ライフサイエンスコーパス: phosphatidyl

1 ability of 5-HT(1A) agonists to activate the phosphatidyl 3'-kinase (PI-3K) prosurvival pathway.

2 s phosphatidylinositol 3,4,5 triphosphate to phosphatidyl 3,4 biphosphate.

3 breast cancer tumorigenicity and stimulates phosphatidyl 3-kinase implicated in colorectal cancer pr

4 -associated protein TRRAP are members of the phosphatidyl 3-kinase-related kinase (PIKK) family.

5 t of rapamycin, an integral component of the phosphatidyl 3-kinase/AKT signaling pathway, with early

6 nce similarities to the catalytic domains of phosphatidyl-3 kinase and other members of this family o

7 However, we did not observe a phosphatidyl-3 kinase or a DNA-dependent protein kinase

8 n p85, a regulator of the signalling protein phosphatidyl-3-OH kinase (PI(3)K), participates in the c

9 at a direct interaction of the channels with phosphatidyl-4,5-bisphosphate (PIP(2)) is critical for o

10 All Kir channels require interaction of phosphatidyl-4,5-bisphosphate (PIP2) at a crystallograph

11 is family may be differentially sensitive to phosphatidyl-4,5-bisphosphate in terms of catalytic acti

12 ion of PI4KB and, consequently, reduction in phosphatidyl-4-phosphate levels may be considered an alt

13 ll possess the predominant natural 19:0/16:0 phosphatidyl acylation pattern were prepared to study th

14 RafC did not bind phosphatidyl alcohols; also, inhibition of PA formation

15 conomical syntheses of three cholesteryl-6-O-phosphatidyl-alpha-D-glucopyranosides (alphaCPG) unique

16 e level, with the remainder occurring at the phosphatidyl-base level; and (c) free Cho originates pre

17 id-binding site and the structural basis for phosphatidyl-based substrate binding and phospholipase A

18 methylation of free bases, phospho-bases, or phosphatidyl-bases.

19 and L chain genes (VH12 and Vkappa4) of anti-phosphatidyl choline (anti-PtC) B cells.

20 toyl oleoyl phosphatidyl choline or dioleoyl phosphatidyl choline (DOPC).

21 omparison, data for a mixture of dipalmitoyl phosphatidyl choline (DPPC), cholesterol, and DOPC are a

22 n either the immobilized artificial membrane-phosphatidyl choline (IAM-PC) stationary phase or the su

23 oxidation products of palmitoyl-arachidonyl-phosphatidyl choline (PAPC), are mediators of inflammati

24 This activity was shown to hydrolyze phosphatidyl choline (PC) and phosphatidyl ethanolamine

25 guide resonance (PWR) studies showed hen egg phosphatidyl choline (PC) bilayers produce amphipathic h

26 Unsaturated soy phosphatidyl choline (PC) liposomes were systematically

27 Murine phosphatidyl choline (PtC)-specific B cells in normal mi

28 Phosphatidyl choline (PtC)-specific B cells segregate to

29 simulation data for bilayers of dipalmitoyl phosphatidyl choline and cholesterol for dipalmitoyl pho

30 a bicelle mixture consisting of dimyristoyl phosphatidyl choline and dihexanoyl phosphatidyl choline

31 rsion of CD1d, in contrast, lacks detectable phosphatidyl choline and the only detectable associated

32 ating in apo E-deficient mice by hydrolyzing phosphatidyl choline as scavenger receptor B1 removes th

33 icients (K(PLW)s), focusing in particular on phosphatidyl choline based lipids.

34 um dodecyl sulfate micelles, and dimyristoyl phosphatidyl choline bilayers.

35 toyl phosphatidyl glycerol, and Lyso-stearyl phosphatidyl choline ligands also showed a high affinity

36 copy of aligned model membranes containing a phosphatidyl choline lipid to investigate the oligomeriz

37 M), cholesterol, and either palmitoyl oleoyl phosphatidyl choline or dioleoyl phosphatidyl choline (D

38 The first enzyme of the phosphatidyl choline production pathway, CHKA, is overex

39 yristoyl phosphatidyl choline and dihexanoyl phosphatidyl choline remains isotropic, but tracer diffu

40 d abundance of phosphatidyl ethanolamine and phosphatidyl choline species, corroborated by DESI-MS, w

41 lamellar liposomes consisting of dimyristoyl phosphatidyl choline, dimyristoyl phosphatidylglycerol,

42 for these LTPs, although the Lyso-Myristoyl Phosphatidyl Choline, Lyso-myristoyl phosphatidyl glycer

43 l) and phospholipids (phosphatidyl glycerol, phosphatidyl choline, phosphatidyl ethanolamine, phospha

44 the most abundant phospholipid in the cell, phosphatidyl choline, while the protease cleavable versi

45 Choline mass (a measure of phosphatidyl choline-specific phospholipase D) also peak

46 actosyl ceramide (LacCer) and di-tridecanoyl-phosphatidyl choline.

47 omyelin and lysophospholipids in addition to phosphatidyl choline.

48 idyl choline and cholesterol for dipalmitoyl phosphatidyl choline:cholesterol ratios of 24:1, 47:3, 1

49 10-(2'-hexadienoyloxy)decanoyl]-sn-glycero-3-phosphatidyl- choline (bis-SorbPC) facilitated liposome

50 nitrobenzo-2-oxa-1,3 diazole)-amino-caproyl phosphatidyl-choline (a fluorescent phospholipid analogu

51 PCs used were 1, 2-dimyristoyl-sn-glycero-3-phosphatidyl-choline (DMPC), 1, 2-dipalmitoyl-sn-glycero

52 in thicker 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidyl-choline (POPC) bilayers with a tilt angle o

53 phospholipid, 1-palmitoyl-2-(5-oxovaleroyl)-phosphatidyl-choline (POVPC), whereas oxidation of fatty

54 increase alveolar and lung-tissue saturated phosphatidyl-choline (Sat PC) in preterm rabbits deliver

55 consisted of a binary mixture of dimyristoyl-phosphatidyl-choline and dihydrocholesterol.

56 The major phospholipid classes, i.e. phosphatidyl-choline and phosphatidyl-inositol, were dif

57 interactions of a coarse grain di-myristoyl-phosphatidyl-choline hydrated bilayer with both a purely

58 Emulsions stabilised by a protein or by phosphatidyl-choline/Tween 80 were submitted to gastro-i

59 ansition temperature (Tm) of identical-chain phosphatidyl-cholines (PCs) in excess H2O is now well kn

60 of several phospholipids (PL) classes, viz., phosphatidyl-cholines (PCs), -ethanolamines (PEs), -seri

61 Dipalmitoyl L-alpha-phosphatidyl-D-myo-inositol 3,4,5-triphosphate (Di-C16-P

62 esters a significant fraction of the L-alpha-phosphatidyl-D-myo-inositol 4,5-bisphosphate (PIP2) on t

63 which phosphatidyl-L-serine was replaced by phosphatidyl-D-serine, phosphatidic acid, or phosphatidy

64 -targeted analog, we synthesized a series of phosphatidyl-ddGs and incubated them with 2.2.15 cells,

65 mined that the first of these compounds is a phosphatidyl-dihydropyridine bisretinoid; to indicate th

66 ClsA, the combined YmdB-ClsC used PE as the phosphatidyl donor to PG to form CL, which demonstrates

67 Dioleoyl phosphatidyl ethanolamine (DOPE) formulations of some of

68 G conjugates of 1, 2-distearoyl-sn-glycero-3-phosphatidyl ethanolamine (DSPE), except that they lacke

69 n to hydrolyze phosphatidyl choline (PC) and phosphatidyl ethanolamine (PE) and was effective in a pH

70 rthoester-distearoylglycerol lipid (POD) and phosphatidyl ethanolamine (PE) has been studied using an

71 s and yeast, Arabidopsis cannot form PC from phosphatidyl ethanolamine (PE), and demonstrates that me

72 icin was encapsulated in polyethylene glycol-phosphatidyl ethanolamine (PEG-PE) conjugated micelles.

73 nforced by additional interactions involving phosphatidyl ethanolamine and cholesterol.

74 or nodules, including increased abundance of phosphatidyl ethanolamine and phosphatidyl choline speci

75 phosphatidyl glycerol, phosphatidyl choline, phosphatidyl ethanolamine, phosphatidyl serine and phosp

76 dyl serine, and in the neutral phospholipid, phosphatidyl ethanolamine, were measured in the sera of

77 dy, we identified 5 members (PhFT1-5) of the phosphatidyl ethanolamine-binding proteins (PEBP) family

78 te esters and by phospholipids, particularly phosphatidyl ethanolamine.

79 methyl-hydroxyethyl ammonium bromide/dioleyl-phosphatidyl-ethanolamine (DMRIE/DOPE) and administered

80 lphosphatidylserine (DOPS) and 1, 2-dioleoyl-phosphatidyl-ethanolamine (DOPE).

81 the headgroups of phosphatidylcholine (PC), phosphatidyl-ethanolamine (PE), phosphatidylinositol (PI

82 A novel glutathione-phosphatidyl-ethanolamine conjugate (Glut-PE) was synthe

83 id membranes that contain phospholipids with phosphatidyl-ethanolamine headgroups.

84 s to membranes containing phospholipids with phosphatidyl-ethanolamine headgroups.

85 tized with OVA and treated with di-palmitoyl-phosphatidyl-ethanolamine polyethylene glycol (DPPE-PEG)

86 probably as the complex lipid, retinylidene-phosphatidyl-ethanolamine.

87 of dioleoyl-phosphatidylcholine or dioleoyl-phosphatidyl-ethanolamine.

88 hatidyl serines, phosphatidyl glycerols, and phosphatidyl ethanolamines.

89 Phosphatidyl glycerol (PG) PLs were suppressed during bo

90 ristoyl Phosphatidyl Choline, Lyso-myristoyl phosphatidyl glycerol, and Lyso-stearyl phosphatidyl cho

91 galactosyldiacylglycerol) and phospholipids (phosphatidyl glycerol, phosphatidyl choline, phosphatidy

92 that polymerizes polyglycerol phosphate from phosphatidyl glycerol.

93 linositol (PI), phosphatidylserine (PS), and phosphatidyl-glycerol (PG) can be unambiguously assigned

94 hosphatidyl inositols, phosphatidyl serines, phosphatidyl glycerols, and phosphatidyl ethanolamines.

95 ained with combinations of squalene (SQ) and phosphatidyl glycerophosphate (PGP) which act synergisti

96 ) specific for C(6)PS, phosphatidic acid, or phosphatidyl(homo)serine and produce a response comparab

97 The phosphatidyl-inosital-3 kinase (PI3K) signaling pathway

98 to alter learned and spontaneous behaviors, phosphatidyl inositide hydrolysis, and the antagonist bi

99 hypothesized that constitutive activation of phosphatidyl-inositide 3 kinase (PI3 kinase) could regul

100 Altered abundance of phosphatidyl inositides (PIs) is a feature of cancer.

101 that mice who are deficient in the glycosyl-phosphatidyl inositol (GPI) -linked protein GFRalpha1 (G

102 essing site close to the C-terminal glycosyl phosphatidyl inositol (GPI) membrane anchor site, which

103 and the sequence predicted it was a glycosyl phosphatidyl inositol (GPI)-anchored protein that had a

104 action was further examined using a glycosyl phosphatidyl inositol (GPI)-linked form of CD45Null (lac

105 ision abnormally delayed (dally), a glycosyl-phosphatidyl inositol (GPI)-linked glypican, as a hepara

106 en used to manipulate and concentrate glycan-phosphatidyl inositol (GPI)-tethered proteins in planar

107 Inhibition of the phosphatidyl inositol (PI) 3-kinase intermediate in IGF-

108 studied biochemical response: stimulation of phosphatidyl inositol (PI) hydrolysis].

109 In vitro phosphatidyl inositol (PI) kinase assay demonstrated tha

110 ERK (extracellular signal-regulated kinase), phosphatidyl inositol 3 (PI3)-kinase/Akt, and RalGEF/Ral

111 oss-linking of the FcepsilonRI activates the phosphatidyl inositol 3 kinase (PI3K) and mitogen-activa

112 epidermal growth factor receptor (ERBB1) or phosphatidyl inositol 3 kinase (PI3K) enhanced BBR3610 t

113 We found that inhibition of Ras, p38, phosphatidyl inositol 3 kinase (PI3K) or Akt signaling r

114 afenib cooperated with clinically relevant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral prot

115 ll as integrin-induced activation of Rho and phosphatidyl inositol 3 kinase, were compromised in Pyk2

116 This metabolic switch depends on the phosphatidyl inositol 3'-kinase/Akt pathway, is antagoni

117 teric site in complex with the head group of phosphatidyl inositol 3,4,5-trisphosphate and N-terminal

118 , RT-PCR using primers flanking the putative phosphatidyl inositol 3-kinase (PI3-K) binding site of E

119 3-methyl-adenine (3-MA), an inhibitor of phosphatidyl inositol 3-kinase (PI3-kinase) prevented in

120 on activation of the IGF-I receptor and the phosphatidyl inositol 3-kinase (PI3-kinase)-Akt pathway

121 ing, CD28 costimulation, and signals through phosphatidyl inositol 3-kinase (PI3K) and related metabo

122 wer cholesterol, possibly via recruitment of phosphatidyl inositol 3-kinase (PI3K) and the serine/thr

123 tivity to myeloid cell leukemia-1 (MCL1) and phosphatidyl inositol 3-kinase (PI3K) inhibitors.

124 Phosphatidyl inositol 3-kinase (PI3K) is activated by IL

125 mitogen-activated protein kinase (MAPK) and phosphatidyl inositol 3-kinase (PI3K) signaling on the s

126 s glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways

127 cation of a pharmacological inhibitor of the phosphatidyl inositol 3-kinase (PI3K).

128 le of nuclear factor kappa B (NF-kappaB) and phosphatidyl inositol 3-kinase (PI3K)/Akt signaling in t

129 was designed to investigate the role of the phosphatidyl inositol 3-kinase (PI3K)/AKT/p70(S6K) signa

130 ecombination, we assessed the effects of the phosphatidyl inositol 3-kinase inhibitor wortmannin on t

131 the pharmacological inhibitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor, and leupeptin

132 the proteasome inhibitor, MG-132, or by the phosphatidyl inositol 3-kinase inhibitor, wortmannin.

133 In contrast, the activity of phosphatidyl inositol 3-kinase is not required for OGD p

134 nases (MAPKs) or protein kinase B/Akt of the phosphatidyl inositol 3-kinase pathway.

135 fects of anisomycin largely involved p38 and phosphatidyl inositol 3-kinase signaling mechanisms.

136 or OGD preconditioning because inhibition of phosphatidyl inositol 3-kinase with a chemical inhibitor

137 f NF-kappaB and found that they included the phosphatidyl inositol 3-kinase, protein kinase C, mitoge

138 ail of EGFR and attenuate phosphorylation of phosphatidyl inositol 3-kinase, which is recruited by EG

139 The phosphatidyl inositol 3-kinase-like kinases (PIKKs), ata

140 /11, protein kinase C, tyrosine kinases, and phosphatidyl inositol 3-kinase.

141 ne mutations that block its interaction with phosphatidyl inositol 3-kinase.

142 rotection was mediated, in part, through the phosphatidyl inositol 3-kinase/Akt and GSK-3beta pathway

143 laces the FRAP/mTOR kinase downstream of the phosphatidyl inositol 3-kinase/Akt-signaling pathway, wh

144 te, and a FYVE domain that selectively binds phosphatidyl inositol 3-phosphate.

145 AP activity is stimulated by lipid messenger phosphatidyl inositol 4,5 bisphoshate (PI4,5P2) and is r

146 ossibly in combination with the reduction in phosphatidyl inositol 4,5 bisphosphate (PIP2).

147 f 0.59 muM and that this activation required phosphatidyl inositol 4,5-bisphosphate (PIP(2)).

148 gamma accumulation at cell-cell contacts and phosphatidyl inositol 4,5-bisphosphate production, which

149 nities for MT1-MMP and TACE, to the glycosyl-phosphatidyl inositol anchor of prions to create a membr

150 hosphatidic acid and phosphorylated forms of phosphatidyl inositol at least in part through the bindi

151 Changes in phosphatidyl inositol bisphosphate (PIP2) concentration

152 Glutamate stimulates phosphatidyl inositol hydrolysis and mobilizes intracell

153 ctasia mutated ( ATM ) gene, a member of the phosphatidyl inositol kinase-like (PIKL) family of prote

154 Consecutive phosphatidyl inositol kinase-like kinase (PIKK)-dependen

155 ocalised production of PI(4,5)P(2) by type 1 phosphatidyl inositol phosphate kinase type 1gamma (PIPK

156 d composition, including bilayers containing phosphatidyl inositol phosphates.

157 LRH-1-which reveal that these receptors bind phosphatidyl inositol second messengers and that ligand

158 Conversion of phosphatidic acid to phosphatidyl inositol was the most active pathway in lam

159 atidyl ethanolamine, phosphatidyl serine and phosphatidyl inositol) under cold stress.

160 re that the N-WASP EVH1 domain does not bind phosphatidyl inositol-(4,5)-bisphosphate, as previously

161 als mediated by SRC family kinases SYK, CBL, phosphatidyl inositol-3 (PI-3) kinase, and Rac are direc

162 r tyrosine kinases, is a potent activator of phosphatidyl inositol-3 kinase (PI3K) and mammalian targ

163 ulated by growth factors and is sensitive to phosphatidyl inositol-3 kinase (PI3K) inhibitors.

164 The phosphatidyl inositol-3 kinase (PI3K) signaling pathway

165 ddition, other signaling pathways, including phosphatidyl inositol-3 kinase (PI3K), have the potentia

166 luding insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian target

167 y inhibitors of ceramide-mediated apoptosis, phosphatidyl inositol-3 kinase activity, or tyrosine kin

168 cellular signal-regulated kinase kinase 1 or phosphatidyl inositol-3 kinase inhibition.

169 Incubation with a phosphatidyl inositol-3 kinase inhibitor or expression o

170 Our results show that inhibiting phosphatidyl inositol-3 kinase or blocking the interacti

171 hand, blockade of Ca2+, phospholipase C, or phosphatidyl inositol-3 kinase signaling pathways did no

172 Radiation-induced activation of the phosphatidyl inositol-3 kinase/Akt signal transduction p

173 he synthesis and biochemical validation of a phosphatidyl inositol-3 phosphate (PI3P) immunogen.

174 in monomers, and wortmannin, an inhibitor of phosphatidyl inositol-3-kinase (PI3-kinase), each disrup

175 growth factor 1 (IGF-1) signalling (IIS) via phosphatidyl inositol-3-kinase (PI3K), phosphoinositide-

176 ylates Chk1-Ser(280), the effect of Erbb2 on phosphatidyl inositol-3-kinase (PI3K)/Akt signaling duri

177 Inhibition of phosphatidyl inositol-3-kinase or mammalian target of ra

178 clic AMP; (ii) mediated by protein kinase C, phosphatidyl inositol-3-kinase, myosin light chain kinas

179 Sac1 is a phosphatidyl inositol-4 phosphate (PI4P) lipid phosphata

180 CD16B is a glycosyl-phosphatidyl inositol-anchored molecule, whereas CD32A i

181 expressing neurons also express the glycosyl-phosphatidyl inositol-linked (GPI-linked) GDNF binding c

182 tastasis-associated protein CD24, a glycosyl phosphatidyl inositol-linked surface protein, as a downs

183 osphorylation of several proteins, including phosphatidyl inositol-specific phospholipase C-gammal.

184 n of a phosphate group to the 3'-position of phosphatidyl inositol.

185 d implicates tubby domains as phosphorylated-phosphatidyl- inositol binding factors.

186 lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes hav

187 R) has been identified as an axonal glycosyl-phosphatidyl-inositol (GPI)-anchored protein, whereas th

188 ough nuclear factor kappa B (NF kappa B) and phosphatidyl-inositol 3 kinase (PI 3-kinase) since addit

189 rivatives or disruption of PDGFRalpha-driven phosphatidyl-inositol 3' kinase (PI3K) activity resulted

190 Nalpha treatment resulted in an mTOR- and/or phosphatidyl-inositol 3'(PI 3') kinase-dependent phospho

191 te myocytes is promoted by activation of the phosphatidyl-inositol 3'-kinase (PI3 kinase) pathway and

192 mma-32P]ATP results in the formation of [32P]phosphatidyl-inositol 3,4, 5-trisphosphate [PtdIns(3,4,5

193 It was also found that though inhibition of phosphatidyl-inositol 3-kinase (PI-3K) by LY294002 in al

194 tions in genes that encode components of the phosphatidyl-inositol 3-kinase (PI3-kinase) signaling pa

195 Extension formation requires phosphatidyl-inositol 3-kinase activity, whereas Rho kin

196 e plasma membrane via the Golgi complex in a phosphatidyl-inositol 3-kinase-dependent and actin-indep

197 g is dependent upon downstream activation of phosphatidyl-inositol 3-kinase/Akt, inactivation of the

198 we show cholesterol and the signaling lipid phosphatidyl-inositol 4,5 bisphosphate (PIP(2)) regulate

199 s to the cell surface by means of a glycosyl-phosphatidyl-inositol anchor.

200 Phosphatidyl-inositol mannosides (PIM) are glycolipids u

201 transduction pathway requires Akt binding to phosphatidyl-inositol phosphates (PIP) on the cell membr

202 pheral membrane proteins which interact with phosphatidyl-inositol phosphates (PIPs) in cell membrane

203 ants and that prevention of this accelerated phosphatidyl-inositol turnover in turn negates suppressi

204 rminal domain with homology to GPI (glycosyl-phosphatidyl-inositol) anchor-containing proteins are se

205 lipid classes, i.e. phosphatidyl-choline and phosphatidyl-inositol, were differentially affected by t

206 In human lymphoblasts, NRG1-mediated phosphatidyl-inositol,3,4,5 triphosphate [PI(3,4,5)P3] s

207 BKM-120 is a CNS-penetrant pan-class I phosphatidyl-inositol-3 kinase (PI3K) inhibitor in clini

208 The phosphatidyl-inositol-3 kinases (PI3K) pathway regulates

209 Activation of phosphatidyl-inositol-3'-OH-kinase (PI3K) and the result

210 inase (PI3K) and the resulting production of phosphatidyl-inositol-3,4,5-trisphosphate (PIP3) are ubi

211 nsequences of biochemical inhibition of KIT, phosphatidyl-inositol-3-kinase (PI3-K), PLCgamma, MAPK/E

212 ain-of-function alterations in MET, HER2, or Phosphatidyl-Inositol-3-Kinase (PI3K), catalytically ina

213 primary classes of effectors, namely, Rafs, phosphatidyl-inositol-3-kinases (PI3Ks) and Ral guanine

214 ARF, an ATP-dependent step that requires the phosphatidyl-inositol-4 kinase Pik1, and third ATP-depen

215 nd sequesters acidic phospholipids including phosphatidyl-inositol-4,5-bisphosphate (PIP2) [7].

216 RF6 during neurite extension by coexpressing phosphatidyl-inositol-4-phosphate 5-Kinase alpha [PI(4)P

217 of Sec2p also binds to the Golgi-associated phosphatidyl-inositol-4-phosphate, which works in concer

218 bisphosphate (PtdInsP2) levels by activating phosphatidyl-inositol-4-phosphate-5-OH kinase (PtdIns-5-

219 ith its binding partners Ypt32p, Sec15p, and phosphatidyl-inositol-4-phosphate.

220 human GPIT is EtN-P-2Manalpha1-4GlcN-(acyl)-phosphatidyl-inositol.

221 eads to an increase in phospholipids such as phosphatidyl inositols, phosphatidyl serines, phosphatid

222 ylcholine (DOPC), POPC, 1-palmitoyl-2-oleoyl-phosphatidyl-L-serine (POPS), or POPS mixed with 1-palmi

223 Membranes containing phosphatidyl-L-serine (PS) and phosphatidylethanolamine

224 The anionic phospholipid, phosphatidyl-L-serine (PS), is sequestered in the inner

225 Lactadherin is a phosphatidyl-L-serine (Ptd-L-Ser)-binding protein that d

226 Thus, while membranes containing phosphatidyl-L-serine enhance condensation of the enzyme

227 ty of protein kinase C provided that 1, 2-sn-phosphatidyl-L-serine is present.

228 Membranes in which phosphatidyl-L-serine was replaced by phosphatidyl-D-ser

229 of enantiomeric membranes containing 2,3-sn-phosphatidyl-L-serine, 2, 3-sn-diacylglycerol, and 2,3-s

230 monolayers comprising either acidic DL-alpha-phosphatidyl-L-serine, dipalmitoyl (DPPS) or zwitterioni

231 ein kinase C specifically recognizes 1, 2-sn-phosphatidyl-L-serine, independently of membrane structu

232 of 28 nM when bound to membranes containing phosphatidyl-L-serine, phosphatidylethanolamine, and pho

233 We found that lactadherin, a phosphatidyl-l-serine-binding protein, blocked >99% of p

234 The largest effect of phosphatidyl-L-serine-containing membranes on the factor

235 hatidylcholine > phosphatidylethanolamine >> phosphatidyl-l-serine.

236 -length protein, stereoselective for sn-1, 2-phosphatidyl-L-serine.

237 n the opposite side of the membrane, whereas phosphatidyl lipids were attracted little to these sites

238 vealed that IgM antibodies failed to bind to phosphatidyl lipids, but did recognize lysophosphatidylc

239 n of a primary alcohol is transferred to the phosphatidyl moiety of the phosphatidic acid product.

240 erases PimA and PimB' (MSMEG_4253) recognize phosphatidyl-myo-inositol (PI) as a lipid acceptor, PimA

241 the binding site for the acceptor substrate, phosphatidyl-myo-inositol (PI).

242 b-restricted T cells by the hexamannosylated phosphatidyl-myo-inositol (PIM(6)), a family of mycobact

243 c(2)) anchor, while syntheses of triacylated-phosphatidyl-myo-inositol dimannoside (Ac(1)PIM(2)) and

244 The precursor of LM, phosphatidyl-myo-inositol dimannoside, had no activity,

245 ving its export to the capsule releasing its phosphatidyl-myo-inositol mannoside lipid anchor.

246 e that initiates the biosynthetic pathway of phosphatidyl-myo-inositol mannoside, lipomannan, and lip

247 Phosphatidyl-myo-inositol mannosides (PIMs) are key glyc

248 (M.tb) envelope is highly mannosylated with phosphatidyl-myo-inositol mannosides (PIMs), lipomannan,

249 sferase (GT) involved in the biosynthesis of phosphatidyl-myo-inositol mannosides (PIMs), which are k

250 nvolved in the biosynthesis of mycobacterial phosphatidyl-myo-inositol mannosides (PIMs).

251 there was a marked reduction of higher order phosphatidyl-myo-inositol mannosides and the presence of

252 Less exposed ManLAM and reduced higher order phosphatidyl-myo-inositol mannosides in strains HN885 an

253 This response is stimulated in part through phosphatidyl-myo-inositol mannosides that are present in

254 ) that initiates the biosynthetic pathway of phosphatidyl-myo-inositol mannosides, lipomannan, and li

255 binomannan, lipomannan, and the higher-order phosphatidyl-myo-inositol mannosides.

256 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) i

257 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) i

258 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) i

259 A preferentially binds to negatively charged phosphatidyl-myo-inositol substrate and non-substrate me

260 abinogalactan-peptidoglycan complex, and the phosphatidyl-myo-inositol-based lipoglycans are key feat

261 E, is generated by phosphate hydrolysis of a phosphatidyl-pyridinium bisretinoid (A2PE) that forms wi

262 e (Ser), but there is also some evidence for phosphatidyl-Ser (Ptd-Ser) decarboxylation.

263 Interestingly, phosphatidyl serine (PS) down-regulated the IFN-gamma pr

264 New studies shed light on the role of the phosphatidyl serine (PS) receptor (PSR).

265 Liposomes with high phosphatidyl serine (PS) were specially formulated to he

266 eptor that binds multiple ligands, including phosphatidyl serine (PS).

267 Other anionic lipids (e.g., phosphatidyl serine and phosphatidic acid), a phosphatid

268 phatidyl choline, phosphatidyl ethanolamine, phosphatidyl serine and phosphatidyl inositol) under col

269 rial membrane potential, exposure of surface phosphatidyl serine as well as induction of caspase 3/7

270 In contrast, phosphatidyl serine caused a concentration-dependent inh

271 e in OSIR at the onset of apoptosis preceded phosphatidyl serine exposure by 5 h.

272 , mitochondrial membrane depolarization, and phosphatidyl serine exposure on the cell surface, which

273 s apoptosis, based on nuclear morphology and phosphatidyl serine exposure, although the apoptotic cel

274 ased on their differential ability to induce phosphatidyl serine exposure, loss of mitochondrial memb

275 First, Annexin V binding to phosphatidyl serine expressed on activated cells was det

276 hromatin condensation (assessed with TOPRO), phosphatidyl serine externalization (Annexin V labeling)

277 associated with early mitochondrial injury, phosphatidyl serine externalization, and DNA degradation

278 hrinkage, plasma membrane microvesiculation, phosphatidyl serine externalization, and proteolysis of

279 neither accompanied by DNA fragmentation nor phosphatidyl serine externalization, characteristics of

280 osis with increased fragmentation of DNA and phosphatidyl serine externalization; activation of caspa

281 These data implicate tumor-derived phosphatidyl serine in the alterations observed in tumor

282 lets possess some element(s) (other than 30% phosphatidyl serine or factor Va), presumably either pro

283 3 protease activity, and flow cytometry for phosphatidyl serine translocation.

284 ively charged phospholipids, cardiolipin and phosphatidyl serine, and differed in their specificity a

285 ively charged phospholipids, cardiolipin and phosphatidyl serine, and in the neutral phospholipid, ph

286 ne exposure of the apoptotic signal molecule phosphatidyl serine, larger cell size, the G1 cell cycle

287 luding granulocyte macrophage-CSF, PGE2, and phosphatidyl serine, that can affect the immune system.

288 E2, granulocyte-macrophage CSF (GM-CSF), and phosphatidyl serine, we evaluated the effects of these p

289 ipid antibodies reduces annexin-V binding to phosphatidyl serine-coated microtiter plates, frozen tha

290 the TUNEL technique, and external display of phosphatidyl serine.

291 -12 protein in cultures treated with PGE2 or phosphatidyl serine.

292 atter labeling scramblase externalization of phosphatidyl serine.

293 at this effect is driven both by EV size and phosphatidyl serine.

294 by this tumor, including PGE(2), GM-CSF, and phosphatidyl serine; however, none of these agents induc

295 Whether examined by esterase staining, phosphatidyl-serine staining, DNA breakage, or caspase-m

296 n antibodies, beta2-glycoprotein I, and anti-phosphatidyl-serine) and 1 in plasma (lupus anticoagulan

297 phosphate (ATP)-dependent aminophospholipid (phosphatidyl-serine) translocase activity.

298 ged lipids, PtdIns3P, phosphatidic acid, and phosphatidyl-serine.

299 hospholipids such as phosphatidyl inositols, phosphatidyl serines, phosphatidyl glycerols, and phosph

300 dylcholine, 10-doxyl phosphatidylcholine, or phosphatidyl-tempocholine, quenching of acrylodan fluore