ライフサイエンスコーパス: GPI

1 GPI biosynthesis is initiated by a multi-subunit enzyme,

2 GPI proteins are found in cholesterol- and sphingolipid-

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

4 GPI use was associated with increased risk of bleeding i

5 GPI use was associated with substantially higher bleedin

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

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

8 binding of aPLs to phospholipid-bound beta(2)GPI arises from the ability of its preexisting J-form to

9 e mice with R. int induced anti-human beta(2)GPI autoantibodies and autoimmune pathologies.

10 Furthermore, beta(2)GPI can adopt multiple conformations (i.e. J-elongated,

11 beta(2)GPI exists in two almost equally populated redox states:

12 APS patients and correlated with anti-beta(2)GPI IgG autoantibodies.

13 propose that targeting the J-form of beta(2)GPI provides a strategy to block pathogenic aPLs in APS.

14 ere, we report that human recombinant beta(2)GPI purified under native conditions is oxidized.

15 Indeed, aPLs prefer membrane-bound beta(2)GPI to that in solution.

16 beta(2)-Glycoprotein I (beta(2)GPI) is an abundant plasma protein displaying phospholip

17 S autoantigen beta(2)-glycoprotein I (beta(2)GPI).

18 R. int immunization of mice induced beta(2)GPI-specific lymphocytes and autoantibodies.

19 sting of two CrRLK1Ls LET1, LET2/MDS1, and a GPI-anchored protein LLG1 that regulates the activation

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

21 ere critical for rapid endocytosis because a GPI-anchored protein induced to misfold at the cell surf

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

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

24 Disruption of GPI7, a GPI anchor-pathway gene, led to a significant reduction

25 GPIHBP1, a GPI-anchored protein of capillary endothelial cells, bin

26 l (GPI)-specific phospholipase D1 (Gpld1), a GPI-degrading enzyme derived from liver, were found to i

27 uPAR is a GPI-anchored cell membrane receptor that shows increased

28 Lymphocyte antigen 6E (LY6E) is a GPI-anchored, interferon-inducible protein that has been

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

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

31 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

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

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

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

35 Here we model IGD by genetically ablating GPI production in the CNS with a conditional mouse allel

36 enzyme, GPI-N-acetylglucosaminyltransferase (GPI-GnT).

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

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

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

40 intact, glycophosphatidylinositol-anchored (GPI-anchored) PrP was relatively unchanged, forming diff

41 on of glycosylphosphatidylinositol-anchored (GPI-anchored) complement inhibitors.

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

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

44 pha-fucosidase, soluble beta-glucosidase and GPI-anchored beta-glucosidase.

45 t, we have now investigated TfR N-glycan and GPI processing.

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

47 erocomplexes of CrRLK1L receptor kinases and GPI-anchored proteins of the LRE and LLG family.

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

49 annotated 31 novel ORFs of which 24 ORFs are GPI-CWPs.

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

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

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

53 Before GPI adjustment, bleeding reductions with bivalirudin ran

54 canonical binding mode between MBL and beta2-GPI.

55 to amplify similar activities of anti-beta2-GPI Abs in APS and possibly act independently of Abs, ra

56 Because beta2-GPI-mediated MBL-dependent thrombin generation was incre

57 beta2-Glycoprotein I (beta2-GPI) is an abundant plasma glycoprotein with unknown phy

58 MBL and isolated domains II and IV of beta2-GPI, whereas the carbohydrate chains, domain I and domai

59 on and the procoagulant effects of the beta2-GPI/MBL complex may contribute to amplify similar activi

60 mannose-binding lectin (MBL) binds to beta2-GPI in Ca(++) and a dose-dependent manner and that this

61 helial cells because binding of MBL to beta2-GPI was detected on the surface of HUVECs, and colocaliz

62 HUVECs, and colocalization of MBL with beta2-GPI was observed on the endothelium of a biopsy specimen

63 GDE3 releases soluble CNTFRalpha by GPI-anchor cleavage from the plasma membrane and from ex

64 lity to adhere to host tissue is mediated by GPI-anchored cell wall proteins (GPI-CWPs); the correspo

65 mechanism of peptide perception in plants by GPI-anchored proteins that act together with a phylogene

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

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

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

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

70 sted bleeding risk compared with clopidogrel-GPIs.

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

72 her IgG2a response than the positive control GPI-0100, a well-studied semisynthetic saponin adjuvant

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

74 Using flow cytometry, GPI-anchor negative erythrocytes (mutants) were scored a

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

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

77 e resulting model of the membrane-bound Dfg5*GPI-CWP complex is validated by molecular dynamics (MD)

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

79 esis is initiated by a multi-subunit enzyme, GPI-N-acetylglucosaminyltransferase (GPI-GnT).

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

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

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

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

84 hy is seen in other IGDs, flow cytometry for GPI-APs should be considered in the work-ups of individu

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

86 s of function of PIGA, which is required for GPI biosynthesis.

87 f IGD which demonstrates a critical role for GPI biosynthesis in cerebellar and white matter developm

88 iously undocumented cell autonomous role for GPI biosynthesis in NCC development.

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

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

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

92 o assemble N-glycans, O-glycans, a C-glycan, GPI-anchors, and polysaccharides, along with their precu

93 ses/LORELEI-like GLYCOLPHOSPHATIDYLINOSITOL (GPI)-ANCHORED PROTEINS (LLG) complexes, or by leucine-ri

94 ma membrane via a glycophosphatidylinositol (GPI) anchor.

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

96 cal assays with BiPNHP, a non-N-glycosylated GPI-anchored reporter.

97 ar plaques forming from poorly glycosylated, GPI-anchorless prions that interact with extracellular H

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

99 Glycosylphosphatidylinositol (GPI) anchoring plays key roles in many biological proces

100 Glycosylphosphatidylinositol (GPI) anchors attach nearly 150 proteins to the cell memb

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

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

103 Glycosylphosphatidylinositol (GPI)-anchored proteins are critical for embryogenesis, n

104 Glycosylphosphatidylinositol (GPI)-anchored proteins are important for virulence of ma

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

106 ttachment of a glycosylphosphatidylinositol (GPI) anchor to C-terminal omega-peptides, which are used

107 rane through a glycosylphosphatidylinositol (GPI) anchor.

108 IP3 fused to a glycosylphosphatidylinositol (GPI) membrane anchor, immobilizing it on the extracellul

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

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

111 uch as CD14, a glycosylphosphatidylinositol (GPI)-anchored protein to the plasma membrane important f

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

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

114 n (Asn514) and glycosylphosphatidylinositol (GPI) anchor (Ser529) sites.

115 quirements and glycosylphosphatidylinositol (GPI) anchor biosynthesis, as well as identification of m

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

117 wn function as glycosylphosphatidylinositol (GPI) anchors in different kingdoms of life.

118 mer comprising glycosylphosphatidylinositol (GPI)-anchored expression site-associated gene 6 (ESAG6 o

119 osition of its glycosylphosphatidylinositol (GPI) anchor.

120 LEI (LRE)-LIKE GLYCOSYLPHOSPHATIDYLINOSITOL (GPI)-ANCHORED PROTEIN 1 (LLG1) to regulate immune signal

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

122 iosynthesis of glycosylphosphatidylinositol (GPI) is required for anchoring proteins to the plasma me

123 expression of glycosylphosphatidylinositol (GPI)-anchored nonsignaling receptors further improved pa

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

125 ma membrane of glycosylphosphatidylinositol (GPI)-anchored proteins.

126 the sorting of glycosylphosphatidylinositol (GPI)-anchored proteins.

127 centrations of glycosylphosphatidylinositol (GPI)-specific phospholipase D1 (Gpld1), a GPI-degrading

128 bility to shed glycosylphosphatidylinositol (GPI)-anchored proteins from the cell surface.

129 The glycosylphosphatidylinositol (GPI) anchor is a post-translational modification added t

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

131 MDS1), and the glycosylphosphatidylinositol (GPI)-anchored protein LLG1 as regulators of mekk1-mkk1/2

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

133 nd encodes the glycosylphosphatidylinositol (GPI)-linked protein doppel, which is expressed on the su

134 ll surface via glycosylphosphatidylinositol (GPI) play various key roles in the human body, particula

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

136 lycosylation, we provide a rationale for how GPI-CWPs are specifically sorted toward the cell wall by

137 s cytotoxicity by targeting Cdc1 activity in GPI-anchor remodeling in the ER.

138 se cell division control protein 1 (Cdc1) in GPI-anchor remodeling is the key target of CTD, independ

139 Variants in several genes participating in GPI biosynthesis and processing lead to decreased cell s

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

141 l UDP-glycosyltransferase, the first step in GPI biosynthesis, with good selectivity over the human f

142 Patients with pathogenic variants in GPI biosynthesis genes develop diverse phenotypes includ

143 cond metric, termed Group Performance Index (GPI), measures performance of each node as an initiator

144 observed in the Deltagpi7 mutant, indicating GPI-anchored proteins are required for immune evasion.

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

146 hored proteins (GPI-APs) and cause inherited GPI deficiency disorders (IGDs).

147 e, suggesting that severe cases of inherited GPI deficiency and DOORS syndrome might share some molec

148 , which is a characteristic of the inherited GPI deficiency but not DOORS syndrome.

149 severe phenotypes associated with inherited GPI deficiency.

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

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

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

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

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

155 HUI-3), and the Glaucoma Profile Instrument (GPI).

156 cy in a mouse glucose-6-phosphate isomerase (GPI)-induced paw swelling model comparable to that seen

157 Its GPI anchor is modified by the addition of 4-6 alpha-gala

158 ol-anchored proteins (GPI-APs), LORELEI-like-GPI-anchored protein 2 (LLG2) and LLG3, as co-receptors

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

160 In fungi, the final destination of many GPI-anchored proteins is their outermost compartment, th

161 Minor GPI processing was also observed, consistent with alpha-

162 malian cells recognize and degrade misfolded GPI-anchored proteins.

163 teins are degraded by proteasomes, misfolded GPI-anchored proteins are primarily degraded in lysosome

164 R itineraries that not only shield misfolded GPI-anchored proteins during their trafficking, but also

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

166 We conclude that BSF trypanosomes can modify GPIs by generating structures reminiscent of those prese

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

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

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

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

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 Defects in the biosynthesis of GPI anchors in humans lead to inherited glycosylphosphat

174 analogue 7 might be the active component of GPI-0100 responsible for its immunostimulant property.

175 and 6 are presumably the major components of GPI-0100, a widely used complex mixture of semisynthetic

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

177 by altering signaling cascades downstream of GPI-anchored substrate cleavage.

178 teins, which are receptors for the export of GPI-anchored proteins and have been shown to bind a spec

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 thereby further establish the importance of GPI-APs as key regulators in plant reproduction processe

186 or the discovery of antifungal inhibitors of GPI-anchoring of proteins, and identify the oligocyclopr

187 ndergoing PCI was maintained irrespective of GPI administration.

188 animal models due to embryonic lethality of GPI biosynthesis gene null mutants.

189 Despite possessing high levels of GPI-anchored glycoconjugates, SMT-null mutants showed si

190 The plasma membrane localization of GPI-anchored proteins was restored in the p24delta3delta

191 port and transport to the plasma membrane of GPI-anchored proteins.

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

193 g lead to decreased cell surface presence of GPI-anchored proteins (GPI-APs) and cause inherited GPI

194 ls showed decreased cell surface presence of GPI-anchored proteins.

195 ls showed decreased cell surface presence of GPI-APs.

196 orrections were within the coding regions of GPI-CWP genes, our genome assembly establishes a high-qu

197 Removal of GPI-anchored proteins in the wild-type strain by hydrofl

198 n prion disease is due to the replication of GPI-anchored prions, with fibrillar plaques forming from

199 Azole sensitivity of GPI-GnT mutants is also due to decreased H3 acetylation

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

201 1 and IgG2a production is similar to that of GPI-0100, indicating a potential mixed and antigen-speci

202 adjuvant activity profile similar to that of GPI-0100, potentiating mixed Th-1/Th-2 immune responses,

203 subfamily catalyze the essential transfer of GPI-anchored substrates from the plasma membrane to the

204 ta1,3-glycoside complex predicts transfer of GPI-CWP toward the nonreducing ends of acceptor glycans

205 The latter show that impaired transfer of GPI-CWPs causes distorted cell-wall integrity as indicat

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

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

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

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

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

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

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

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

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

215 -0.80%) and negligible for transradial PCI (GPI-adjusted risk difference, 0.09%; 95% CI: -0.32%, 0.5

216 y stained for glycosyl phosphatidylinositol (GPI)-anchored proteins; CD55 and CD59.

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

218 .01-8.17; P = .04) but not with heparin plus GPI (0 vs 3 [0.3%]; P = .30).

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

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

221 bivalirudin and 1412 receiving heparin plus GPI.

222 Ps associated with expression levels of post-GPI attachment to proteins 3, GSDMB, or gasdermin A (3.1

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

224 l surface presence of GPI-anchored proteins (GPI-APs) and cause inherited GPI deficiency disorders (I

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

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

227 cosylphosphatidylinositol-anchored proteins (GPI-APs), LORELEI-like-GPI-anchored protein 2 (LLG2) and

228 mediated by GPI-anchored cell wall proteins (GPI-CWPs); the corresponding genes contain long tandem r

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

230 ed BdBGLC2 (Bd2g51280), which has a putative GPI-anchor sequence, was found associated with the plasm

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

232 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

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

234 arms in subsets receiving and not receiving GPIs.

235 expression of glycosyltransferases, regulate GPI processing.

236 eir physico-chemical properties, to regulate GPI-anchored protein transport and maintain homeostasis

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

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

239 Patients requiring bailout or rescue GPI therapy were excluded.

240 iscriminate between plasma membrane-resident GPI-anchored proteins and those transferred to the cell

241 tion is via H3 acetylation of the respective GPI-GnT gene promoters by Rtt109.

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

243 een at 37 degrees C with RUSH VSVG or a RUSH GPI-anchored construct using a biotin pulse to release t

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

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

248 broblasts rescued the levels of cell surface GPI-APs.

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

250 The Clpex mutation decreases surface GPI expression.

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 We found that GPI-anchored proteins mostly localized to the ER in p24d

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

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

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

259 Theoretical arguments suggest that GPI anchorage could be important for these receptors to

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

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

262 The GPI anchoring can regulate subcellular localization of t

263 The GPI-anchored proteins were found to highly accumulate in

264 asing the spacing between E6 protein and the GPI omega-site (aa 4-7) resulted in extensive post-trans

265 direct interaction between p24delta5 and the GPI-anchored protein arabinogalactan protein4 (AGP4).

266 GPI transamidase complex, which attaches the GPI anchor to proteins.

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

268 Exchanging the GPI anchor for a nonraft transmembrane sequence redirect

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

270 caused by mutations in genes involved in the GPI biosynthesis and remodeling pathway.

271 Our results indicate the GPI anchoring facilitates the penetration of M. oryzae i

272 Biosynthesis and remodeling of the GPI anchor requires the activity of over 20 distinct gen

273 tensive post-translational processing of the GPI anchor to a form that was TL/ECL-reactive, suggestin

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

275 Here, we reveal the roles of the GPI anchoring in Magnaporthe oryzae during plant infecti

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

277 nt to Proteins-2 (Pgap2), a component of the GPI biosynthesis pathway.

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

279 PIGK encodes a component of the GPI transamidase complex, which attaches the GPI anchor

280 T mice, underscoring the pivotal role of the GPI-anchor in driving the aggregate conformation and dis

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

282 glycan fragment screening to reassemble the GPI-core glycan in a U-shaped conformation within its bi

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

284 , transfection with WT PIGK also rescued the GPI-AP levels, but transfection with the two tested muta

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

286 B, which transfers the third mannose to the GPI.

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

288 Thus, GPI anchor remodeling is independent of protein folding

289 nly be a structurally defined alternative to GPI-0100 but also provide a valuable clue for rational d

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

291 ed a novel mouse model of NCC-specific total GPI deficiency.

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

293 We showed previously that two GPI-GnT subunits, encoded by CaGPI2 and CaGPI19, are mut

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

295 fically sorted toward the cell wall by using GPI-core glycan modifications.

296 eins and those transferred to the cell wall (GPI-CWP).

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

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 embrane and only a truncated version without GPI-anchor complemented the mutant, proving that Brachyp