ライフサイエンスコーパス: phosphoinositol

1 and to have a high-affinity binding site for phosphoinositols.

2 uced Akt activity was partially dependent on phosphoinositol 3' kinase (PI 3'K) since a PI 3'K inhibi

3 ferase fusion proteins of the p85 subunit of phosphoinositol 3'-kinase, Grb2, and Syp, paralleling re

4 naling proteins including the p85 subunit of phosphoinositol 3'-kinase, phospholipase Cgamma, and Ras

5 effectors, including phospholipase C-gamma, phosphoinositol 3'-kinase, RAS, and signal transducer an

6 phosphatase that catalyzes the conversion of phosphoinositol 3,4,5-triphosphate to phosphoinositol 4,

7 o the phosphatidylinositol 3-kinase products phosphoinositol 3,4,5-trisphosphate and phosphoinositol

8 ucts phosphoinositol 3,4,5-trisphosphate and phosphoinositol 3,4-bisphosphate.

9 required for focal adhesion kinase-dependent phosphoinositol 3-hydroxykinase activation and cellular

10 ty is dependent on beta(1) integrin-mediated phosphoinositol 3-hydroxykinase stimulation and the leve

11 We have now found that phosphoinositol 3-kinase (PI 3-K) activity is significan

12 DNA-dependent protein kinase (DNA-PK), has a phosphoinositol 3-kinase (PI 3-K) domain close to its C-

13 hypothesized that NPM-ALK signaling through phosphoinositol 3-kinase (PI 3-kinase) and AKT would reg

14 signaling cascades, including the Jak-STAT, phosphoinositol 3-kinase (PI 3-kinase), and mitogen-acti

15 Activation of VEGF receptors (VEGFRs), phosphoinositol 3-kinase (PI-3K) or Rac1 was measured in

16 mitogen-activated protein kinase (MAPK) and phosphoinositol 3-kinase (PI-3K), leading to both prolif

17 activates focal adhesion kinase (FAK), Src, phosphoinositol 3-kinase (PI3-K), c-Cbl, and RhoA GTPase

18 Insulin-like growth factor 1 (IGF1) and phosphoinositol 3-kinase (PI3K) acted upstream of Akt wh

19 rophic response was equivalently attenuated, phosphoinositol 3-kinase (PI3K) activation was blunted,

20 Investigations of phosphoinositol 3-kinase (PI3K) and its downstream effec

21 Phosphoinositol 3-kinase (PI3K) is important in GPIb-IX-

22 ternal, but not internal, application of the phosphoinositol 3-kinase (PI3K) or Janus kinase 2 (Jak2)

23 lipid phosphatase that, by antagonizing the phosphoinositol 3-kinase (PI3K) pathway, also inhibits f

24 istance has been linked to activation of the phosphoinositol 3-kinase (PI3K) pathway.

25 in containing transforming protein (Shc) and phosphoinositol 3-kinase (PI3K) phosphorylation levels i

26 monstrate that the TPO-induced activation of phosphoinositol 3-kinase (PI3K), a signaling intermediat

27 phosphatase SHP-2, the subsequent binding of phosphoinositol 3-kinase (PI3K), and diminished PI3K sig

28 upon B cell receptor (BCR) crosslinking in a phosphoinositol 3-kinase (PI3K)-dependent manner; howeve

29 signaling networks involving Raf-ERK1/2 and phosphoinositol 3-kinase (PI3K)-mechanistic target of ra

30 ming the placental phenotype of mice lacking phosphoinositol 3-kinase (PI3K)-p110alpha.

31 Finally, we found that phosphoinositol 3-kinase activation synergistically enha

32 ation of either GT1b or GD3 content affected phosphoinositol 3-kinase activation, and inhibition of t

33 ups had reduced levels of insulin-stimulated phosphoinositol 3-kinase and Akt kinase activities and r

34 ors promote myoblast differentiation through phosphoinositol 3-kinase and Akt signaling.

35 Integrin activation is mediated by phosphoinositol 3-kinase and is followed by an increase

36 owth factor-beta(1) nor by inhibition of the phosphoinositol 3-kinase and MAP kinase pathways.

37 orter protein, metabolic signaling pathways (phosphoinositol 3-kinase and mitogen-activated protein k

38 was sensitive to pharmacologic inhibition of phosphoinositol 3-kinase and protein kinase C, but adhes

39 for mitogen-activated protein kinase 1/2 and phosphoinositol 3-kinase but not the IL-33 signaling moi

40 ew of the fact that the signaling pathway of phosphoinositol 3-kinase controls microfilament rearrang

41 e, calcineurin A, nitric-oxide synthase, and phosphoinositol 3-kinase had no effect.

42 codynamic biomarkers for both proteasome and phosphoinositol 3-kinase inhibition were used.

43 ement by a pathway that was sensitive to the phosphoinositol 3-kinase inhibitor wortmannin and to the

44 In contrast, phosphoinositol 3-kinase inhibitor wortmannin, or extrac

45 ster (an inhibitor of NOS) and wortmannin (a phosphoinositol 3-kinase inhibitor).

46 , and ganglioside depletion, suggesting that phosphoinositol 3-kinase is an intermediate in both the

47 In U1A-derived cells, the p85/p110 phosphoinositol 3-kinase isoform was associated with IFN

48 of Rac1, phosphorylated Akt as a readout for phosphoinositol 3-kinase signaling, and VEGFR2 activatio

49 ll spreading through alpha(5)beta(1)/FAK and phosphoinositol 3-kinase signaling, whereas GD3-modulate

50 ntiation and a new pathway from CB1R through phosphoinositol 3-kinase to the transcription factor pai

51 re significantly reduced the levels of total phosphoinositol 3-kinase, Akt kinase, phospho-BAD (inact

52 kinases, phospholipase C, calcium elevation, phosphoinositol 3-kinase, and multiple amplification mec

53 EBV-negative BLs exhibit activation of phosphoinositol 3-kinase, but do not have elevated level

54 PI3Kgamma, a G-protein-coupled type 1B phosphoinositol 3-kinase, exhibits a basal glucose-indep

55 ular signal-regulated kinase, p38 kinase, or phosphoinositol 3-kinase, Janus kinase 3 (JAK3) inhibiti

56 sformed immune cells results from effects of phosphoinositol 3-kinase-Akt-mechanistic target of rapam

57 s, is independent of PKA, and results in the phosphoinositol 3-kinase-dependent activation of AKT.

58 cells from DNA-damaging agents by activating phosphoinositol 3-kinase-dependent and Akt-dependent ant

59 xpressing myeloid progenitor cells induced a phosphoinositol 3-kinase-dependent increase in beta-cate

60 s GD3-modulated spreading appears to involve phosphoinositol 3-kinase-dependent protein kinase C sign

61 Wortmannin, which blocks phosphoinositol 3-kinase-dependent signaling, has little

62 udy correlates with the intricate pathway of phosphoinositol 3-kinase-mediated nuclear translocation

63 dent and is mediated by protein kinase C and phosphoinositol 3-kinase.

64 anner similar to its interaction with p85 of phosphoinositol 3-kinase.

65 ot to LTD(4), was resistant to inhibitors of phosphoinositol 3-kinase.

66 Insulin-like growth factor 1 activated the phosphoinositol 3-kinase/Akt and forkhead box O1 pathway

67 atheroprotective flow activates Nrf2 via the phosphoinositol 3-kinase/Akt pathway, and this activatio

68 ed protein kinase pathways and antiapoptotic phosphoinositol 3-kinase/AKT pathways were examined in c

69 ced survival signaling via activation of the phosphoinositol 3-kinase/AKT signaling pathway.

70 homeostasis are primarily the result of the phosphoinositol 3-kinase/Akt-dependent activation of Nrf

71 , Ras/extracellular signal-regulated kinase, phosphoinositol 3-kinase/mammalian target of rapamycin (

72 Phosphoinositol 3-kinases (PI3Ks) gamma and delta are ke

73 lized via caveolae required microtubules and phosphoinositol 3-kinases and was inhibited in cells exp

74 We show that a C-terminal phosphoinositol 3-phosphate (PI3P)-binding domain, also

75 hoinositol(3,4,5)P3, phosphoinositol(3,5)P2, phosphoinositol(3,4)P2 and several other phosphoinositid

76 ospholipids, including phosphatidic acid and phosphoinositol(3,4,5)P3, phosphoinositol(3,5)P2, phosph

77 sphatidic acid and phosphoinositol(3,4,5)P3, phosphoinositol(3,5)P2, phosphoinositol(3,4)P2 and sever

78 ss-of-function mutations in FIG4, encoding a phosphoinositol(3,5)P2-phosphatase.

79 molog (PTEN) loss or activating mutations of phosphoinositol-3 (PI3) kinase (PIK3CA) may be associate

80 and activator of transcription-3 (STAT3) and phosphoinositol-3 kinase (PI 3-kinase).

81 ivation of alpha(IIb)beta(3) integrin, or on phosphoinositol-3 kinase (PI3K) activity.

82 the mitogen-activated protein kinase (MAPK), phosphoinositol-3 kinase (PI3K) and phospholipase C gamm

83 activation is dependent upon the activity of phosphoinositol-3 kinase (PI3K) and that transient but n

84 The phosphoinositol-3 kinase (PI3K) inhibitor LY294002 also

85 The phosphoinositol-3 kinase (PI3K) pathway is frequently dy

86 The prosurvival signaling molecule, phosphoinositol-3 kinase (PI3K), has previously been lin

87 and tensin homolog) and the activity of the phosphoinositol-3 kinase (PI3K)-AKT signaling pathway in

88 It is known that radiation activates the phosphoinositol-3 kinase (PI3K)/Akt pathway and that inh

89 re activated by the binding of BDNF to TrkB: phosphoinositol-3 kinase (PI3K); Ras-MEK and phospholipa

90 rylation of phospholipase Cgamma (PLCgamma), phosphoinositol-3 kinase and SHC.

91 effectors, including c-Raf-1, A-Raf, B-Raf, phosphoinositol-3 kinase delta, RalGDS, and Rin1.

92 nsistent with this hypothesis, the selective phosphoinositol-3 kinase inhibitor LY294002 blocked the

93 reatment of lung tumor-bearing mice with the phosphoinositol-3 kinase inhibitor LY294002 induced a ra

94 , two ERK kinase MAP inhibitors, whereas the phosphoinositol-3 kinase inhibitors wortmannin and 2-(4-

95 uding the Sprouty-related protein SPRED1 and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2/p8

96 Axl activation activates downstream phosphoinositol-3 kinase signaling, and Axl knockdown by

97 ignaling, and Axl knockdown by siRNA impairs phosphoinositol-3 kinase signaling.

98 ding Janus family tyrosine protein kinase 2, phosphoinositol-3 kinase, and mitogen-activated protein

99 as mitogen-activated protein kinase (MAPK), phosphoinositol-3 kinase, and RhoA have also been shown

100 ifested primarily in excessive EGF-dependent phosphoinositol-3 kinase/Akt activity.

101 and the subsequent activation through src of phosphoinositol-3 kinase/Akt and ras/mitogen-activated p

102 sed AKT phosphorylation, suggesting that the phosphoinositol-3 kinase/AKT pathway mediated the surviv

103 kinase A/CREB signaling module and p110beta phosphoinositol-3' kinase, establishing a novel signal t

104 and PI-828 and by antibodies raised against phosphoinositol-3,4,5-trisphosphate (PIP(3)), the produc

105 rotein kinase kinase (MAPKK) pathway and the phosphoinositol-3-kinase (PI-3-K) pathway.

106 hannel activity was selectively inhibited by phosphoinositol-3-kinase (PI-3-kinase) inhibitors wortma

107 gulate FLIP in a manner that is dependent on phosphoinositol-3-kinase (PI3K) and Akt signaling.

108 r of which is believed to be mediated by the phosphoinositol-3-kinase (PI3K) and Akt/PKB pro-apoptoti

109 eted p85alpha, the regulatory subunit of the phosphoinositol-3-kinase (PI3K) heterodimer, causing p85

110 to wild-type ES cells and that inhibition of phosphoinositol-3-kinase (PI3K) in HEK293 cells elicits

111 inase (MAPK) pathway signaling and increased phosphoinositol-3-kinase (PI3K) pathway signaling in iso

112 mitogen-activated protein kinase (MAPK) and phosphoinositol-3-kinase (PI3K) pathways.

113 by phosphatase and tension homolog (PTEN) - phosphoinositol-3-kinase (PI3K) signaling involving PTEN

114 atase and tumor suppressor PTEN inhibits the phosphoinositol-3-kinase (PI3K) signaling pathway and pl

115 rapamycin (mTOR) is an important mediator of phosphoinositol-3-kinase (PI3K) signaling.

116 regulatory subunit of class IA lipid kinase phosphoinositol-3-kinase (PI3K), but not of p85 beta, or

117 ents it from interacting with and activating phosphoinositol-3-kinase (PI3K), which is required to st

118 eleted On Chromosome 10 (PTEN) regulates the phosphoinositol-3-kinase (PI3K)-AKT signaling pathway.

119 l hypothalamus via the intracellular enzyme, phosphoinositol-3-kinase (PI3K).

120 Phosphoinositol-3-kinase (PI3K)/protein kinase B (AKT) a

121 nding to collagen VII, which in turn, led to phosphoinositol-3-kinase activation and protection from

122 Inhibition of phosphoinositol-3-kinase activity by wortmannin induced

123 is via its lipid phosphatase activity in the phosphoinositol-3-kinase and AKT pathway as well as inhi

124 hat there is an Akt-independent link between phosphoinositol-3-kinase and glycogen synthase kinase3 a

125 m may influence signaling pathways including phosphoinositol-3-kinase and mitogen-activated protein k

126 t failed to affect phosphorylation of Akt by phosphoinositol-3-kinase induced by either TLR2- or TLR4

127 a telangiectasia and Rad3-related (ATR) is a phosphoinositol-3-kinase like kinase (PIKK) that initiat

128 Pharmacological inhibition of phosphoinositol-3-kinase or mTOR in PTEN(-/-) cells rest

129 Phosphoinositol-3-kinase signaling pathway was analyzed

130 owed growth and invasion in vitro, inhibited phosphoinositol-3-kinase signaling, and inhibited melano

131 Overexpression of constitutively active p110 phosphoinositol-3-kinase subunit was sufficient to resto

132 Inhibition of the phosphoinositol-3-kinase-AKT-mTOR pathway mitigates the

133 did not interact with survival signaling of phosphoinositol-3-kinase.

134 including phospholipase C gamma 1, SHP2, and phosphoinositol-3-kinase.

135 ty phosphatase that negatively regulates the phosphoinositol-3-kinase/Akt pathway and mediates cell-c

136 ressor is a phosphatase that antagonizes the phosphoinositol-3-kinase/AKT signaling pathway and suppr

137 wing to DNA damage, by a mechanism involving phosphoinositol-3-kinase/c-Akt signaling.

138 ary enamine attached to the C20 that inhibit phosphoinositol-3-OH kinase (PI3K) by producing wortmann

139 le of RIAM interacts with GTP-bound RAP1 and phosphoinositol 4,5 bisphosphate but this interaction is

140 The PH domain bound phosphoinositol 4,5-bisphosphate (PI(4,5)P(2)) and was r

141 M8 activity is sensitive to the phospholipid phosphoinositol 4,5-bisphosphate (PIP2), a substrate for

142 ion of phosphoinositol 3,4,5-triphosphate to phosphoinositol 4,5-bisphosphate and thereby inhibits PI

143 Vt can bind F-Actin and phosphoinositol 4,5-bisphosphate, and association with t

144 liposomes composed of phosphatidylserine and phosphoinositol 4,5-bisphosphate, with moderate affinity

145 lserine-binding protein) and PLCdelta1-PH (a phosphoinositol 4,5-bisphosphate-binding protein) in mic

146 Reversal of the modulation was blocked by a phosphoinositol 4-kinase inhibitor, indicating a require

147 he HCV replication complex with its product, phosphoinositol 4-phosphate (PI4P).

148 tudies link synaptojanin 1 (synj1), the main phosphoinositol (4,5)-biphosphate phosphatase (PI(4,5)P2

149 her directly or indirectly, neither LIS1 nor phosphoinositol-4 kinase (PI4K) were detected in any of

150 TRPC1 channel activity was inhibited by anti-phosphoinositol-4,5-bisphosphate (PIP(2)) antibodies and

151 In addition, the phosphoinositol-4,5-bisphosphate (PIP(2)) binding protei

152 are tightly regulated by the membrane lipid phosphoinositol-4,5-bisphosphate (PIP(2)).

153 nositol-4-phosphate-5-kinase (PIP5K) to form phosphoinositol-4,5-bisphosphate (PIP2) at the phagocyti

154 Phosphoinositol-4,5-bisphosphate (PIP2) can directly or

155 k on bullfrog hair cells showed an effect of phosphoinositol-4,5-bisphosphate (PIP2) depletion on MET

156 Contrary to studies that suggested that phosphoinositol-4,5-bisphosphate (PIP2) only induces vin

157 t requires active (high-affinity) integrins, phosphoinositol-4,5-bisphosphate (PIP2), talin, and immo

158 c1-dependent pathway involves recruitment of phosphoinositol-4-phosphate-5-kinase (PIP5K) to form pho

159 nin, and overexpression of nla regulates the phosphoinositol 5' phosphatase activity of synaptojanin.

160 Ig domain bound to the membrane by a glycan phosphoinositol anchor was unable to induce actin polyme

161 lated negatively by Ca(2+) and positively by phosphoinositol and cholesterol lipids.

162 des-derived sphingolipids including ceramide phosphoinositol and deoxy-sphingolipids.

163 ingle catalytic domain possessing both lipid phosphoinositol and protein phosphatase activities.

164 For discrimination between anionic (phosphoinositol) and zwitterionic (phosphocholine, phosp

165 Phosphoinositols are an important class of phospholipids

166 The results reinforce the notion that phosphoinositols are important second messengers in cold

167 protein E4 (ApoE4)-specific changes in brain phosphoinositol biphosphate (PIP(2)) homeostasis to the

168 We have found that the levels of phosphoinositol biphosphate (PIP2) are reduced in postmo

169 er exposure to repetitive blast-induced TBI, phosphoinositol biphosphate (PIP2) levels in hippocampal

170 onversely, channel opening is potentiated by phosphoinositol bisphosphate (PIP(2)), which binds to Ki

171 PLA2beta on chromosome 15 in a region near a phosphoinositol bisphosphate phosphatase.

172 osis or with phosphoinositol caps (producing phosphoinositol-capped LAM [PILAM]) in Mycobacterium sme

173 ped LAM [ManLAM]) in M. tuberculosis or with phosphoinositol caps (producing phosphoinositol-capped L

174 zeta is mediated through a pathway involving phosphoinositol-dependent kinase-1 (PDK1).

175 om myo-inositol-phosphate (MIP) synthesis to phosphoinositol dihydroceramide, determined the crystal

176 hogen-recognition receptors for the ceramide phosphoinositol glycan core (CPI-GC) of the dominant sur

177 y may serve as a source of hormone-sensitive phosphoinositol glycans.

178 gamma R linked to the membrane via a glycan phosphoinositol (GPI) anchor.

179 rical relationship in the recognition of the phosphoinositol head group at the binding motif.

180 in, thereby maintaining the integrity of the phosphoinositol head group essential for selective recog

181 result from the addition of a PtdIns-derived phosphoinositol head group to ceramides through Aur1p.

182 he presented antigen, selecting for both the phosphoinositol headgroup and glycerol neck region via a

183 igh affinity (IC50 = 36 pM) and potency in a phosphoinositol hydrolysis assay (IC50 = 0.714 pM) for m

184 also a potent inhibitor (IC(50)=0.16 nM) of phosphoinositol hydrolysis stimulated by ET-1, and it an

185 amma (PLC-gamma) activation, PDGF-BB induced phosphoinositol hydrolysis was completely abolished in t

186 the less active 1R,3S-t-ACPD failed to alter phosphoinositol hydrolysis.

187 ited in these organisms at the step in which phosphoinositol is transferred to ceramide, resulting in

188 beta treatment stimulated IFNAR-1-associated phosphoinositol kinase activity equally in either U1.wt

189 of the mitogen-activated protein kinase and phosphoinositol kinase pathways.

190 Inhibiting the PIKfyve phosphoinositol kinase reduced alpha-syn aggregation and

191 he protein kinase A (PKA), protein kinase C, phosphoinositol kinase, or p38 MAPK pathways.

192 panel of 21 serine/threonine, tyrosine, and phosphoinositol kinases, in addition to the conventional

193 enotypic screening converge to implicate the phosphoinositol kinases, receptor tyrosine kinases, MAP

194 the transmembrane FcgammaRII and the glycan phosphoinositol-linked FcgammaRIIIB.

195 nase Btk with the membrane through PH domain-phosphoinositol lipid interactions.

196 tdIns(3,4,5)P3 or a similar 3-phosphorylated phosphoinositol lipid, resulting in actin filament disru

197 ss depends upon Gi-mediated production of 3'-phosphoinositol lipids (PI3Ps), the activated form of Ra

198 rast, the mutant (K679,687N), unable to bind phosphoinositol lipids, translocates to the cytoplasm.

199 PI3Ks), which transduce signals via membrane phosphoinositol lipids.

200 erine, the C2B domain interacts with several phosphoinositol lipids.

201 e the first genetic evidence indicating that phosphoinositols mediate ABA and stress signal transduct

202 rf6, a process that initiates alterations in phosphoinositol metabolism critical for a lineage-specif

203 oplasmic reticulum-to-Golgi vesicle traffic, phosphoinositol metabolism, AMPylation, deAMPylation, pr

204 7), and 1-oleoyl-2-arachidonoyl-sn-glycero-3-phosphoinositol (OR = 0.77; 95% CI = 0.66-0.90) were inv

205 studies revealed that PIN clusters depend on phosphoinositol pathways, cytoskeletal structures and sp

206 The lipid phosphoinositol phosphatase activity is essential for PT

207 coordinates CME and ADBE by controlling the phosphoinositol phosphatase activity of synaptojanin (Sy

208 tional domain analyses reveal that Synj's 5'-phosphoinositol phosphatase activity suppresses ADBE, wh

209 ved from yeast to humans, which contains two phosphoinositol phosphatase domains and a proline-rich d

210 The 5'-phosphoinositol phosphatase SHIP negatively regulates si

211 APOE4-VLDL reduces PI(3,4,5)P3, through the phosphoinositol phosphatase SHIP2, and not through PTEN.

212 d expression of a PIP2-degrading enzyme, the phosphoinositol phosphatase synaptojanin 1 (synj1), in A

213 determine partitioning of the most abundant phosphoinositol phosphates, PI(4)P and PI(4,5)P2 into mo

214 chain" phosphoinositides, usually dioctanoyl phosphoinositol phosphates.

215 e characterized by high levels of ceramides, phosphoinositols, phosphocholines, and sphingomyelins.

216 logical membranes is mediated by protein and phosphoinositol phospholipid interactions.

217 -1), +/+ 44%, db/+ 61% decrease, P<0.05; and phosphoinositol (PI) 3-kinase (p85alpha), +/+ 33%, db/+

218 en species (ROS)-dependent regulation of the phosphoinositol (PI) 3-kinase pathway in steatosis induc

219 xpression of certain liver genes through the phosphoinositol (PI) 3-kinase/Akt pathway.

220 EG enrichment in plant-pathogen interaction, phosphoinositol, plant hormones, and other signaling pat

221 of PC-phospholipase D, phospholipase A2, or phosphoinositol-PLC were not affected.

222 ies are mainly directed against the acylated phosphoinositol portion of GPIs.

223 and PI(3,4)P(2), changing the balance of two phosphoinositol products of phosphoinositide 3-kinase, P

224 may serve to generate a very specific set of phosphoinositol products, possibly involved in regulatin

225 exes with many signaling proteins, including phosphoinositol (PtdIns) 3-kinase (EC 2.7.1.137), Cbl, G

226 nt facilitator lipids (e.g., gangliosides or phosphoinositols), revealing a plausible regulatory effe

227 ence suggests that the charge density on the phosphoinositol ring represents a key factor in determin

228 t by cannabimimetic CB1 receptor, G protein, phosphoinositol signal transduction pathway, and Ca(2+)-

229 he present study investigates if the classic phosphoinositol signaling pathway involving Galphaq-medi

230 involved in migration, ECM interaction, and phosphoinositol signaling were significantly downregulat

231 Furthermore, phosphoinositol specific phospholipase-C (PLC) activity

232 sphate production or reduced ability of this phosphoinositol to release stored Ca2+.

233 n catalyzed by phosphatidylinositol:ceramide phosphoinositol transferase (IPC synthase).

234 phatidylinositol:mannose-inositol-P-ceramide phosphoinositol transferase).

235 nergy was uncoupled by pretreatment with the phosphoinositol-tris phosphate kinase [PI3K] inhibitor,

236 ugh a leptin receptor-mediated production of phosphoinositol-trisphosphate [PIP3].

237 EP4) that have divergent effects on cAMP and phosphoinositol turnover and different anatomical distri

238 ctive at blocking 5-HT(2C) receptor-mediated phosphoinositol turnover.

239 values in functional assays measuring [(3)H]phosphoinositol turnover: 5-HT2C = 8.1; 5-HT2A = 6.8; 5-

240 ers of 1,2-di(9Z-octadecenoyl)-sn-glycero-3-[phosphoinositol-x,y-bisphosphate] (PI(3,4)P2, PI(3,5)P2,