K) signaling pathway.

11 LPA receptor antagonists, and inhibitors of phosphoinositide 3 kinase.

12 oss of HACE1 impaired KSHV infection-induced phosphoinositide 3-kinase (PI3-K), protein kinase C-zeta

13 B cell adaptor for phosphoinositide 3-kinase (PI3K) (BCAP) is a signaling a

14 of connexin channels in a system mediated by phosphoinositide 3-kinase (PI3K) activation, which allow

15 led that platelet DREAM positively regulates phosphoinositide 3-kinase (PI3K) activity during platele

16 evels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased

17 The phosphoinositide 3-kinase (PI3K) and RAS signaling pathw

18 tin A was recently shown to strongly inhibit phosphoinositide 3-kinase (PI3K) and the mammalian targe

19 Phosphoinositide 3-kinase (PI3K) and the proteasome path

20 enetics screen of kinase inhibitors revealed phosphoinositide 3-kinase (PI3K) as a central player tra

21 PIK3CD encodes the phosphoinositide 3-kinase (PI3K) catalytic subunit, p110

22 Phosphoinositide 3-kinase (PI3K) comprised of the p110be

23 orylation of the P85 subunit in the P85-P110 phosphoinositide 3-kinase (PI3K) heterodimer, which redu

24 Depletion of CD2AP or phosphoinositide 3-kinase (PI3K) inhibition results in l

25 Phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 abo

26 ated protein kinase kinase MEK1/2, MEK5, and phosphoinositide 3-kinase (PI3K) inhibitors.

27 Phosphoinositide 3-kinase (PI3K) is deregulated in a wid

28 ches, we found that the p110delta isoform of phosphoinositide 3-kinase (PI3K) is involved in anterogr

29 but not by AG1478, indicating that Gi/o and phosphoinositide 3-kinase (PI3K) mediate the increase in

30 sly documented that systemic inactivation of phosphoinositide 3-kinase (PI3K) p110alpha, the principa

31 s identified known interactions of BCAP with phosphoinositide 3-kinase (PI3K) p85 subunit and NCK ada

32 th factor receptor (EGFR) and its downstream phosphoinositide 3-kinase (PI3K) pathway are commonly de

33 Defects in the phosphoinositide 3-kinase (PI3K) pathway are shared char

34 in-1 to initiate signaling by the downstream phosphoinositide 3-kinase (PI3K) pathway, with consequen

35 therapies is constitutive activation of the phosphoinositide 3-kinase (PI3K) pathway.

36 ng, and FGFR3 preferentially used downstream phosphoinositide 3-kinase (PI3K) pathways, whereas FGFR2

37 hat inactivation of the p110delta isoform of phosphoinositide 3-kinase (PI3K) reduces anterograde axo

38 ith distinct genetic bases for perturbed BCR/phosphoinositide 3-kinase (PI3K) signaling and dysregula

39 To study the role of phosphoinositide 3-kinase (PI3K) signaling in pericyte b

40 Class IA phosphoinositide 3-kinase (PI3K) signaling is critical f

41 e sought to dissect the effects of increased phosphoinositide 3-kinase (PI3K) signaling on CD4(+) T-c

42 Ralpha), produced in tumour cells, activates phosphoinositide 3-kinase (PI3K) signalling by binding t

43 turn, the Gbetagamma complex signals through phosphoinositide 3-kinase (PI3K) to regulate kinocilium

44 (PDGF) signaling recruits the p85 subunit of Phosphoinositide 3-kinase (PI3K) to regulate mammalian l

45 adipose tissue, specifically at the level of phosphoinositide 3-kinase (PI3K), a key IIS effector mol

46 d to activation of the catalytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that co

47 vated by CD44, including phospholipase C and phosphoinositide 3-kinase (PI3K), also attenuated HMWH-i

48 encoding the p110delta catalytic subunit of phosphoinositide 3-kinase (PI3K), have highly penetrant

49 ncover the role of Vps34, the sole class III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs

50 encoding the catalytic p110delta subunit of phosphoinositide 3-kinase (PI3K), result in hyperactivat

51 ind that growth factor signaling through the phosphoinositide 3-kinase (PI3K)-Akt pathway induces acu

52 INSM1 modulates the phosphoinositide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT

53 inase 1 (PDK1) is a pivotal regulator in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway t

54 The ubiquitous, growth factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network

55 CD133, but not GLIS3 or WNT, is required for phosphoinositide 3-kinase (PI3K)/AKT Ser/Thr kinase (AKT

56 Hyperactivated phosphoinositide 3-kinase (PI3K)/Akt serine/threonine ki

57 t vitreous activate the signaling pathway of phosphoinositide 3-kinase (PI3K)/Akt, which plays a crit

58 w that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K)/Akt-dependent manner, r

59 We also identify active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in

60 Prior studies suggest that phosphoinositide 3-kinase (PI3K)/mammalian target of rap

61 The phosphoinositide 3-kinase (PI3K)/mechanistic target of r

62 The phosphoinositide 3-kinase (PI3K)beta isoform is uniquely

63 Classically Class IB phosphoinositide 3-kinase (PI3Kgamma) plays a role in ex

64 3CA are frequent in human breast cancer, and phosphoinositide 3-kinase alpha (PI3Kalpha) inhibitors h

65 osolic calcium, and downstream activation of phosphoinositide 3-kinase and extracellular signal-regul

66 Phosphoinositide 3-kinase beta (PI3Kbeta) is regulated b

67 ys, including calcium, protein kinase C, and phosphoinositide 3-kinase but not extracellular signal-r

68 The protein expression of phosphoinositide 3-kinase catalytic subunit PI3K(p110alp

69 contrast, inhibition of phospholipase C and phosphoinositide 3-kinase did not prevent stimulating ef

70 ung fibroblasts through its interaction with phosphoinositide 3-kinase gamma (PI3Kgamma), forming nan

71 dependent on activation of G(i), ERK1/2, and phosphoinositide 3-kinase gamma/Akt at a molecular level

72 endent on the activities of the lipid kinase phosphoinositide 3-kinase in addition to the Rho GTPases

73 as independent of the regulatory function of phosphoinositide 3-kinase in mediating the metabolic act

74 However, treatment with the phosphoinositide 3-kinase inhibitor wortmannin did not d

75 a detoxified TLR4 agonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, prevented the LPS-m

76 can then be reactivated by the addition of a phosphoinositide 3-kinase inhibitor, which has previousl

77 cluding several chemoimmunotherapy regimens, phosphoinositide 3-kinase inhibitors, and lenalidomide p

78 Here we demonstrate that phosphoinositide 3-kinase p110alpha in the fetus and the

79 either mitogen-activated protein kinases or phosphoinositide 3-kinase prevented the MP-induced endot

80 mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase signaling but in different for

81 links TCR signaling to mTORC2 activation via phosphoinositide 3-kinase signaling.

82 Activation of ERK, phosphoinositide 3-kinase, and NADPH oxidase-mediated re

83 s (phospholipases Cepsilon and Cgamma1), and phosphoinositide 3-kinase, in nociceptors.

84 activator of transcription-5 (JAK2-STAT5) or phosphoinositide 3-kinase-Akt (PI3K-Akt) pathways to med

85 is response was mediated in part through the phosphoinositide 3-kinase-AKT signaling pathway.

86 rophy, insulin resistance and reduced muscle phosphoinositide 3-kinase-Akt signalling are common char

87 gh activation of estrogen receptor (ER)alpha-phosphoinositide 3-kinase-Akt-Foxo1 signaling, which can

88 sib, a first-in-class oral dual inhibitor of phosphoinositide 3-kinase-delta,-gamma, in RR iNHL in a

89 d phospholipase C (PLC)-driven (females) and phosphoinositide 3-kinase-driven (males) phospholipid me

90 38alpha kinase, c-Jun N-terminal kinase-1/2, phosphoinositide 3-kinase-gamma, and p50 and p65 nuclear

91 tion of the 5' to 3' exonuclease EXO1 by the phosphoinositide 3-kinase-like kinases ATM (ataxia telan

92 hat GPER1 mediates the effects of E2 via the phosphoinositide 3-kinase-protein kinase B-mechanistic t

93 te that this BPA effect involves ERalpha and phosphoinositide 3-kinase.

94 lcium, protein kinase C, and to some extent, phosphoinositide 3-kinase.

95 ived neurons, enriched in pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI

96 le protein inhibitor), gedatolisib (PKI-587, phosphoinositide 3-kinase/mammalian target of rampamycin

97 through the aberrant expression of the TYRO3/phosphoinositide 3-kinase/protein kinase B signal transd

98 everal signal transduction pathways, such as phosphoinositide 3-kinase/protein kinase B, which are cr

99 phosphoinositide 3-kinase/protein kinase B/mammalian tar

100 Class Ia phosphoinositide 3-kinases (PI3K) are critical mediators

101 The phosphoinositide 3-kinases (PI3Ks) are a family of lipid

102 ted protein kinases (MAPKs) ERK and p38, the phosphoinositide 3-kinases (PI3Ks), and the kinase mTOR.

103 lpha regulatory (PIK3R1) subunit of class IA phosphoinositide 3-kinases (PI3Ks).

104 mic aberrations in neurofibromin 1 (NF1) and phosphoinositide 3-kinases/mammalian target of rapamycin

105 Class I phosphoinositide 3-OH kinase (PI3K) signaling is central

106 fy a kinase-independent function of class II phosphoinositide 3-OH kinase alpha (PI3K-C2alpha) acting

107 l is mediated by a signaling axis comprising phosphoinositide 3-phosphate kinase, Akt Ser/Thr kinase,

108 In PC12 cells, inhibition of phosphoinositide-3 kinase (PI3K) activity blocked export

109 a 4-gene predictive signature containing the phosphoinositide-3 kinase (PI3K) inhibitor, PTEN, for id

110 re we report that the regulatory subunits of phosphoinositide-3 kinase (PI3K)-p85alpha (PIK3R1) and p

111 racellular signal-regulated kinase 1/2, p38, phosphoinositide-3 kinase signaling pathways.

112 sib is a second-generation oral inhibitor of phosphoinositide-3 kinase, downstream of the B-cell rece

113 3-RAF1 aberrantly activate both the MAPK and phosphoinositide-3 kinase/mammalian target of rapamycin

114 Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha

115 holipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kinase (PI3K), and subsequently to ph

116 s in PIK3R1 encoding a regulatory subunit of phosphoinositide-3-kinase (PI3K).

117 erine/threonine protein kinase that mediates phosphoinositide-3-kinase (PI3K)/AKT signalling.

118 The phosphoinositide-3-kinase (PI3K)/mammalian target of rap

119 Phosphoinositide-3-kinase delta (PI3Kdelta) is a critica

120 se tensin homolog), thereby activating PI3K (phosphoinositide-3-kinase) and mTOR (mammalian target of

121 Bruton's tyrosine kinase, phospholipase and phosphoinositide-3-kinase, calcium, and phosphoinositide

122 Phosphoinositide-3-kinase-delta (PI3Kdelta), a lipid kin

123 We investigated a next-generation phosphoinositide-3-kinase-delta inhibitor (PI3K-deltai),

124 The survival signaling pathway phosphoinositide-3-kinase/protein kinase B that regulate

125 Phosphoinositide-3-kinases (PI3Ks) are part of signal tr

126 erse membrane cargo by the tubby domain in a phosphoinositide 4,5-bisphosphate (PI(4,5)P2)-dependent

127 e kinase (pMEK), protein kinase B (pAkt), or phosphoinositide-4,5-bisphosphate 3-kinase (pPI3K).

128 require the production of PI(3,4)P(2) by the phosphoinositide 5'-phosphatase SHIP2.

129 Loss of the phosphoinositide 5-phosphatase OCRL causes accumulation

130 ynamics is established by the cilia-enriched phosphoinositide 5-phosphatase, Inpp5e.

131 , the underlying molecular mechanisms of how phosphoinositides act in the ER stress response remain e

132 We also demonstrate that these phosphoinositides activate ADAP1's enzymatic activity to

133 Other soluble phosphoinositides also interacted with the 4HB but less

134 irm the critical proviral function of PI(3)P phosphoinositide and the early endosomal compartment in

135 ivity that phosphorylates the 3'-hydroxyl of phosphoinositides and a protein-kinase activity that inc

136 The cleaved N-terminal domain binds phosphoinositides and cardiolipin, forms membrane-disrup

137 pids and forming essential binding sites for phosphoinositides and cholesterol that are functionally

138 Two important identifiers are phosphoinositides and GTP-bound GTPases, which provide w

139 e functional domains for in vitro binding to phosphoinositides and liposomes and for plant cell membr

140 Phosphoinositides and phosphatidic acid are small anioni

141 Thus, resolution involves phosphoinositides and tethering of phagolysosomes to the

142 cal models: one representing the dynamics of phosphoinositides and the other explaining how phosphati

143 d PtdIns3P, others interact with alternative phosphoinositides, and a precise understanding of how th

144 osphorylate the 3-OH of the inositol ring of phosphoinositides, and deregulation of this pathway has

145 chanisms by which the biological outcomes of phosphoinositide are diversified.

146 That phosphoinositides are dynamically elevated in response t

147 Phosphoinositides are signaling lipids that regulate num

148 We propose that Nir2 functions to replenish phosphoinositides at the HCV replication organelle to ma

149 ion of the primary cilium and maintenance of phosphoinositide balance in nondividing cells.

150 ically to various di- and tri-phosphorylated phosphoinositides, bind both PtdIns3P and other phosphoi

151 ma membrane via the actions of an N-terminal phosphoinositide-binding domain.

152 c reticulum localization, kinesin-binding or phosphoinositide-binding properties abrogated the regene

153 therefore suggested to be the plant-specific phosphoinositide-binding protein whose expression is con

154 exin A11 (ANXA11), an RNA granule-associated phosphoinositide-binding protein, acts as a molecular te

155 Here, we report that a phosphoinositide-binding protein, SMALLER TRICHOMES WITH

156 mity to the basolateral plasma membrane, and phosphoinositide-binding residues of Septin2 are require

157 t P4-ATPase Drs2, ATP8A2 is not regulated by phosphoinositides but undergoes phosphorylation on the s

158 fluorescence spectroscopy demonstrated that phosphoinositides change the local conformation of the N

159 tecting' sensors that selectively report the phosphoinositide composition of clathrin-associated stru

160 ised sensory signaling alters cilia membrane phosphoinositide composition via TUB-1-dependent traffic

161 d GAK correlates with temporal variations in phosphoinositide composition, consistent with a lipid-sw

162 t this problem, we target the resynthesis of phosphoinositides consumed during intracellular transduc

163 Luminal pH and phosphoinositide content are fundamental features of org

164 Pharmacologic alteration of cellular phosphoinositide content with miltefosine reduces ZFYVE2

165 e of these sensors to follow the dynamics of phosphoinositide conversion during endocytosis.

166 and VAPs completes our understanding of the phosphoinositide cycle between the ER and HCV ROs.

167 ular signal-regulated kinase-ribosomal S6 PK-phosphoinositide-dependent kinase (ERK-RSK-PDK) complex

168 The PI3K/phosphoinositide-dependent kinase (PDK) 1 pathway repres

169 ) via phosphatidyl inositol-3-kinase (PI3K), phosphoinositide-dependent kinase 1 (PDK1 or PDPK1), and

170 ARE disruption also results in constitutive phosphoinositide-dependent kinase 1 gain of function.

171 weak TCR signals were sufficient to activate phosphoinositide-dependent kinase-1 to phosphorylate AKT

172 3-Phosphoinositide-dependent protein kinase 1 (PDK1) is a

173 rn controlled by GC-specific upregulation of phosphoinositide-dependent protein kinase PDK1 and the p

174 Phosphoinositide-dependent protein kinase-1 (PDK1) is re

175 TIPE2 functioned as a local enhancer of phosphoinositide-dependent signaling and cytoskeleton re

176 3'-Phosphoinositide-dependent-Kinase-1 (PDK1) is a master r

177 compaction of Tom1 VHS, suggesting that the phosphoinositide destabilizes the protein domain.

178 These lipids include phosphoinositides, diacylglycerol, phosphatidic acid, an

179 Phosphoinositides, diacylglycerolpyrophosphate, ceramide

180 We find further that the phosphoinositide-directed activities of both PIKfyve and

181 tes, including lysophosphatidylinositols and phosphoinositides, displayed anti-DENV2 activity.

182 uggests that, in addition to being required, phosphoinositides drive downstream pathways.

183 complex cannot access membrane-incorporated phosphoinositides due to steric constraints.

184 To investigate the spatial distribution of phosphoinositides during arbuscular mycorrhizal symbiosi

185 act with SNX9, an actin regulator that binds phosphoinositides during endocytosis and at invadopodia.

186 ppo signaling, and uncover the importance of phosphoinositide dynamics, specifically PI(4,5)P(2), in

187 Membrane phosphoinositides, especially phosphatidylinositol 4,5-b

188 tidylinositol 4-kinase, completes a cycle of phosphoinositide flow between the ER and viral replicati

189 Phosphoinositides function as lipid signals in plant dev

190 Here, we show that phosphoinositide-generating enzyme, PIPKIgamma, expressi

191 Phosphoinositides have a pivotal role in the maturation

192 sed of kinases, GTPases, and lipids, such as phosphoinositides, helps to coordinate all of these proc

193 oculocerebrorenal syndrome protein) disrupt phosphoinositide homeostasis along the endolysosomal pat

194 y activate Golgi localized, prohypertrophic, phosphoinositide hydrolysis, that is not accessed by cel

195 all vesicle trafficking, autophagy relies on phosphoinositide identity, concentration, and localizati

196 dimeric proteins which tether by binding the phosphoinositides in both membranes.

197 Here we studied the role of phosphoinositides in phagolysosome resolution.

198 position of actin-associated proteins and of phosphoinositides in the membrane.

199 It bound to multiple bioactive phosphoinositides in vitro.

200 PI(4)P phosphatase and its substrate, PI(4)P phosphoinositide, in promoting viral replication.

201 CD of ATG16L1 that mediate direct binding to phosphoinositides, including phosphatidylinositol 3-phos

202 n due to a reduced capacity to re-synthesize phosphoinositides, including phosphatidylinositol-(4,5)-

203 r downstream recruitment of WD-repeat domain phosphoinositide-interacting protein (WIPI)2, a protein

204 Genetic ablation of WD repeat domain, phosphoinositide-interacting protein 2 in B cells alone

205 any studies focus on signaling molecules and phosphoinositides involved in initiating macropinocytosi

206 The requirement for a phosphoinositide is conventionally studied by depleting

207 examples of how we have used HDX-MS to study phosphoinositide kinases and the protein kinase Akt.

208 that clathrin-coated vesicles have a dynamic phosphoinositide landscape, and we have proposed that li

209 f synaptic strength and show that changes in phosphoinositide levels correlate with changes in endoso

210 betaII-spectrin required phosphoinositide lipid binding to promote axonal transpo

211 ate that TRPV1 activity is enhanced when the phosphoinositide lipid content is reduced, and the C-ter

212 ed response to capsaicin, independent of the phosphoinositide lipid content.

213 spholipase C-coupled receptors that regulate phosphoinositide lipid content.

214 lows IQGAP1 to help control the amplitude of phosphoinositide lipid messenger signaling by coordinati

215 udies show that TRPM8 requires the signaling phosphoinositide lipid PIP(2) to function.

216 y an enhanced response to capsaicin, whereas phosphoinositide lipid supplementation reduces TRPV1-med

217 Phosphoinositide lipids (PPIs) are enriched in the nucle

218 Phosphorylated phosphoinositide lipids (PPIs) are low-abundance signali

219 itol (PI) 3-phosphates being the predominant phosphoinositide lipids at endosomes and lysosomes, wher

220 TRPV1 worms with low levels of phosphoinositide lipids display an enhanced response to

221 Here, we determined the effect of phosphoinositide lipids on TRPV1 function by combining g

222 of autism disease mutations and the role of phosphoinositide lipids to promote homodimerization that

223 ind to phosphatidylinositol phospholipids or phosphoinositides, markers of organelle identity in the

224 ced pro-inflammatory responses by inhibiting phosphoinositide-mediated activation of TAK1.

225 BCAP couples TLR signaling to phosphoinositide metabolism and inhibits MyD88-directed

226 R-domain containing proteins, Arfaptins, and phosphoinositide-metabolizing enzymes.

227 ide a mechanistic link between RTK-initiated phosphoinositide microdomains and Arf6 during signal tra

228 P binds preferentially to monophosphorylated phosphoinositides, of which PtdIns(4)P is most abundant

229 to nitrocellulose membranes immobilized with phosphoinositides or sulfatide, but not with cardiolipin

230 sphoinositides, bind both PtdIns3P and other phosphoinositides, or associate with none of the lipids

231 iacylglycerol kinase (DGK), an enzyme of the phosphoinositide pathway, reduces ENaC function.

232 ase domain of synaptojanin 1 (SJ1/PARK20), a phosphoinositide phosphatase implicated in synaptic vesi

233 s activated by loss of the tumour suppressor phosphoinositide phosphatase PTEN.

234 Fig4 is a phosphoinositide phosphatase that converts PI3,5P2 to PI

235 Synaptojanin1 (synj1) is a phosphoinositide phosphatase with dual SAC1 and 5'-phosp

236 Synaptojanin1 (Synj1) is a phosphoinositide phosphatase, important in clathrin unco

237 Here, we screen for phosphoinositide phosphatases that influence autophagy i

238 e, the kinase that synthesizes the endosomal phosphoinositide phosphatidylinositol-3,5-bisphosphate,

239 The phosphoinositide, phosphatidylinositol 4,5-bisphosphate

240 selective alpha-1A agonist A61603-stimulated phosphoinositide-phospholipase C and myocyte contraction

241 Synthesis of the phosphoinositide PI(3)P by the autophagic class III phos

242 mobile G-actin pool in spines depends on the phosphoinositide PI(3,4,5)P3 and involves the actin mono

243 Thus, a neuronal program dependent on the phosphoinositide PI(3,4,5)P3 is sufficient to trigger al

244 The phosphoinositide PI(3,5)P(2), generated exclusively by t

245 The phosphoinositide PI(4,5)P(2) has been of particular inte

246 rane recruitment of TIRAP is mediated by its phosphoinositide (PI)-binding motif (PBM).

247 d enrichment in several pathways, including "Phosphoinositides (PI) and their downstream targets" (Bo

248 Phosphoinositides (PI) are key regulators of cellular or

249 e Ca(2+)-mobilizing messenger, NAADP and the phosphoinositide, PI(3,5)P(2), respectively.

250 By phosphorylating the phosphoinositide- (PI) binding domain of Daple, Akt abol

251 demonstrate that GOLPH3, upon binding to the phosphoinositide PI4P, induces curvature of synthetic me

252 eutrophil function by modulating appropriate phosphoinositide (PIP) signaling.

253 around signaling patches of Ras, Rac and the phosphoinositide PIP3 in the plasma membrane.

254 he associations of alpha-Syn with the acidic phosphoinositides (PIPs), phosphatidylinositol 4,5-bisph

255 Phosphoinositides (PIs) are phospholipids that perform c

256 Phosphoinositides (PIs) regulate a myriad of cellular fu

257 Phosphoinositides play crucial roles in intracellular me

258 SopE and SopB target MYO6 to coordinate phosphoinositide production at invasion foci, facilitati

259 Limiting phosphoinositide production leads to a blockage of the a

260 eclin 1-Vps34 complex and thereby inhibiting phosphoinositide production.

261 s suggest that stimulus-induced elevation of phosphoinositides provides a way for these stimuli to se

262 eby controls Collybistin-2-interactions with phosphoinositides (PtdInsPs) in the plasma membrane.

263 is also remarkable for having revealed that phosphoinositide recognition by a PH domain can be switc

264 We show that selective phosphoinositide recognition by cytohesin-1 isoforms pro

265 Our results suggest inhibition of phosphoinositide recycling provides a useful anti-angiog

266 that systemic or EC specific suppression of phosphoinositide recycling results in reduced tumor grow

267 (RXR) motifs that are required for NGF- and phosphoinositide-regulated DOR export from intracellular

268 tic variation affects expression of VAC14, a phosphoinositide-regulating protein, to influence suscep

269 rther exploring the mechanisms underlying PM phosphoinositide regulation.

270 the small modulatory membrane protein PIRT (phosphoinositide regulator of TRP).

271 in HIV-1, fully quantitative analysis of all phosphoinositides remains technically challenging and th

272 e phosphatidic acid, phosphatidylserine, and phosphoinositides, represent a small percentage of membr

273 Quantitative analyses of phosphoinositides revealed strong enrichment of PIP(2),

274 In contrast, phosphoinositide-rich membranes recruit and activate tal

275 ediate chemokine-induced local generation of phosphoinositide second messengers, but inhibit global a

276 by TIPE2 (TNFAIP8L2), a transfer protein for phosphoinositide second messengers.

277 of OsPIP5K1 and its product PI(4,5)P(2) , a phosphoinositide secondary messenger, in nuclear bodies.

278 ause almost all GBM tumors have dysregulated phosphoinositide signaling as part of that process, we h

279 linositol-transfer proteins (PITPs) regulate phosphoinositide signaling in eukaryotic cells.

280 between membranes in vitro, and to stimulate phosphoinositide signaling in vivo, Sfh5 does not exhibi

281 Coordinated phosphoinositide signaling is critical both for phagocyt

282 demonstrate that platelet PITPalpha-mediated phosphoinositide signaling is inconsequential for in viv

283 Phosphoinositide signaling lipids are essential for seve

284 Here, we show that the phosphoinositide signaling modulated by phosphatidylinos

285 s (HCV) is known for its ability to modulate phosphoinositide signaling pathways for its replication.

286 et of rapamycin (mTOR) activation, increased phosphoinositide signaling, and microRNA downregulation.

287 tin polymerization, membrane processing, and phosphoinositide signaling.

288 and phosphoinositide-3-kinase, calcium, and phosphoinositide signaling.

289 w that FplA binds with high affinity to host phosphoinositide-signaling lipids, revealing a potential

290 to a previously unrecognized role of nuclear phosphoinositide signalling in regulating p53 stability

291 of rice shoots, likely to be through nuclear phosphoinositide signals, and provides insights into the

292 its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglyc

293 rted that Arabidopsis (Arabidopsis thaliana) phosphoinositide-specific phospholipase C2 functions in

294 INPP5E's phosphoinositide substrates PI(4,5)P2 and PI(3,4,5)P3 ac

295 atidylinositol 3-phosphate (PtdIns(3)P) is a phosphoinositide that is rapidly synthesized and degrade

296 There are seven species of phosphoinositides that are interconverted by lipid kinas

297 s activity towards PI(4,5)P(2) and PI3P, two phosphoinositides that function at the early stages of m

298 mino acid residues and acidic lipids such as phosphoinositides that play a primary role in these inte

299 The phosphoinositide, which is present in the plasmalemma be

300 to demonstration of the enrichment of PI(4)P phosphoinositide within the replication compartment.