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

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

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

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

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

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

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

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

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

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

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

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

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

25 Unsaturated soy phosphatidyl choline (PC) liposomes were systematically

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 omyelin and lysophospholipids in addition to phosphatidyl choline.

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

46 10-(2'-hexadienoyloxy)decanoyl]-sn-glycero-3-phosphatidyl- choline (bis-SorbPC) facilitated liposome

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Dioleoyl phosphatidyl ethanolamine (DOPE) formulations of some of

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

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

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

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

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

70 te esters and by phospholipids, particularly phosphatidyl ethanolamine.

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

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

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

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

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

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

77 hatidyl serines, phosphatidyl glycerols, and phosphatidyl ethanolamines.

78 Phosphatidyl glycerol (PG) PLs were suppressed during bo

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

80 that polymerizes polyglycerol phosphate from phosphatidyl glycerol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 3-methyl-adenine (3-MA), an inhibitor of phosphatidyl inositol 3-kinase (PI3-kinase) prevented in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 /11, protein kinase C, tyrosine kinases, and phosphatidyl inositol 3-kinase.

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

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

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

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

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

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

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

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

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

136 Changes in phosphatidyl inositol bisphosphate (PIP2) concentration

137 Glutamate stimulates phosphatidyl inositol hydrolysis and mobilizes intracell

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

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

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

141 d composition, including bilayers containing phosphatidyl inositol phosphates.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Phosphatidyl-inositol mannosides (PIM) are glycolipids u

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 3 protease activity, and flow cytometry for phosphatidyl serine translocation.

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

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

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

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

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

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

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

269 -12 protein in cultures treated with PGE2 or phosphatidyl serine.

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

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

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

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

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

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

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