ライフサイエンスコーパス: bisphosphate

1 enates rather than carboxylates ribulose-1,5-bisphosphate.

2 oteins that deplete phosphatidylinositol 4,5-bisphosphate.

3 the PFK-1 allosteric activator fructose 2,6-bisphosphate.

4 omology domain with phosphatidylinositol 4,5-bisphosphate.

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

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

7 sphatidylserine and phosphatidylinositol 4,5-bisphosphate.

8 hannel activated by phosphatidylinositol 3,5-bisphosphate.

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

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

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

12 phates, including its substrate ribulose 1,5-bisphosphate.

13 the signaling lipid phosphatidylinositol-4,5-bisphosphate.

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

15 to glucose 6-phosphate via beta-glucose 1,6-bisphosphate.

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

17 ast in part through phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) activation and linked to an

18 ysiological signal, phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) activity, indeed regulates

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

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

21 ein kinase B (pAkt), or phosphoinositide-4,5-bisphosphate 3-kinase (pPI3K).

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

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

24 ic mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic (PIK3CA) subunit are mor

25 nse mutation in the Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Alpha (PIK3CA) g

26 replicated PIK3CD (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta) sites wer

27 Pik3cg, encoding phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (Pi3kgamma

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

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

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

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

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

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

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

35 ro-glycolytic enzyme that forms fructose-2,6-bisphosphate, a powerful allosteric activator of 6-phosp

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

37 targets were the glycolytic enzymes fructose bisphosphate aldolase (FBPA) and glyceraldehyde-3-phosph

38 ied candidate biomarkers (myosin-9, fructose-bisphosphate aldolase and plectin).

39 Loss of hepatic fructose-1, 6-bisphosphate aldolase B (Aldob) leads to a paradoxical u

40 phosphate (S7P) to SBP, after which fructose-bisphosphate aldolase cleaves SBP into dihydroxyacetone

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

42 the naturally occurring enzyme fructose 1,6 bisphosphate aldolase.

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

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

45 mitoyl-sn-glycero-3-phosphatidylinositol-4,5-bisphosphate and Atto488-1,2-dipalmitoyl-sn-glycero-3-ph

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

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

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

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

50 c binding of SVB to phosphatidylinositol 3,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphat

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

52 substrates, bicarbonate, CO(2) and ribulose bisphosphate and the product 3-phosphoglycerate associat

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

54 te and its product phosphatidylinositol 3, 5-bisphosphate, and a WIPI-binding protein, ATG2A, but do

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

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

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

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

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

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

61 with GTP-bound RAP1 and phosphoinositol 4,5 bisphosphate but this interaction is inhibited by the N-

62 The oxygenation of ribulose 1,5-bisphosphate by Rubisco is the first step in photorespir

63 the cbbL genes (67%-82%) coding the ribulose-bisphosphate carboxylase large chain in the Calvin cycle

64 arboxysomes are BMCs containing ribulose-1,5-bisphosphate carboxylase oxygenase and carbonic anhydras

65 (LHCA1, LHCB1, and LHCB4), the ribulose 1.5-bisphosphate carboxylase subunits (rbcL and RbcS), and e

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

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

68 ize toxic glycolate formed when ribulose-1,5-bisphosphate carboxylase-oxygenase oxygenates rather tha

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

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

71 Ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) activase (R

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

73 tosynthetic CO(2) fixing enzyme ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco) forms dead-

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

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

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

77 Ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco) is the corn

78 Ribulose 1,5-bisphosphate carboxylase/oxygenase (RuBisCO) is the most

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

80 uester the CO(2)-fixing enzymes ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) to enhance

81 ymes, and immunolocalization of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) to show tha

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

83 ate, phosphate dikinase (PPDK), ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO), and phosph

84 The key enzyme of the CBB cycle, ribulose-bisphosphate carboxylase/oxygenase (RubisCO), is a main

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

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

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

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

89 ation relies on the function of ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco).

90 raising the CO(2) concentration for Ribulose bisphosphate carboxylase/oxygenase (Rubisco).

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

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

93 Rubisco (d-ribulose 1,5-bisphosphate carboxylase/oxygenase) is responsible for t

94 he CO(2)-fixing enzyme Rubisco (ribulose 1,5-bisphosphate carboxylase/oxygenase) to release tightly b

95 e carbon-fixing enzyme Rubisco (ribulose-1,5-bisphosphate carboxylase/oxygenase), a major component o

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

97 and O(2) at the active site of ribulose-1,5-bisphosphate carboxylase/oxygenase.

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

99 urthermore, we report the INPP1/inositol 1,4-bisphosphate complex which illuminates key features of t

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

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

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

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

106 nzyme that produces phosphatidylinositol 4,5-bisphosphate, directly interacts with Rab7a and plays cr

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

108 membrane containing phosphatidylinositol 4,5 bisphosphate, even if phosphatidylserine (PS) is present

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

110 We show that the PKM2 activator fructose 1,6-bisphosphate (FBP) alone promotes tetramerisation and in

111 tructural reorganization of the fructose 1,6-bisphosphate (FBP), an allosteric activator, binding sit

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

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

114 tor alanine (Ala) and activator fructose-1,6-bisphosphate (Fru-1,6-BP) in human liver pyruvate kinase

115 on, and 3) prevented binding of fructose-1,6-bisphosphate (Fru-1,6-BP).

116 phosphorylating agents, such as fructose 1,6-bisphosphate, generate phosphorylated forms of both conf

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

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

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

120 Here we show that diverse meso-bisphosphates in combination with alkylzirconium nucleop

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

122 odulator of channel-phosphatidylinositol 4,5-bisphosphate interactions.

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

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

125 s are activated and phosphatidylinositol-4,5-bisphosphate is concentrated.

126 al phosphoinositide phosphatidylinositol-3,5-bisphosphate, is an essential regulator of lysosomal bio

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

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

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

130 find clustering of phosphatidylinositol 4,5-bisphosphate-like lipids that induce a directional membr

131 When we include phosphatidylinositol 4,5-bisphosphate-like lipids that preferentially interact wi

132 117 mumol CO2 m(-2) s(-1)) and ribulose-1:5-bisphosphate limited carboxylation rate (Jmax 213 mumol

133 aining PS even if a phosphatidylinositol 4,5 bisphosphate membrane is presented in trans.

134 of plasma membrane phosphatidylinositol 4,5-bisphosphate microdomains at nascent sheaths, followed b

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

136 ition, we observe a phosphatidylinositol-4,5-bisphosphate molecule forming a bridge between the membr

137 ntamer contains two phosphatidylinositol-4,5-bisphosphate molecules, the head groups of which occupy

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

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

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

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

142 to accumulation of phosphatidylinositol 4,5-bisphosphate PI(4,5)P2 in endolysosomes, driving local h

143 The membrane lipid phosphatidylinositol-3,4-bisphosphate (PI(3,4)P(2)) is an important signaling eff

144 lipid messenger, phosphatidylinositol (3,4)-bisphosphate (PI(3,4)P(2)), are not well understood.

145 e (PI(4,5)P(2)) and phosphatidylinositol 3,4-bisphosphate (PI(3,4)P(2)).

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

147 this, the effect of phosphatidylinositol 3,5-bisphosphate (PI(3,5)P(2)) on vacuole fusion remains unk

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

149 al signaling lipid, phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2), is required for full assembly

150 teins interact with phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) and are either activated or i

151 oinositides (PIPs), phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) and phosphatidylinositol 3,4-

152 ) channel-dependent phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) compartmentalization governs

153 ther explaining how phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) influences ENaC activity and,

154 Since phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) maintains TRPC4 and TRPC5 cha

155 ase Cbeta (PLCbeta)/phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) signaling pathway.

156 RTKs can hydrolyze phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) within the nucleus, leading t

157 phosphates, such as phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)), are enriched at the cell sur

158 trix (MA) domain to phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)).

159 oluble analogs of phosphatidylinositol (4,5)-bisphosphate (PI(4,5)P(2)).

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

161 generated elevated phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and reduced phosphatidylinosito

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

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

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

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

166 e C (PLC)s degrade phosphatidylinositol-4, 5-bisphosphate (PI(4,5)P2) lipids and regulate multiple ce

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

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

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

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

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

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

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

174 Phosphatidylinositol-4,5-bisphosphate (PI-4,5-P(2) ) is critical for synaptic ves

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

176 5-trisphosphate and phosphatidylinositol-3,4-bisphosphate [PI(3,4)P2] and consequently recruit plecks

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

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

179 mbrane phospholipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2) or PIP(2)] for activity.

180 robust decrease in phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)] levels, which is a major cont

181 the synthesis of phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P(2)], a key regulator of dynamic e

182 o the hydrolysis of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].

183 and membrane lipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].

184 +) and modulated by phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)].

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

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

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

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

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

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

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

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

193 R) interacts with phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2], a PM-specific acidic lipid.

194 by its binding to phosphatidylinositol-(4,5)-bisphosphate [PI(4,5)P2], and MA binding to cellular RNA

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

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

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

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

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

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

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

202 through hydrolysing phosphatidylinositol 4,5-bisphosphate (PIP(2) ) to produce the initial proton sig

203 odally regulated by phosphatidylinositol 4,5-bisphosphate (PIP(2) ), the substrate hydrolysed by PLC,

204 channel opening by phosphatidylinositol 4,5-bisphosphate (PIP(2) ).

205 channel opening by phosphatidylinositol 4,5-bisphosphate (PIP(2) ).

206 membrane lipids: Phosphatidylinositol (4, 5)-bisphosphate (PIP(2)) activates the channel; a secondary

207 lasma membrane, such as phosphatidylinositol-bisphosphate (PIP(2)) and phosphatidylserine (PS).

208 ng carboxy-terminal phosphatidylinositol 4,5-bisphosphate (PIP(2)) binding domains, or the entire C t

209 Phosphatidylinositol 4,5-bisphosphate (PIP(2)) has a significantly lower mobile f

210 identify a unique phosphatidylinositol (4,5)-bisphosphate (PIP(2)) interaction profile near intracell

211 that is promoted by phosphatidylinositol 4,5-bisphosphate (PIP(2)) is also phosphorylation-dependent,

212 that cannot bind to phosphatidylinositol 4,5-bisphosphate (PIP(2)) or that constitutively adopt a clo

213 mbrane phospholipid phosphatidylinositol 4,5-bisphosphate (PIP(2)) regulates the activity of diverse

214 Here we show that phosphatidylinositol (4,5)-bisphosphate (PIP(2)) regulates TMEM16A channel activati

215 h direct binding of phosphatidylinositol 4,5-bisphosphate (PIP(2)) stabilized the oligomers, the stab

216 ptors both consumes phosphatidylinositol 4,5-bisphosphate (PIP(2)) via phosphalipase Cbeta hydrolysis

217 s liposomes lacking phosphatidylinositol-4,5-bisphosphate (PIP(2)) with greater Ca(2+) sensitivity th

218 ation by increasing phosphatidylinositol 4,5-bisphosphate (PIP(2)), and our molecular dynamics simula

219 asma membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP(2)), but it is unclear whether PIP(2)

220 and membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP(2)), but lack of structural informatio

221 he phospholipid, phosphatidylinositol (4, 5)-bisphosphate (PIP(2)), directly interacts with the DAT N

222 e phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP(2)), has long been established as a ma

223 anes, in particular phosphatidylinositol 4,5-bisphosphate (PIP(2)), initially suggested they act as c

224 annels regulated by phosphatidylinositol 4,5-bisphosphate (PIP(2)).

225 with affinity for phosphatidylinositol-(4,5)-bisphosphate (PIP(2)).

226 and is modulated by phosphatidylinositol 4,5-bisphosphate (PIP(2)).

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

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

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

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

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

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

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

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

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

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

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

238 The lipid phosphatidylinositol 4,5-bisphosphate (PIP2) forms nanoscopic clusters in cell pl

239 d redistribution of phosphatidylinositol 4,5-bisphosphate (PIP2) from the plasma membrane to actin ri

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

241 Phosphatidylinositol-4,5-bisphosphate (PIP2) is an important signaling lipid in e

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

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

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

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

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

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

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

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

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

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

252 itides, including phosphatidylinositol-(4,5)-bisphosphate (PIP2), resulting in VEGF-exacerbated defec

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

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

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

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

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

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

259 sts, we noticed the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding protein, myristoylated alani

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

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

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

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

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

265 es identified are metabolism of fructose-1,6-bisphosphate, production of glycerol-3-phosphate and com

266 mechanism whereby the levels of fructose 2,6-bisphosphate promote mitochondrial PDK4 levels and ident

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

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

269 A)) and its product phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).

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

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

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

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

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

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

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

277 ificity for binding phosphatidylinositol-4,5-bisphosphate (PtdIns4,5P2).

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

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

283 addition of CO(2) onto enolized ribulose 1,5-bisphosphate (RuBP), producing 3-phosphoglycerate which

284 ng inhibitory molecules such as ribulose-1,5-bisphosphate (RuBP).

285 TP to produce the Rubisco substrate ribulose bisphosphate (RuBP).

286 tic clostridia rely on the sedoheptulose 1,7-bisphosphate (SBP) pathway, using pyrophosphate-dependen

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

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

289 pathways, including phosphatidylinositol-3,5-bisphosphate synthesis and retrograde transport from the

290 ally interacts with phosphatidylinositol 4,5-bisphosphate to stabilize MA orientation.

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

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

293 In addition, C(2)-symmetric chiral bisphosphates undergo stereospecific reactions and a rac

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

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

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

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

298 Pfk2 catalyzes the synthesis of fructose-2,6-bisphosphate, which acts as a potent allosteric activato

299 res inhibition by the regulator fructose 1,6-bisphosphate, which senses the upper-glycolytic flux and

300 , the reaction intermediate beta-glucose 1,6-bisphosphate, whose concentration depends on the beta-gl