ライフサイエンスコーパス: bisphosphate

1 verting fructose-6-phosphate to fructose-1,6-bisphosphate.

2 ence of the allosteric effector fructose 2,6-bisphosphate.

3 pends on binding to phosphatidylinositol 4,5-bisphosphate.

4 ts the synthesis of phosphatidylinositol 4,5-bisphosphate.

5 ks hydrolysis of phosphatidylinostitol (4,5)-bisphosphate.

6 n interactions with phosphatidylinositol 4,5-bisphosphate.

7 in the presence of phosphatidylinositol 4,5-bisphosphate.

8 omology domain with phosphatidylinositol 4,5-bisphosphate.

9 ge of the CO2 acceptor molecule ribulose 1,5-bisphosphate.

10 sphatidylserine and phosphatidylinositol 4,5-bisphosphate.

11 hannel activated by phosphatidylinositol 3,5-bisphosphate.

12 tol-3-phosphate and phosphatidylinositol-3,5-bisphosphate.

13 e, forming the much more stable fructose 1,6-bisphosphate.

14 itol-5-phosphate to phosphatidylinositol-4,5-bisphosphate.

15 Bisphosphate 3'-nucleotidase (BPNT-1) is a lithium-sensi

16 ubunit alpha of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) frequently mutated in cance

17 ion via the FAK-Src-phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K) signaling pathway.

18 ne kinase (Syk) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K).

19 g components of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT signalling cascade that

20 Phosphatidylinositol-4,5-bisphosphate 3-kinase 1A, activated in Schwann cells by

21 , a key effector of phosphatidylinositol-4,5-bisphosphate 3-kinase 1A, was previously implicated in C

22 the Janus Kinase 2/phosphatidylinositol-4,5-bisphosphate 3-kinase pathway.

23 ls, and blockage of phosphatidylinositol-4,5-bisphosphate 3-kinase, Akt, or p38 downstream mitogen-ac

24 activating PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha, PI(3)Kal

25 ear factor kappa B, phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt, and p38 signaling pathways.

26 The phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt/ mammalian target of rapamycin

27 Although phosphatidylinositol 4,5-bisphosphate, 3-phosphate, and 3,5-bisphosphate are comm

28 ions activating the phosphatidylinositol-4,5-bisphosphate-3-kinase (PI3K)-protein kinase B (AKT)-mamm

29 GFR2 interacts with phosphatidylinositol-4,5-bisphosphate-3-kinase and AKT to inactivate p21.

30 VEGFR2 to activate phosphatidylinositol-4,5-bisphosphate-3-kinase and AKT, resulting in inactivation

31 am molecule FIG4 (phosphatidylinositol (3,5)-bisphosphate 5-phosphatase) as significantly up-regulate

32 ttack on the aldehyde and yield tagatose 1,6-bisphosphate, a competitive inhibitor of the enzyme.

33 d associated with phosphatidylinositol (3,5)-bisphosphate, a key component of late endosomes/lysosome

34 for the first time explain how fructose 1,6-bisphosphate affects the active site.

35 The current model posits that fructose-1,6-bisphosphate aldolase (ALD) provides a critical link bet

36 d that it inhibits E. coli class II fructose bisphosphate aldolase, but not RNA polymerase.

37 dentification of calpain, Sm29, and fructose-bisphosphate aldolase, themselves potential vaccine anti

38 ing bifunctional unidirectional fructose 1,6-bisphosphate aldolase/phosphatase, have been identified.

39 pleting the pool of phosphatidylinositol-4,5-bisphosphate, an activator of multiple actin-regulatory

40 y identified enzymes generate mevalonate 3,5-bisphosphate and a new decarboxylase we describe here, m

41 spholipid vesicles, phosphatidylinositol 4,5-bisphosphate and Ca(2+), or by the identity of the fluor

42 ne phosphoinositide phosphatidylinositol 4,5-bisphosphate and cargo relieves this autoinhibition, tri

43 though inactive, does bind alpha-glucose 1,6-bisphosphate and changes conformation.

44 vels [increase in phosphatidylinositol (3,5)-bisphosphate and decrease in phosphatidylinositol 3-phos

45 s in the absence of phosphatidylinositol 4,5-bisphosphate and is facilitated by palmitoylation of a s

46 interaction with phosphatidylinositol-(4,5)-bisphosphate and its subsequent cleavage from the precur

47 aling phospholipids phosphatidylinositol 4,5-bisphosphate and phosphatidic acid.

48 d messengers, i.e., phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphat

49 tides, particularly phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate, are i

50 t whereas levels of phosphatidylinositol-3,4-bisphosphate and phosphatidylinositol-3,4,5-trisphosphat

51 exin binding lipids phosphatidylinositol-4,5-bisphosphate and phosphatidylserine in different composi

52 nase that generates phosphatidylinositol-3,5-bisphosphate and, directly or indirectly, phosphatidylin

53 hed in cholesterol, phosphatidylinositol 4,5-bisphosphate, and gangliosidic lipids.

54 d by cold, voltage, phosphatidylinositol 4,5-bisphosphate, and menthol.

55 ate and synthesizes phosphatidylinositol 3,5-bisphosphate, and plays a critical role in endolysosomal

56 rates, fructose 1-phosphate and fructose 1,6-bisphosphate, and provides an excellent model system for

57 ing phospholipid phosphatidylinositol-(4, 5)-bisphosphate, and the c-Abl-interacting protein CrkII ar

58 sitol 4,5-bisphosphate, 3-phosphate, and 3,5-bisphosphate are commonly considered as hallmarks of the

59 nd accumulation of phosphatidylinositol(3,4)-bisphosphate at invadopodia is a key determinant for inv

60 converts PIP3 to phosphatidylinositol (4,5)-bisphosphate at the plasma membrane.

61 yl transfer steps using a beta-D-glucose 1,6-bisphosphate (betaG16BP) intermediate.

62 ature involving the phosphatidylinositol 4,5-bisphosphate binding residue (L1008), but was independen

63 out cold sensor and phosphatidylinositol 4,5-bisphosphate binding sites, which are both located in th

64 ility studies, demonstrate that fructose 1,6-bisphosphate binding to the allosteric domain causes a s

65 e of Lys-170 in the phosphatidylinositol 4,5-bisphosphate-binding site.

66 sphatidylserine and phosphatidylinositol 4,5-bisphosphate but not other anionic phospholipids.

67 ysis, we demonstrated that alpha-glucose 1,6-bisphosphate can adopt two low energy orientations as re

68 CO2-fixing Calvin cycle enzyme, ribulose 1,5-bisphosphate carboxylase (RubisCO), prevents photohetero

69 lutionary adaptation is that of ribulose-1,5-bisphosphate carboxylase (RubisCO), the enzyme responsib

70 ng the key Calvin Cycle enzyme, Ribulose 1,5 bisphosphate carboxylase oxygenase (Rubisco).

71 volved in photosynthesis (e.g., ribulose-1,5-bisphosphate carboxylase oxygenase genes rbcS and rbcL),

72 The ratios of PEPC and PPDK to ribulose bisphosphate carboxylase were substantially lower than 1

73 carbon dioxide may be fixed via the ribulose bisphosphate carboxylase, Wood-Ljungdahl pathway or redu

74 ry of nearly 100 genes encoding ribulose-1,5 bisphosphate carboxylase-oxygenase subunit proteins of t

75 ound many copies of the enzymes ribulose 1,5-bisphosphate carboxylase/ oxygenase and carbonic anhydra

76 e two key carboxysomal enzymes, ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) and carboni

77 arbon fixation by concentrating ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) and its sub

78 The enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) catalyzes t

79 trates the carbon-fixing enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) in a paracr

80 Ribulose 1,5-bisphosphate carboxylase/oxygenase (RubisCO) is a critic

81 hotosynthetic CO2-fixing enzyme ribulose 1,5-bisphosphate carboxylase/oxygenase (rubisco) is inhibite

82 Ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) is the key

83 In photosynthetic organisms, D-ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) is the majo

84 encies of the CO2-fixing enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) often limit

85 Ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) plays a cri

86 mes compartmentalize the enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) with carbon

87 ts suffers from the reaction of ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco) with O2 ins

88 O2 concentration at the site of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco), simultaneo

89 Ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO), the carbox

90 ion around the carboxylating enzyme ribulose bisphosphate carboxylase/oxygenase (RuBisCO).

91 tion-state analog-bound form II ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco).

92 enhancing the CO2 fixing enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco).

93 the TP of the small subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase and its reverse pepti

94 nservation of Mg(2+) within the ribulose-1,5-bisphosphate carboxylase/oxygenase family of enzymes.

95 Cb) using a simple kinetic model of ribulose bisphosphate carboxylase/oxygenase function.

96 ns both the denitrification and ribulose 1,5-bisphosphate carboxylase/oxygenase gene clusters, unders

97 boxylase, class II aldolase, or ribulose 1,5-bisphosphate carboxylase/oxygenase, large subunit (RuBis

98 to model maximal rates of RuBP (ribulose-1,5-bisphosphate) carboxylation (Vcmax ) and electron transp

99 tetramers show that binding of fructose 2,6-bisphosphate cools the enzyme and reduces dynamic moveme

100 carboxylase we describe here, mevalonate 3,5-bisphosphate decarboxylase, produces isopentenyl phospha

101 maturation through phosphatidylinositol-3,5-bisphosphate-dependent activation of TRPML1, whereas che

102 We show that phosphatidylinositol 4,5-bisphosphate-dependent FGF2 oligomerization concomitant

103 anism that involves phosphatidylinositol 4,5-bisphosphate-dependent insertion of FGF2 oligomers into

104 macropinosomes in a phosphatidylinositol 3,5-bisphosphate-dependent manner and localize to their cont

105 es that may control phosphatidylinositol 4,5-bisphosphate-dependent membrane translocation as part of

106 Rac1-dependent and phosphatidylinositol 4,5-bisphosphate-dependent signaling cascade that suppresses

107 s ability to induce phosphatidylinositol 4,5-bisphosphate depletion after agonist stimulation.

108 aused resistance to phosphatidylinositol 4,5-bisphosphate depletion, and increased KCNQ2 current ampl

109 ing by mutations or phosphatidylinositol 4,5-bisphosphate depletion, we show that KCNE1 affects both

110 in plasma membrane phosphatidylinositol 4,5-bisphosphate depletion.

111 echanism whereby the binding of fructose 1,6-bisphosphate destabilizes an alpha-helix that bridges th

112 lasma membrane to phosphatidylinositol (4,5)-bisphosphate-enriched domains.

113 mplexans express one or both of fructose 1,6-bisphosphate (F16BP) aldolase and 2-deoxyribose 5-phosph

114 colytic flux via their product, fructose-2,6-bisphosphate (F26BP), which activates 6-phosphofructo-1-

115 Fructose-1,6-bisphosphate (FBP) aldolase, a glycolytic enzyme, cataly

116 the pathway and the levels of fructose (1,6) bisphosphate (FBP), are predictive of the rate and contr

117 sine 5'-monophosphate (AMP) and fructose 1,6-bisphosphate (FBP), respectively.

118 ation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activa

119 catalytic ability to synthesize fructose-2,6-bisphosphate (Fru-2,6-P(2)), the key glycolysis alloster

120 amine the physiological role of fructose 2,6-bisphosphate (Fru-2,6-P2 ) during photosynthesis, growth

121 The effects of AMP and fructose 2,6-bisphosphate (Fru-2,6-P2) on porcine fructose-1,6-bispho

122 ure is required for phosphatidylinositol 4,5-bisphosphate homeostasis mediated by Nir2 at ER-PM junct

123 C activity, causing phosphatidylinositol 4,5-bisphosphate hydrolysis and inositol 1,4,5-trisphosphate

124 rrent inhibition or phosphatidylinositol 4,5-bisphosphate hydrolysis.

125 the continuous accumulation of fructose 1,6-bisphosphate in a permanently frozen solution as followe

126 p5e and accumulates phosphatidylinositol 4,5-bisphosphate in distal cilia.

127 ling studies showed accumulated fructose 1,6-bisphosphate in FK866-treated cells mainly derived from

128 differentially sensitive to phosphatidyl-4,5-bisphosphate in terms of catalytic activation enhancemen

129 ne, including PIP2 (phosphatidylinositol-4,5-bisphosphate) in the inner leaflet, and GM3 (monosialodi

130 ith the fluorescent phosphatidylinositol 4,5-bisphosphate/inositol 1,4,5-trisphosphate biosensor GFP-

131 Our data show that the octose 1,8-bisphosphate intermediate is first converted to octose 1

132 ozymes to hydrolyze phosphatidylinositol 4,5-bisphosphate into the second messengers diacylglycerol a

133 detect inositol phosphate (IP), inositol 4,5-bisphosphate (IP2 ), inositol 1,4,5-trisphosphate (IP3 )

134 els of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolytic activity b

135 binding of ENTH to phosphatidylinositol 4,5-bisphosphate leads to a substantial increase in adhesion

136 ylation of the common substrate ribulose-1,5-bisphosphate leads to photosynthetic carbon assimilation

137 hereby, modulates phosphatidylinositol (4,5)-bisphosphate levels and adhesion.

138 A and protein levels as well as fructose-2,6-bisphosphate levels were increased in aLivGHRkd mice, su

139 117 mumol CO2 m(-2) s(-1)) and ribulose-1:5-bisphosphate limited carboxylation rate (Jmax 213 mumol

140 Upon binding to the phosphatidylinositol 4,5-bisphosphate lipid, the wild-type Merlin adopts a more o

141 a circular array of phosphatidylinositol(4,5)bisphosphate microdomains, and that their constriction w

142 nolayers containing phosphatidylinositol-4,5-bisphosphate, mimicking presence of this phosphoinositid

143 phosphoinositide phosphatidylinositol (4,5)-bisphosphate or altered the subcellular localization of

144 lective SND1 inhibitor 3', 5'-deoxythymidine bisphosphate (pdTp), inhibited tumor formation without e

145 se-phosphate isomerase and sedoheptulose 1,7-bisphosphate phosphatase.

146 not for the homologous phosphatidylinositol bisphosphate phosphatases Inp52/Sjl2 and Inp53/Sjl3.

147 nd their modulation of internal ribulose-1,5-bisphosphate, phosphoglycerate, and Ci pools when grown

148 sicular signaling lipid phosphatidylinositol bisphosphate PI(3,5)P2 modulates TPC2 activity to contro

149 e (PI(3,4,5)P3) and phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2), suggesting that the macropinos

150 Phosphatidylinositol 3,5-bisphosphate (PI(3,5)P(2)), an endosomal signaling lipid

151 binding partner of phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) and demonstrate that their inte

152 The PPI phosphatidylinositol (3,5)-bisphosphate (PI(3,5)P2) is essential in multiple organ

153 the signaling lipid phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2).

154 eta followed by PIP 5-kinase produced PI-4,5-bisphosphate (PI(4,5)P2 or PIP2).

155 PM), where it binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and directs HIV-1 assembly.

156 CAPS binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and SNARE proteins and is propo

157 omote hydrolysis of phosphatidylinositol 4,5 bisphosphate (PI(4,5)P2) by functioning with synaptojani

158 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) has been recognized as an impor

159 hat the signaling lipid phosphoinositide 4,5-bisphosphate (PI(4,5)P2) has opposite effects on the fun

160 The phosphatidylinositol (4,5) bisphosphate (PI(4,5)P2) head binds preferentially to th

161 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is a minor component of total p

162 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is a negatively charged phospho

163 Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) resides predominantly in the pl

164 to the phospholipid phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a marker for the plasma membra

165 he phosphoinositide phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2), and Tec kinase, as well as mem

166 tion of Ca(2+) with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the main lipid marker of the p

167 s of proteins with phosphatidylinositol(4,5)-bisphosphate (PI(4,5)P2), which is highly enriched in th

168 y the tubby domain in a phosphoinositide 4,5-bisphosphate (PI(4,5)P2)-dependent manner, ciliary deliv

169 ted from cells in a phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2)-dependent manner.

170 Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/S

171 biological product, phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2).

172 y dephosphorylates phosphatidylinositide 4,5 bisphosphate (PI(4,5)P2).

173 PI 4,5-bisphosphate (PI[4,5]P2) interacts with and modulates th

174 er, steady-state PM phosphatidylinositol 4,5-bisphosphate (PI[4,5]P2) levels, important for localizat

175 5-trisphosphate and phosphatidylinositol-3,4-bisphosphate [PI(3,4)P2] and consequently recruit plecks

176 domain in Lpd and phosphatidylinositol (3,4)-bisphosphate [PI(3,4)P2] on the bacterial surface and by

177 the signaling lipid phosphatidylinositol-3,5-bisphosphate [PI(3,5)P2] is required in neurons and in O

178 e low abundant PIP, phosphatidylinositol 3,5-bisphosphate [PI(3,5)P2], because mutations in PI(3,5)P2

179 tidic acid (PA) and phosphatidylinositol(3,5)bisphosphate [PI(3,5)P2].

180 logical levels of phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2] and by cholesterol.

181 llular host factors phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and ubiquitin for its activatio

182 kinase C (PKC) and phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] are obligatory for native TRPC1

183 Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] is a minor phospholipid in the

184 osphoinositide phosphatidylinositol (PI) 4,5-bisphosphate [PI(4,5)P2] is a well-known precursor for i

185 Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] is an important cofactor for io

186 Phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] is essential for exocytosis.

187 of plasma membrane phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] leads to a decrease in exocytos

188 EM24 transports the phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] precursor phosphatidylinositol

189 pha to synthesize phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P2] rather than to remove PI5P.

190 lasma membrane (PM) phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] regulates the activity of many

191 gh interaction with phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], but pathophysiologic triggers

192 sitides, especially phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], regulate the activities of man

193 s in the absence of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2].

194 ng lipids including phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2].

195 cidic phospholipid, phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].

196 sma membrane marker phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].

197 phosphoinositide, phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2].

198 specific binding to phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].

199 of FAK initiated by phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].

200 that Mcp5 binds to phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2].

201 adecenoyl)-sn-glycero-3-[phosphoinositol-x,y-bisphosphate] (PI(3,4)P2, PI(3,5)P2, PI(4,5)P2).

202 sed the dynamics of phosphatidylinositol 3,5-bisphosphate (PI3,5P2) and greatly reduced V-ATPase prot

203 at the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) directly stimulates heterologously

204 ated that the lipid phosphatidylinositol 4,5-bisphosphate (PIP2 ) enabled the slow AHP component (sAH

205 f1/Brag2 complex with a phosphatidylinositol bisphosphate (PIP2) -containing lipid bilayer, using coa

206 Phosphatidylinositol 4,5-bisphosphate (PIP2) affects the functions of many target

207 nges in response to phosphatidylinositol-4,5-bisphosphate (PIP2) and cargo binding at multiple sites.

208 ion is dependent on phosphatidylinositol 4,5-bisphosphate (PIP2) and is related to SNARE complex form

209 binding of ezrin to phosphatidylinositol 4,5-bisphosphate (PIP2) and phosphorylation of a conserved t

210 lated with synaptic phosphatidylinositol 4,5-bisphosphate (PIP2) and that alterations in PIP2 at the

211 e interplay between Phosphatidylinositol 4,5-bisphosphate (PIP2) and the F-actin network.

212 Here, we identify phosphatidylinositol 4,5-bisphosphate (PIP2) as a critical regulator of the polar

213 Phosphatidylinositol (PI) 4,5-bisphosphate (PIP2) at the plasma membrane (PM) constitu

214 ed the influence of phosphatidylinositol-4,5-bisphosphate (PIP2) availability on SGN electrophysiolog

215 ivation of ezrin by phosphatidylinositol-4,5-bisphosphate (PIP2) binding and a threonine phosphorylat

216 Phosphoinositol-4,5-bisphosphate (PIP2) can directly or indirectly modify io

217 C2B-SNAP25 and C2B-phosphatidylinositol 4,5-bisphosphate (PIP2) complexes, revealing how Rabphilin-3

218 ells showed an effect of phosphoinositol-4,5-bisphosphate (PIP2) depletion on MET current amplitude a

219 Galphaq activation, phosphatidylinositol 4,5-bisphosphate (PIP2) depletion, and diacylglycerol produc

220 y is potentiated by phosphatidylinositol 4,5-bisphosphate (PIP2) depletion.

221 at the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) directly stimulates NBCe1-A in an ex

222 eceptors signal via phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis.

223 the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) is a potent inhibitory gating modifi

224 Plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2) is required for Ca(2+)-triggered ves

225 and a later fall in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the primary cultured cardi

226 colocalized with a phosphatidylinositol 4,5-bisphosphate (PIP2) marker in pollen tubes.

227 PLCzeta targets its phosphatidylinositol 4,5-bisphosphate (PIP2) membrane substrate.

228 dies that suggested that phosphoinositol-4,5-bisphosphate (PIP2) only induces vinculin homodimers, wh

229 We found that phosphatidylinositol-4,5-bisphosphate (PIP2) or clotrimazole is necessary for cha

230 preferentially with phosphatidylinositol 4,5-bisphosphate (PIP2) through the PH domain.

231 constitutive lipid phosphatidylinositol-4,5-bisphosphate (PIP2) to produce the signaling lipid phosp

232 the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) to propagate diverse intracellular r

233 d, cardiolipin, and phosphatidylinositol 4,5-bisphosphate (PIP2)) PLs containing palmitoyl-oleoyl and

234 e common gating ligand, phosphatidylinositol bisphosphate (PIP2), although these exhibit opposite cou

235 FAs, a DAG metabolite), phosphatidylinositol bisphosphate (PIP2), and H(+) as possible channel activa

236 ete plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2), and these interactions provide a mo

237 anner that requires phosphatidylinositol-4,5-bisphosphate (PIP2), but is otherwise distinct from rece

238 almodulin (CaM) and phosphatidylinositol-4,5-bisphosphate (PIP2), but the role of CaM in channel func

239 Phosphatidylinositol-4,5-bisphosphate (PIP2), one of the key phospholipids, direc

240 by PLC breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2), the mechanism by which the PLC path

241 yo-inositol-derived phosphatidylinositol 4,5-bisphosphate (PIP2), the mechanisms and functional conse

242 mbrane phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2), the source of the Ca(2+)-releasing

243 uence that binds to phosphatidylinositol(4,5)bisphosphate (PIP2), the substrate of PLCbeta1b.

244 MARCKS) and release phosphatidylinositol-4,5-bisphosphate (PIP2), thereby stimulating production of t

245 esis and depends on phosphatidylinositol 4,5-bisphosphate (PIP2), underlies the effects of 2-AG.

246 ence and absence of phosphatidylinositol 4,5-bisphosphate (PIP2), we found that PIP2 increases alpha-

247 tingent on membrane phosphatidylinositol 4,5-bisphosphate (PIP2), which is fundamental for maintainin

248 ugmented in vivo by phosphatidylinositol 4,5-bisphosphate (PIP2), which is generated from myo-inosito

249 cluded by screening phosphatidylinositol 4,5-bisphosphate (PIP2)-negative charges with poly-l-lysine

250 Phosphatidylinositol 4,5-bisphosphate (PIP2)-sensitive transient receptor potenti

251 second messenger phosphatidylinositol (4,5)-bisphosphate (PIP2).

252 mbrane phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2).

253 annels is the lipid phosphatidylinositol 4,5-bisphosphate (PIP2).

254 imilar reduction in phosphatidylinositol 4,5-bisphosphate (PIP2).

255 he regulatory lipid phosphatidylinositol 4,5-bisphosphate (PIP2).

256 -C2gamma produces a phosphatidylinositol-3,4-bisphosphate pool specifically required for delayed and

257 of plasma membrane phosphatidylinositol 4,5-bisphosphate pools but only during strong stimulation of

258 tol 4-phosphate and phosphatidylinositol 4,5-bisphosphate pools.

259 llular clathrin and phosphatidylinositol-3,4-bisphosphate predict the excitability of the plasma memb

260 dges of cells where phosphatidylinositol-3,4-bisphosphate-produced by the dephosphorylation of phosph

261 ucture reveals that phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2) binds to the N terminus of

262 Phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2) helps control various endol

263 Phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2), a master architect of endo

264 ed signalling lipid phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2), whereas other phosphoinosi

265 hate (PtsIns5P) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).

266 calcium-activated, phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) -modulated, non-selective c

267 ,5)P3) 3-kinase and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) 3-kinase activities.

268 serine (PtdSer) and phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) have been implicated in the

269 ral organization of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) landmarks for polarized mem

270 an enzyme producing phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), stabilizes Mig6 expression

271 el interaction with phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-binding protein Amer1/WTX/F

272 otor domain and its phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-binding tail domain.

273 sic lysine patch to phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2).

274 or the synthesis of phosphatidylinositol-3,5-bisphosphate [PtdIns(3,5)P2] and for the regulation of e

275 hate (PtdIns4P) and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] as well as PtdIns4P 5-kinas

276 latory phospholipid phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] is critical for polar tip g

277 ation of photosynthates between ribulose 1,5-bisphosphate regeneration and starch synthesis.

278 mpared in the model, and increasing ribulose bisphosphate regeneration rate will allow for further im

279 but a single lipid (phosphatidylinositol-4,5-bisphosphate) regulates many LPS responses, including en

280 uctive binding of its substrate ribulose-1,5-bisphosphate (RuBP) and other sugar phosphates.

281 that functions to scavenge the ribulose-1,5-bisphosphate (RuBP) by-product of purine/pyrimidine meta

282 g CO2 as sole source of carbon, ribulose-1,5-bisphosphate (RuBP) carboxylase/oxygenase (Rubisco) cata

283 to generate enough ATP to allow ribulose-1,5-bisphosphate (RuBP) regeneration in BS.

284 ue to the accumulation of toxic ribulose-1,5-bisphosphate (RuBP).

285 ly highly organized phosphatidylinositol-4,5-bisphosphate signaling program required for establishmen

286 present here the first structural model of a bisphosphate substrate bound to human phosphomannomutase

287 doheptulose) and six-carbon (fructose) sugar bisphosphate substrates.

288 chain is composed of two domains, requires a bisphosphate sugar (either mannose or glucose) as activa

289 r RNA decapping and phosphatidylinositol 3,5-bisphosphate synthesis were also identified as targets o

290 yme responsible for phosphatidylinositol 4,5-bisphosphate synthesis, is modified by small ubiquitin-l

291 tidylserine, and/or phosphatidylinositol-4,5-bisphosphate, thus providing a mechanistic model for the

292 neogenesis is the conversion of fructose 1,6-bisphosphate to fructose 6-phosphate by a fructose bisph

293 isoforms hydrolyze phosphatidylinositol 4,5-bisphosphate to the second messengers inositol 1,4,5-tri

294 presence of 2.5 mum phosphatidylinositol 4,5-bisphosphate, TRPV1 channels demonstrated rapid activati

295 replace radioactive phosphatidylinositol 4,5-bisphosphate used in conventional PLC assays and will en

296 membrane-localized phosphatidylinositol-4,5-bisphosphate using the pleckstrin-homology domain (PHD)

297 hyl)-propane-1,3-diyltetrakis(2-chloroethyl) bisphosphate (V6)).

298 he regulatory lipid phosphatidylinositol 4,5-bisphosphate was enriched at sites of cell wall invagina

299 nts, the levels of PtdIns monophosphates and bisphosphates were changed, with opposite effects on the

300 glucose led to accumulation of fructose-1,6-bisphosphate, which has been associated with toxicity in