ライフサイエンスコーパス: GPI

1 GPI proteins are found in cholesterol- and sphingolipid-

2 GPI use was 50.5% during UFH PCIs and 12.0% during bival

3 GPI use was associated with increased risk of bleeding i

4 GPI use was associated with substantially higher bleedin

5 GPI-80 colocalized on the surface of HSPCs with Integrin

6 GPI-80 expression also enabled tracking of HSPCs once th

7 GPI-anchored proteins (GPI-APs) are essential for plant

8 GPI-VHH JM4, but not GPI-VHH JM2, in transduced CD4(+) c

9 ng which time it may cleave approximately 10 GPI-anchored proteins before dissociating.

10 smembrane glycerophosphodiesterase GDE3 as a GPI-specific phospholipase C that cleaves and releases u

11 tors, including folate receptor (FR) beta, a GPI-anchored protein belonging to the folate receptor fa

12 ns interact with eosinophils through CD48, a GPI-anchored receptor important in allergy mainly as exp

13 In contrast, PrP(C) containing a GPI anchor from which the sialic acid had been removed (

14 ERAD and provide evidence that it contains a GPI anchor, ruling out that a GPI anchor obstructs ERAD.

15 e show that the folate-receptor 1 (FolR1), a GPI-anchored cell surface molecule, specifically marks m

16 We describe GlycoFRET for a GPI-anchored receptor, a G-protein-coupled receptor, and

17 to atgpi8-1, indicating that either TMM is a GPI-AP or there is another GPI-AP regulating stomata dev

18 s and following the C-terminal addition of a GPI-anchor (from surface antigen EtSAG1) mCherry was exp

19 amily (ERf) genes suggest the existence of a GPI-AP in a branch of the ERf signaling pathway that reg

20 val [CI]: 0.55 to 1.01) or did not receive a GPI (3.6% vs. 4.4%; OR: 0.82; 95% CI: 0.72 to 0.94; Pint

21 Overall, 3,173 patients (12.7%) received a GPI, most commonly eptifibatide (69.4%).

22 Reck, a GPI-anchored membrane protein, and Gpr124, an orphan GPC

23 it contains a GPI anchor, ruling out that a GPI anchor obstructs ERAD.

24 r degradation, leading to predictions that a GPI anchor sterically obstructs ERAD.

25 ta clustering in atgpi8-1, indicating that a GPI-AP functions upstream of the MAP kinase cascade.

26 that by genetically linking the VHHs with a GPI attachment signal, VHHs are targeted to the lipid ra

27 that by genetically linking the VHHs with a GPI attachment signal, VHHs are targeted to the lipid ra

28 After GPI adjustment in the IV, more than half the bleeding re

29 amine phosphate, which is removed soon after GPI is attached to the protein.

30 eling of its GPI anchor, which occurs in all GPI-APs and provides a protein-independent ER export sig

31 e (SP) and glycophosphatidylinositol-anchor (GPI) sequences, were examined.

32 teristics of fluorescent lipid analogues and GPI-anchored proteins (GPI-APs) in the live-cell plasma

33 e to segregation of transmembrane PrP(C) and GPI-anchored PrP(res) in distinct membrane environments.

34 tein (PfRipr) lack transmembrane domains and GPI anchors.

35 ion of PrP(C) gives rise to glycosylated and GPI-anchored PrP(Sc) The question of the sialylation sta

36 nal modifications, such as glycosylation and GPI anchoring, can affect the transmissibility of prions

37 P modifications, including glycosylation and GPI anchoring, may also influence cross-species infectiv

38 tabolic engineering of cell-surface GPIs and GPI-anchored proteins by using inositol derivatives carr

39 The azide-labeled GPIs and GPI-anchored proteins were then tagged with biotin on li

40 ric VLPs (cVLPs) containing influenza HA and GPI-anchored CCL28 as antigen and mucosal adjuvant, resp

41 ch contains just two Mmps (secreted Mmp1 and GPI-anchored Mmp2) and one secreted Timp.

42 icagrelor was used in 18.1% of patients, and GPI was used in 84.8% of the control group.

43 -acylation (palmitoylation), prenylation and GPI anchors but until recently little was truly known ab

44 y suggests that antigen fusions with SP2 and GPI of EtSAG1 may be promising candidates to examine ind

45 t either TMM is a GPI-AP or there is another GPI-AP regulating stomata development whose function is

46 l (C-term) region, which potentially acts as GPI-addition signal peptide.

47 ecruiting PrP(C) with both sialo- and asialo-GPIs is a common feature of PrP(Sc) The mixtures of sial

48 of PrP(Sc) The mixtures of sialo- and asialo-GPIs were observed in PrP(Sc) universally regardless of

49 brains reported that both sialo- and asialo-GPIs were present in PrP(Sc), with the majority being as

50 t in PrP(Sc), with the majority being asialo-GPIs.

51 ably, the proportion of sialo- versus asialo-GPIs was found to be controlled by host, tissue, and cel

52 r selecting PrP(C) with sialo- versus asialo-GPIs.

53 ted into PrP(Sc), whereas PrP(C) with asialo-GPIs inhibited conversion.

54 , a Cys protease that transfers an assembled GPI anchor to proteins.

55 ransamidase (GPIT), the enzyme that attaches GPI anchors to proteins as they enter the lumen of the e

56 FLA4 is likely to be GPI-anchored, is highly N-glycosylated and carries two O

57 CyRPA was demonstrated to be GPI-linked, localized in the micronemes, and essential f

58 Before GPI adjustment, bleeding reductions with bivalirudin ran

59 -GPI compared with wild-type mice, but beta2-GPI is not deposited on ischemic intestinal tissue.

60 e serum protein, beta2-glycoprotein I (beta2-GPI).

61 During reperfusion, binding of beta2-GPI by naturally occurring Abs results in an excessive i

62 R, TLR2(-/-) mice have increased serum beta2-GPI compared with wild-type mice, but beta2-GPI is not d

63 ell viability were observed in biochemically GPI-AP-deficient cells and were further increased in PIG

64 tached to cells by an anchor molecule called GPI.

65 CD34(+)CD38(lo/-)CD90(+)GPI-80(+) HSPCs were the sole population that maintained

66 in and PAR-2 are co-expressed in HeLa cells, GPI-anchored testisin specifically releases the PAR-2 te

67 inds to phosphatidylcholine (PC) and cleaves GPI-anchored proteins off eukaryotic plasma membranes.

68 between the cangrelor alone and clopidogrel-GPI groups (2.6% vs 3.3%; odds ratio [OR], 0.79; 95% CI,

69 ebo) and receiving routine GPIs (clopidogrel-GPI).

70 Patients in the clopidogrel-GPI group were more likely to be male (75.6% vs 71.9%),

71 th cangrelor alone compared with clopidogrel-GPI (0.3% vs 0.7%; OR, 0.43; 95% CI, 0.11-1.66).

72 sted bleeding risk compared with clopidogrel-GPIs.

73 ored proteins (GPI-APs) carrying a conserved GPI modification signal.

74 Here we have identified a conserved GPI-linked parasite protein, Cysteine-rich protective an

75 we show that products of both genes contain GPI-anchors, and unexpectedly, that GPI-anchored MMPs pr

76 The cVLPs containing GPI-CCL28 showed in-vitro chemotactic activity towards s

77 provide strong evidence that in cell culture GPI anchor-directed membrane association of PrP(C) is re

78 These data suggest that female-derived GPI-anchored ENODLs play an essential role in male-femal

79 In the present study, we developed GPI-anchored variable regions (VHHs) of two heavy chain-

80 rion infection where cells expressing either GPI-anchored PrP(C) or transmembrane-anchored PrP(C), wh

81 e showed that primary CD4 T cells expressing GPI-scFv X5 were resistant to CCR5 (R5)-, CXCR4 (X4)-, a

82 Finally, GPI-scFv X5-transduced CD4 T cells, after being cotransf

83 Finally, GPI-VHH JM4-transduced human primary CD4 T cells efficie

84 For GPI, the hospital LOS (14.64 versus 10.31 days; P = 0.00

85 For GPI-APs, we detect two molecular pools in living cells;

86 ng LRE variants lacking domains critical for GPI anchor addition also rescued lre female gametophyte

87 dings should have important implications for GPI-anchored antibody-based therapy against HIV-1.

88 s the M8CM, but not the domains required for GPI anchor addition.

89 To elucidate how BtPI-PLC searches for GPI-anchored proteins on the membrane surface, we measur

90 Despite variation in indications for GPIs, baseline characteristics were well balanced betwee

91 turated acyl-chains are required for forming GPI-anchor nanoclusters.

92 Four GPI-anchorless prion strains caused a nearly identical c

93 ell population maintained independently from GPI(pos)CD56(dim).

94 The removal of sialic acid from GPIs prevented the targeting of either the isolated GPIs

95 nsisting of the glycerophosphatidylinositol (GPI)-anchored, ligand binding receptor GDNF family recep

96 IFT4 was constructed by fusing a glycolipid (GPI)-anchoring sequence and incorporated into Env-enrich

97 f cells through a glycophosphatidylinositol (GPI) anchor.

98 ma membrane via a glycophosphatidylinositol (GPI) anchor.

99 e mice expressing glycophosphatidylinositol (GPI)-anchorless prion protein, PrP(C), together with hyd

100 Glycosylphosphatidylinositol (GPI) anchoring of the prion protein (PrP(C)) influences

101 Glycosylphosphatidylinositol (GPI) is a glycolipid that anchors >150 various proteins

102 Glycosylphosphatidylinositol (GPI) membrane anchoring of the prion protein (PrP(C)) di

103 Glycosylphosphatidylinositol (GPI) transamidase (GPIT), the enzyme that attaches GPI a

104 Glycosylphosphatidylinositol (GPI)-anchored proteins are ubiquitously expressed in the

105 BST2 with a glycosylphosphatidylinositol (GPI) anchor signal deletion, which is not expressed at t

106 P linked via a glycosylphosphatidylinositol (GPI) anchor to the cell membrane (mGFP-GPI).

107 rane through a glycosylphosphatidylinositol (GPI) anchor.

108 CD177 is a glycosylphosphatidylinositol (GPI)-anchored protein expressed by a variable proportion

109 or (uPAR) is a glycosylphosphatidylinositol (GPI)-anchored protein that promotes tissue remodeling, t

110 we employed a glycosylphosphatidylinositol (GPI)-scFv X5 approach to confer resistance of human prim

111 ation but also glycosylphosphatidylinositol (GPI) anchor side-chain modification.

112 synthesis, and glycosylphosphatidylinositol (GPI)-anchor biosynthesis.

113 Besides glycosylphosphatidylinositol (GPI) anchors and N-glycosylation, O-fucosylation has bee

114 we constructed glycosylphosphatidylinositol (GPI)-anchored VHH JM2 and JM4 along with an E4 control a

115 osition of its glycosylphosphatidylinositol (GPI) anchor.

116 n nature, many glycosylphosphatidylinositol (GPI)-anchored proteins localize in the lipid rafts.

117 expression of glycosylphosphatidylinositol (GPI) anchors on their cell surface, allowing quantificat

118 he cleavage of glycosylphosphatidylinositol (GPI)-anchored proteins, disrupted plasma membrane locali

119 nd a predicted glycosylphosphatidylinositol (GPI) anchor motif.

120 des a putative glycosylphosphatidylinositol (GPI)-anchored surface protein with a modified eight-cyst

121 d a sialylated glycosylphosphatidylinositol (GPI) anchor.

122 the C-terminal glycosylphosphatidylinositol (GPI) anchor-truncated form, inhibited HBV virion egress

123 y a C-terminal glycosylphosphatidylinositol (GPI) linkage.

124 he role of the glycosylphosphatidylinositol (GPI) anchor attached to PrP(C) in prion formation was ex

125 ication of the glycosylphosphatidylinositol (GPI)-anchored glycoprotein Juno as the egg plasma membra

126 inked with the glycosylphosphatidylinositol (GPI)-anchored serine protease prostasin, which is a co-f

127 ed to bivalirudin (n = 2,889) or heparin +/- GPI (n = 2,911).

128 8 patients to bivalirudin versus heparin +/- GPI before primary PCI.

129 gulation with bivalirudin versus heparin +/- GPI for primary PCI, given the evolution in primary PCI.

130 Bivalirudin compared with heparin +/- GPI resulted in reduced 30-day rates of major bleeding (

131 , and transfusions compared with heparin +/- GPI, results that were consistent with evolution in PCI

132 nts compared with 16 of 40 (40.0%) heparin+/-GPI-treated patients (adjusted hazard ratio, 0.12; 95% C

133 patients versus 16 of 2456 (0.7%) heparin+/-GPI-treated patients (P=0.007).

134 lower after bivalirudin than after heparin+/-GPI.

135 were similar with bivalirudin and heparin+/-GPI (1.0% versus 1.4%, P=0.24).

136 er rates of early ST compared with heparin+/-GPI (2.5% versus 1.6%, P=0.04), because of more acute (<

137 ted with bivalirudin compared with heparin+/-GPI because of increased ST within 4 hours after primary

138 ignaling network and, furthermore, highlight GPI-anchor hydrolysis as a cell-intrinsic mechanism to a

139 eting of either the isolated GPIs or the IgG-GPI conjugate to synapses.

140 region that carries the functional domain in GPI-APs, in Pd-resident proteins further enhances Pd acc

141 ndings should have important implications in GPI-anchored antibody-based therapy against HIV-1.

142 at TbRFT1 plays a direct or indirect role in GPI anchor glycosylation in the Golgi apparatus.

143 The TTOT for Gram-positive infection (GPI) was improved (64.04 versus 41.61 h; P = 0.082).

144 of these genes are known to cause inherited GPI deficiencies (IGDs), and all are inherited as recess

145 ferences in glycoprotein IIb/IIIa inhibitor (GPI) use, a test of mediation was performed using the IV

146 heparin+/-a glycoprotein IIb/IIIa inhibitor (GPI).

147 heparin + a glycoprotein IIb/IIIa inhibitor (GPI).

148 us glycoprotein IIb/IIIa receptor inhibitor (GPI) is used.

149 iated with glycoprotein IIb/IIIa inhibitors (GPIs) and a potent P2Y12 antagonist, cangrelor, in patie

150 nal use of glycoprotein IIb/IIIa inhibitors (GPIs) in patients with ST-segment elevation myocardial i

151 ot receive glycoprotein IIb/IIIa inhibitors (GPIs).

152 Isolated GPIs (derived from PrP(C)) were also targeted to synapse

153 evented the targeting of either the isolated GPIs or the IgG-GPI conjugate to synapses.

154 RAD is caused by canonical remodeling of its GPI anchor, which occurs in all GPI-APs and provides a p

155 The strategy can be used to label GPI-anchored proteins with various tags for biological s

156 The azide-labeled GPIs and GPI-anchored proteins were then tagged with bio

157 LORELEI and the seedling-expressed LRE-like GPI-AP1 (LLG1) bind to the extracellular juxtamembrane r

158 ass spectrometry demonstrated that the major GPI-anchored proteins of T. brucei procyclic forms have

159 Mutations in many GPI biosynthesis genes have been described to date in pa

160 mine how oxidized lipid species disrupt mGFP-GPI nanoplatforms in the plasma membrane.

161 found a dose-response relationship for mGFP-GPI nanoplatform disintegration upon addition of POVPC,

162 itol (GPI) anchor to the cell membrane (mGFP-GPI).

163 we analyzed the degradation of the misfolded GPI-AP Gas1* in yeast.

164 ace, allowing quantification of PIGA-mutant (GPI-negative) HSPC-derived peripheral blood cell populat

165 ated by lipid packing defects, possibly near GPI-anchored proteins, and the protein diffuses on the m

166 Expression of GPI-VHH JM4, but not GPI-VHH E4 and JM2, on the surface of transduced TZM.bl

167 GPI-VHH JM4, but not GPI-VHH JM2, in transduced CD4(+) cell lines and human p

168 Thus, the novel GPI-GIFT4-containging VLPs have the potential to be deve

169 of GPI-APs or by structural abnormalities of GPI.

170 s enzyme, leading to reduced accumulation of GPI-anchored proteins.

171 We studied the adjuvanticity of GPI-anchored CCL28 co-incorporated with influenza HA-ant

172 es have been implicated in the biogenesis of GPI-anchored proteins.

173 y control is limited for the entire class of GPI-APs, many of them being clinically relevant.

174 Notch signalling through surface cleavage of GPI-anchored proteins, is targeted by Prdx4 oxidative ac

175 protein partially rescued the deficiency of GPI-anchored proteins.

176 We show that diffusion of GPI-anchored proteins also becomes temperature dependent

177 Thus cell surface diffusion of GPI-anchored proteins and transmembrane proteins that as

178 Previous in vivo studies on the effects of GPI anchoring on prion infectivity have not examined cro

179 ential influence of endogenous expression of GPI-anchored PrP(C) To further explore these questions,

180 aused by the decreased surface expression of GPI-APs or by structural abnormalities of GPI.

181 Expression of GPI-VHH JM4, but not GPI-VHH E4 and JM2, on the surface

182 the plasma membrane by examining the flow of GPI-anchored proteins.

183 The fraction of GPI-negative cells within the CD56(dim) NK cells was mar

184 cursor lipid or defective galactosylation of GPI intermediates in the endoplasmic reticulum, but rath

185 Incorporation of GPI-anchored GIFT4 into VLPs as a molecular adjuvant rep

186 ndergoing PCI was maintained irrespective of GPI administration.

187 this study, we tested the effect of lack of GPI anchoring on a species barrier model using mice expr

188 There were significantly reduced levels of GPI-anchored proteins (CD55 and CD59) on the surface of

189 alities in the synthesis and localization of GPI-anchored surface molecules.

190 edge, the first evidence of the mechanism of GPI-AP sorting in plants.

191 suggest that pharmacological modification of GPI glycosylation might constitute a novel therapeutic a

192 For one strain, passage of GPI-anchorless prions into wild type mice led to the eme

193 likely to be determined by the specifics of GPI biosynthesis.

194 c analogues to a level comparable to that of GPI-0100 and suitable for immunological studies and clin

195 have adjuvant activity comparable to that of GPI-0100.

196 re involved in biosynthesis and transport of GPI-anchored proteins (GPI-APs).

197 lirudin or with heparin with optional use of GPI resulted in similar 1-year mortality.

198 versy, we analyzed the sialylation status of GPIs within PrP(Sc) generated in the brain, spleen, or c

199 c) The question of the sialylation status of GPIs within PrP(Sc) has been controversial.

200 work suggests that the sialylation status of GPIs within PrP(Sc) is regulated in a cell-, tissue-, or

201 bivalirudin was because of the lower use of GPIs (risk difference, -0.84%; 95% CI: -1.11%, -0.57%),

202 re, in part, explained by the greater use of GPIs with UFH.

203 by confocal microscopy and flow cytometry on GPI-AP-deficient cells incubated with aHUS serum compare

204 Only GPI-anchored PrP(C) supported persistent PrP(res) propag

205 he prion protein, PrP(res) We show that only GPI-anchored PrP(C) was able to convert to PrP(res) and

206 r low-molecular-weight heparin plus optional GPIs (control group).

207 r low-molecular-weight heparin plus optional GPIs on 1-year mortality.

208 nknown, particularly in the context of other GPI-APs not associated with Pd Here, we conducted a comp

209 valirudin were largest for transfemoral PCI (GPI-adjusted risk difference, -1.11%; 95% CI: -1.43%, -0

210 -0.80%) and negligible for transradial PCI (GPI-adjusted risk difference, 0.09%; 95% CI: -0.32%, 0.5

211 the two Pd-resident and two unrelated non-Pd GPI-APs in Arabidopsis (Arabidopsis thaliana).

212 modification signal from both Pd- and non-Pd GPI-APs is able to target a reporter protein to Pd, like

213 cate that segregation between Pd- and non-Pd GPI-APs occurs prior to Pd targeting, providing, to our

214 However, in non-Pd GPI-APs, the ectodomain overrides the Pd targeting funct

215 antigen is a glycosyl-phosphatidylinositol (GPI)-linked glycoprotein and has been shown to be critic

216 the odr-2 glycosylated phosphatidylinositol (GPI)-linked signaling gene in the SMB neurons.

217 .01-8.17; P = .04) but not with heparin plus GPI (0 vs 3 [0.3%]; P = .30).

218 n but not patients treated with heparin plus GPI, possibly because of the rapid offset of bivalirudin

219 andomized 1:1 to bivalirudin or heparin plus GPI.

220 bivalirudin and 1412 receiving heparin plus GPI.

221 cleavage site 3 aa upstream of the predicted GPI anchor attachment site of ARTC2.2.

222 nterface and further suggest that preventing GPI anchoring of CaValpha2delta1 averts its cell-surface

223 lycosylphosphatidylinositol-anchored protein GPI-80, that is functionally required for their self-ren

224 hosphatidylinositol-anchored surface protein GPI-80 defines a subpopulation of human fetal liver hema

225 ycosylphosphatidylinositol-anchored protein (GPI-AP) LORELEI and the seedling-expressed LRE-like GPI-

226 GPI-anchored proteins (GPI-APs) are essential for plant growth and development;

227 glycophosphatidylinositol-anchored proteins (GPI-APs) are, however, generally poor ERAD substrates an

228 cosylphosphatidylinositol-anchored proteins (GPI-APs) carrying a conserved GPI modification signal.

229 t lipid analogues and GPI-anchored proteins (GPI-APs) in the live-cell plasma membrane and in actin c

230 esis and transport of GPI-anchored proteins (GPI-APs).

231 ol- anchored complement regulatory proteins (GPI-AP).

232 We studied the effect of PrP GPI anchoring using a mouse-to-human species barrier mod

233 n microsomes from wild-type mice or purified GPI-anchorless amyloid fibrils).

234 itro labeling experiments using radiolabeled GPI precursors showed that GPI underglycosylation was no

235 71; 95% CI: 0.25 to 1.99) or did not receive GPIs (0.2% vs. 0.1%; OR: 1.56; 95% CI: 0.80 to 3.04; Pin

236 ents assigned to cangrelor but not receiving GPIs (cangrelor alone) and 1211 patients assigned to clo

237 arms in subsets receiving and not receiving GPIs.

238 ARTC2.2 is a toxin-related, GPI-anchored ADP-ribosyltransferase expressed by murine

239 PION PCI, in which routine or bailout/rescue GPI use was at the site investigator's discretion.

240 Only bailout/rescue GPI use was permitted, except in CHAMPION PCI, in which

241 Patients requiring bailout or rescue GPI therapy were excluded.

242 opidogrel (or placebo) and receiving routine GPIs (clopidogrel-GPI).

243 lable individual samples showed that several GPI-anchored proteins had decreased cell-surface abundan

244 tent with the hypothesis that the sialylated GPI anchor attached to PrP(C) acts as a synapse homing s

245 ies showed that pretreatment with sialylated GPIs prevented the targeting of PrP(C) to synapses.

246 cells claimed that only PrP(C) with sialylo-GPIs could be recruited into PrP(Sc), whereas PrP(C) wit

247 of the GPI signal and determines a specific GPI-dependent non-Pd localization of these proteins at t

248 ntrol cells ex vivo In a hu-PBL mouse study, GPI-scFv X5-transduced CD4 T cells were selected in peri

249 levated tumor expression of the cell surface GPI-linked CD24 protein signals poor patient prognosis i

250 or the metabolic engineering of cell-surface GPIs and GPI-anchored proteins by using inositol derivat

251 Furthermore, sgRNA targeting GPI anchor protein pathway genes induced loss of functio

252 how that CD4 T cells were protected and that GPI-scFv X5-transduced cells were selected in HIV-1-infe

253 n virus replication in vivo We conclude that GPI-scFv X5-modified CD4 T cells could potentially be us

254 We conclude that GPI-scFv X5-modified CD4 T cells could potentially be us

255 In contrast, we find that GPI-anchored proteins exhibit temperature-independent di

256 HXMS studies revealed that GPI-anchorless PrP(Sc) is characterized by substantially

257 We show that GPI modification is necessary and sufficient for deliver

258 Moreover, we show that GPI-scFv X5-transduced CD4 T cells exerted a negative ef

259 sing radiolabeled GPI precursors showed that GPI underglycosylation was not the result of decreased f

260 The results strongly suggest that GPI anchoring and the localization of PrP(C) to rafts ar

261 c analysis of atgpi8-1 mutants suggests that GPI-APs are important for root and shoot growth, stomata

262 contain GPI-anchors, and unexpectedly, that GPI-anchored MMPs promote cell adhesion when they are re

263 interactions between PfRH5, PfRipr, and the GPI-anchored CyRPA clearly defines the components of the

264 Signaling by the GPI anchor mutant also depended on Y6 of BST2.

265 Exchanging the GPI anchor for a nonraft transmembrane sequence redirect

266 either an acyl chain or sialic acid from the GPI anchor reduced the targeting of PrP(C) to synapses.

267 as almost completely abolished; however, the GPI-APs had normal surface levels and normal structure,

268 analysis of maturing DCs, we identified the GPI-anchored protein semaphorin 7A (Sema7A) as being hig

269 omozygous recessive sequence variants in the GPI biosynthesis gene PIGY.

270 d pathogenic variants in PIGG, a gene in the GPI pathway.

271 and functional synaptogenesis, including the GPI-anchored heparan sulfate proteoglycan (HSPG) Wnt co-

272 ng both BG_pap and PDCB1 to Pd Moreover, the GPI modification signal from both Pd- and non-Pd GPI-APs

273 Thus, the lack of the GPI anchor on prions reduced the effect of the mouse-hum

274 Thus, the lack of the GPI anchor on the PrPres from tg44 mice appeared to redu

275 s complex orchestrates the attachment of the GPI anchor to the C terminus of precursor proteins in th

276 s a transmembrane (TM) domain instead of the GPI anchor.

277 ings show that the sialic acid moiety of the GPI attached to PrP(C) modifies local membrane microenvi

278 not the result of decreased formation of the GPI precursor lipid or defective galactosylation of GPI

279 n overrides the Pd targeting function of the GPI signal and determines a specific GPI-dependent non-P

280 se genes associated with deficiencies of the GPI-anchor biosynthesis pathway and also serves to highl

281 domain and was unaffected by removal of the GPI-modification signal, a highly conserved N-glycan or

282 ure N-linked glycans and did not require the GPI anchor for localization.

283 ane microdomains enriched at Pd As such, the GPI modification serves as a primary Pd sorting signal i

284 Thus, the results suggest that the GPI-anchored CCL28 induces significantly higher mucosal

285 whereas a small number are restricted to the GPI-anchored protein CD59 for initial membrane recogniti

286 When the GPI was incorporated, mCherry was observed on the sporoz

287 to synapses, as was IgG conjugated to these GPIs.

288 Thus, GPI anchor remodeling is independent of protein folding

289 Thus, GPI-anchored CCL28 in influenza VLPs act as a strong imm

290 lity given current practices with respect to GPI use and access site.

291 of T. brucei procyclic forms have truncated GPI anchor side chains in TbRFT1 null parasites when com

292 cts containing either a C-terminal wild-type GPI anchor signal sequence or a nonraft transmembrane se

293 ed a novel parasite ligand, Plasmodium vivax GPI-anchored micronemal antigen (PvGAMA), that bound hum

294 Consistently, LRE-cYFP-TM, where GPI anchor addition domains were replaced with a single-

295 r for FER and elucidate a mechanism by which GPI-APs enable the signaling capacity of a cell surface

296 eover, transduction of CEMss-CCR5 cells with GPI-VHH JM4, but not with GPI-VHH E4, confers resistance

297 (ITGAM), which in leukocytes cooperates with GPI-80 to support migration.

298 HIV-1-permissive CD4 T cells engineered with GPI-scFv X5 are resistant to R5-, X4-, or dual-tropic vi

299 4 cells in hu-PBL mice compared to mice with GPI-scFv AB65-transduced CD4 T cells.

300 ss-CCR5 cells with GPI-VHH JM4, but not with GPI-VHH E4, confers resistance to both cell-free and T c

301 oding for arabinogalactans and proteins with GPI anchors.