ライフサイエンスコーパス: glycophorin

1 r connected to actin from outside a cell via glycophorin.

2 ism for the phenotypic diversity of membrane glycophorins.

3 of coronary causes with an antibody against glycophorin A (a protein specific to erythrocytes that f

4 ), CD19 (B lymphocytes), CD16 (Fc receptor), glycophorin A (erythroid lineage cells), and CD71 (trans

5 esidue motifs (GxxxG) in the dimerization of Glycophorin A (GpA) and helped to elucidate the associat

6 The EBA-175/glycophorin A (GPA) and Rh5/basigin ligand-receptor inte

7 Band 3 and glycophorin A (GPA) are the 2 most abundant integral pro

8 We chose glycophorin A (GPA) as a model integral protein to begin

9 to get an unequivocal estimate of the use of glycophorin A (GPA) as a receptor, we found that the 175

10 protein (MCP) and human erythrocyte protein glycophorin A (GpA) contain a GxxxG motif in their TM do

11 The PufX-dimer model on the basis of the glycophorin A (GpA) dimer was constructed, and its robus

12 Human red cell glycophorin A (GPA) enhances the expression of band 3 an

13 ransmembrane domain of the human erythrocyte glycophorin A (GpA) fused to the carboxyl terminus of mo

14 Glycophorin A (GpA) is a well-documented test system for

15 Here we examine this issue using the glycophorin A (GpA) model system, whose homodimeric TM h

16 site strains, plays a key role by binding to glycophorin A (GPA) on the red cell surface, although th

17 alpha-helical MPs bacteriorhodopsin (bR) and glycophorin A (GpA) shows that lost buried surface area

18 We have used the glycophorin A (GPA) somatic cell mutation assay to analy

19 known transmembrane dimerization domain from Glycophorin A (GpA) stimulated dimerization, but was not

20 105 hydrophobic single-point mutants of the glycophorin A (GpA) transmembrane domain.

21 Researchers have studied glycophorin A (GpA) transmembrane helices embedded in so

22 aternity subjects (n = 120); and (b) somatic glycophorin A (GPA) variants in erythrocytes from a grou

23 cture of the dimeric transmembrane domain of glycophorin A (GpA) was determined by solution nuclear m

24 antibody (scFv Ter-119) that binds to mouse glycophorin A (GPA) with a variant human single-chain lo

25 ncy virus type 1 (HIV-1) GP41, human CD4 and glycophorin A (GpA), and influenza virus hemagglutinin (

26 al target genes, including GYPA that encodes glycophorin A (GPA), and the up-regulation of members of

27 -/- red blood cells are completely devoid of glycophorin A (GPA), as assessed by Western blot and imm

28 ein (gp), Rh gp, Landsteiner Wiener (LW) gp, glycophorin A (GPA), Band 3, Lutheran (Lu) gp, and Duffy

29 In GASright dimers, such as glycophorin A (GpA), BNIP3, and members of the ErbB fami

30 inding site into a natural membrane protein, glycophorin A (GpA), structurally characterized by the d

31 h weaker than the dimerization propensity of glycophorin A (GpA), the well-characterized "membrane di

32 A (M2-TMP), and the transmembrane domain of glycophorin A (GpA).

33 -helix from the erythrocyte membrane protein glycophorin A (GPA).

34 he products of C3 cleavage, onto erythrocyte glycophorin A (GPA).

35 we find that the transmembrane helix dimer, glycophorin A (GpATM), is actually much less stable in t

36 Glycophorin A (GYPA) and B (GYPB), which determine MN an

37 imarily on the erythrocyte sialoglycoprotein glycophorin A (GYPA) and erythrocyte-binding antigen 175

38 sfused with RBCs expressing transgenic human glycophorin A (hGPA) antigen in the absence of inflammat

39 that specifically binds the human RBC marker glycophorin A (huGYPA).

40 Using nulls lacking glycophorin A [En(a-)], glycophorin B (S-s-U-) or a comb

41 deformability of erythrocytes by binding to glycophorin A and activating a phosphorylation cascade t

42 lux was partially rescued by coexpression of glycophorin A and also rescued by coexpression of wild-t

43 , glycophorin B (S-s-U-) or a combination of glycophorin A and B (Mk/Mk) we showed that erythrocytes

44 evidence suggest a close interaction between glycophorin A and band 3 during their biosynthesis.

45 he membrane over five alpha-helical turns in glycophorin A and integrin.

46 Larger amounts of both glycophorin A and iron were associated with larger necro

47 Only traces of glycophorin A and iron were found in lesions with pathol

48 interface that strikingly resembles that of glycophorin A and is mediated by an AxxxG motif similar

49 with a pattern similar to that of Bcl-xL and glycophorin A and opposite that of Bcl-2.

50 he replacement of its TM domain with that of glycophorin A and retained signaling.

51 Further, glycophorin A and Rh-associated antigen, which normally

52 lores the possible ligands existing on human glycophorin A and tests their ability to inhibit erythro

53 tional landscapes in the membrane domains of Glycophorin A and the ErbB2 oncogene, and find that inse

54 However, for the glycophorin A and the M2 proton channels, we tend to pre

55 50% of mice develop alloantibodies to human glycophorin A antigen, we found reduced in vitro and in

56 sialic acids on the erythrocyte glycoprotein glycophorin A are a crucial factor for erythrocyte recog

57 utations, band 3, Rh-associated antigen, and glycophorin A are deficient.

58 ith Abs and complement bound to CR1, DAF, or glycophorin A are incubated with model human macrophages

59 ng sites for the heavily sialylated receptor glycophorin A are proposed based on a complex of RII wit

60 ovary (CHO) cells transiently expressing the glycophorin A binding domain of EBA-175, a P falciparum

61 x with the strongly dimerizing TM helix from glycophorin A blocked T-pilus biogenesis in A. tumefacie

62 his study, we report that IC bound to DAF or glycophorin A by an Ab linkage are also transferred to m

63 Increasing the skeletal association of glycophorin A by liganding its extrafacial domain reduce

64 e directly the free energy of association of Glycophorin A by means of extensive parallel Monte Carlo

65 Glycophorin A contains a GxxxG motif that is found in ma

66 The hydrophobic transmembrane domain of glycophorin A contains a sequence motif that mediates di

67 The transmembrane helix of glycophorin A contains a seven-residue motif, LIxxGVxxGV

68 n helices having the structural motif of the glycophorin A dimer and the GxxxG pair.

69 These results refine the structure of the glycophorin A dimer in membrane bilayers and highlight t

70 n the presence of an intact GxxxG motif, the glycophorin A dimer stability can be modulated over a sp

71 Starting from the glycophorin A dimer structure determined by NMR, we perf

72 ine our previously proposed structure of the glycophorin A dimer which revealed that the methyl group

73 f GASright, the GxxxG-containing fold of the glycophorin A dimer, is optimal for the formation of ext

74 imilar to the helix-helix interaction of the glycophorin A dimer, where two transmembrane helices ass

75 To explore the residue interactions in the glycophorin A dimerization motif, an alanine scan double

76 The wide variations in glycophorin a dimmer, stability with the detergent used,

77 gth of the intramembrane dimerization of the glycophorin A domain could be compared quantitatively wi

78 These results indicate that glycophorin A epitopes responsible for antibody and para

79 a progressive decrease in size, increase in glycophorin A expression, and chromatin and nuclear cond

80 n production, and erythroid membrane protein glycophorin A expression.

81 nic mice were generated expressing the human glycophorin A gene and were used to examine how the indu

82 imer interface modulates the strength of the glycophorin A GxxxG-mediated transmembrane dimerization

83 ion of either of the two Gly residues in the glycophorin A GxxxG-motif by Ala or Ser using the recent

84 rgent affects the secondary structure of the glycophorin A helix as measured by far-UV circular dichr

85 dimerization, we used the well-characterized glycophorin A homodimer as a positive standard.

86 of TM helices is laid out and is applied to glycophorin A in both micelles and bilayers.

87 lculated standard association free energy of glycophorin A in N-dodecylphosphocholine micelles is in

88 crosis or thin caps had a marked increase in glycophorin A in regions of cholesterol clefts surrounde

89 serve that the binding of the IgM mAb-C3b to glycophorin A induces a novel unclustering of CR1.

90 Dimerization of the transmembrane domain of glycophorin A is mediated by a seven residue motif LIxxG

91 demonstrate, in an isogenic background, that glycophorin A is required for efficient strain-specific

92 Glycophorin A is the major transmembrane sialoglycoprote

93 ous studies reveal that a single face of the glycophorin A monomer contains a specific glycine-contai

94 The changes in association free energy for glycophorin A mutants can be explained primarily by chan

95 s a merozoite ligand that binds its receptor glycophorin A on erythrocytes during invasion.

96 y to sialic acid and the peptide backbone of glycophorin A on erythrocytes.

97 itions also express normal surface antigens: glycophorin A on erythroid cells, CD15 on myeloid cells,

98 parum invasion ligand, reported to recognize glycophorin A on the surface of erythrocytes.

99 by expressing chimeric proteins of VHHs with Glycophorin A or Kell.

100 acid-dependent pathways requires the EBA-175-glycophorin A pathway for erythrocyte invasion.

101 invasion is partially limited to the EBA-175-glycophorin A pathway, using chymotrypsin-treated erythr

102 data were compared with spectra of monomeric glycophorin A peptides deuterated at Val84.

103 n of EBA-175 is the ligand that binds to the glycophorin A receptor on human erythrocytes and is ther

104 n B retain the ability to bind but a lack of glycophorin A reduced adherence by exflagellating microg

105 dimerization of the transmembrane domain of glycophorin A reproducibly lower the TOXCAT signal more

106 d-tethered peptide both contained the native glycophorin A sequence, the microbeads readily accumulat

107 As for the glycophorin A structure, we find backbone-to-backbone at

108 identity with a transmembrane segment within glycophorin A that forms a portion of its dimer interfac

109 Although the overall sensitivity of glycophorin A tm dimerization to mutagenesis is found to

110 membrane (TM) domain of the chimera with the glycophorin A TM domain causes intramembrane dimerizatio

111 kinases and are critical for stabilizing the glycophorin A TM domain dimer.

112 e TOXCAT system has been used to investigate glycophorin A tm-mediated dimerization.

113 a concentration similar to that required by glycophorin A to block the binding of erythrocyte-bindin

114 the pIgR's transmembrane domain with that of glycophorin A to force dimerization or with a mutant gly

115 portion of the single transmembrane helix of glycophorin A to investigate the structural role of glyc

116 Red blood cells (RBCs) from human glycophorin A transgenic (hGPA-Tg) or wild-type (WT) mic

117 Accompanying experimental results for the glycophorin A transmembrane alpha-helix dimer measured i

118 Deuterium spectra of the glycophorin A transmembrane dimer were obtained using sy

119 part of the strong interaction motif in the glycophorin A transmembrane dimer, in which the pair is

120 able as the dimerization of the well-studied glycophorin A transmembrane dimer, the murine EpoR trans

121 equilibrium studies for point mutants of the glycophorin A transmembrane domain dimer indicate that s

122 support a long standing assumption about the glycophorin A transmembrane domain, that detergents unco

123 ccur between monomer and dimer states of the glycophorin A transmembrane helices during the time-scal

124 s heterodimerization of wild-type and mutant glycophorin A transmembrane helices.

125 steric trap method to the well-characterized glycophorin A transmembrane helix (GpATM) reveals a dime

126 rotein structure, the stability of the human glycophorin A transmembrane helix dimer has been analyze

127 ively examine the sequence dependence of the glycophorin A transmembrane helix dimerization.

128 We find that the glycophorin A transmembrane helix dimerizes with a disso

129 ergy transfer to measure dimerization of the glycophorin A transmembrane helix in detergent micelles.

130 We show that glycines in the glycophorin A transmembrane helix promote extended beta-

131 protein-protein interaction residues in the glycophorin A transmembrane helix-helix dimer was carrie

132 , as a model system, the dimerization of the glycophorin A transmembrane helix.

133 t reported for the right-handed dimer of the glycophorin A transmembrane peptide in similar detergent

134 The 27-residue human erythrocyte protein Glycophorin A transmembrane peptide sequence: KKITLIIFG(

135 stablish a robust protocol for incorporating glycophorin A transmembrane peptides into membrane bilay

136 merization domain with the human erythrocyte glycophorin A transmembrane segment (GpA TM).

137 The results demonstrate that the glycophorin A transmembrane sequence dimerizes when its

138 chain Ab fragment with specificity for mouse glycophorin A was placed under transcriptional control o

139 f the single-spanned transmembrane domain of glycophorin A was used as a model system.

140 ody staining showed that they were CD 45(-), glycophorin A(+) and CD 71(+).

141 o promote both phenotypic (CD36(+), CD33(-), glycophorin A(+)) and morphologic differentiation of the

142 Two trans-membrane helices, WALP-19 and glycophorin A(71-98), were synthesized with Ala-d3 in th

143 rilliant red hemoglobinization, CD71/CD325a (glycophorin A) expression, and exclusively embryonic/fet

144 population of CD43(+)(Leukosialin)/CD235(+)(Glycophorin A) hematopoietic cells, accompanied by incre

145 cells in PV, CD19+, CD3+, CD34+, CD33+, and glycophorin A+ cells and granulocytes were isolated from

146 dritic (CD1a+) cells, 41% of RBC precursors (glycophorin A+), and 32% of monocytic (CD14(+)) cells ex

147 teraction that was comparable in affinity to glycophorin A, a well-studied human blood group antigen

148 ells mutated at a selectively neutral locus, glycophorin A, allow observation of individual stem-cell

149 recedes the appearance of the glycophorin C, glycophorin A, and band III erythroid lineage markers bu

150 nally found at the dimerization interface in glycophorin A, and it promotes dimerization in model sys

151 ne alpha-helices, such as residues 69-101 of glycophorin A, are notoriously difficult to prepare in q

152 4, Na-K-ATPase, sodium/hydrogen exchanger 1, glycophorin A, CD47, Duffy, and Kell is reduced.

153 duced by the strongly dimerizing TM helix of glycophorin A, confirming that the alpha(IIb) TM domain

154 or glycoprotein found on human erythrocytes, glycophorin A, during invasion.

155 However, only one erythrocyte receptor, Glycophorin A, has a well-established cognate parasite l

156 parasite ligand that binds to sialic acid on glycophorin A, in the invasion of erythrocytes by 10 P.

157 ion of the major integral proteins band 3 or glycophorin A, indicating that AQP1 does not exist as a

158 Our predictions of glycophorin A, neu, the M2 channel and phospholamban res

159 Monosaccharides present on human glycophorin A, neuraminyl lactoses, bovine and porcine s

160 c acid moiety of glycophorins, predominantly glycophorin A, or a more complex interaction involving t

161 Tandem spectra of glycopeptides from fetuin, glycophorin A, ovalbumin and gp120 tryptic digests were

162 aced by the strongly dimerizing TM domain of glycophorin A, the EpoR could tolerate the replacement o

163 ding-like domains involved in the binding to glycophorin A, the functional role of regions III-V is l

164 of transmembrane helices of three proteins--glycophorin A, the M2 proton channel, and phospholamban-

165 assay and immunofluorescence, we found that glycophorin A, the most abundant sialoglycoprotein on er

166 te ligand erythrocyte binding antigen 175 to glycophorin A, the most common invasion profile in a pre

167 characterized is the transmembrane domain of glycophorin A, the most extensively studied membrane pro

168 hat BAEBL can bind to erythrocytes that lack glycophorin A, the receptor for EBA-175.

169 ding of EBA-175 to its erythrocyte receptor, glycophorin A, using either native or recombinant EBA-17

170 wn specific skeletal association, band 3 and glycophorin A, were differentially depleted in vesicles.

171 In addition to glycophorin A, where triplets are strongly correlated wi

172 the G79-C(alpha)-H...I76-O hydrogen bond in glycophorin A, whereas a mutagenesis study showed that t

173 Using glycophorin A-bound IC, we observe competition between t

174 viously undescribed mechanism in which large glycophorin A-containing vesicles forming at the cytosol

175 is characterized by the generation of large glycophorin A-decorated vesicles of autophagic origin.

176 These glycophorin A-like helix-helix interactions are enriched

177 Analysis of chimerism in immature (glycophorin A-positive [GYPA(+)], CD71(hi)) and mature (

178 DBMC), NT-DBMC further depleted of CD15+ and glycophorin A-positive cells (NT-LP/DBMC), or purified C

179 FACS on glycophorin A-positive cells showed that approximately 0

180 study was designed to assess the binding of glycophorin A-specific antibodies to polyethylene glycol

181 The binding of glycophorin A-specific antibodies was assessed by hemagg

182 demonstrated a dose-dependent inhibition of glycophorin A-specific antibody binding, CHO cell rosett

183 5 (EBA-175), which binds erythrocyte surface glycophorin A.

184 in a number of membrane proteins, including glycophorin A.

185 f transmembrane sequences, including that of glycophorin A.

186 gM mAb-C3b and IC-C3b substrates attached to glycophorin A.

187 ly reported right-handed motif described for glycophorin A.

188 d with dimerization in other proteins, e.g., glycophorin A.

189 e experimentally determined GxxxG pattern of glycophorin A.

190 interface rotated by 50 degrees relative to glycophorin A.

191 to the transmembrane dimerization domain of glycophorin A.

192 that used by the GXXXG dimerization motif of glycophorin A.

193 shown to be important in the dimerization of glycophorin A.

194 ed in neovessel-containing areas enriched in glycophorin A.

195 imers, GASright, whose best-known example is glycophorin A.

196 ersely related to increases in expression of glycophorin A.

197 ion in E. coli is very weak when compared to glycophorin A.

198 -175) binds to its receptor, sialic acids on glycophorin A.

199 lic acids as well as the protein backbone of glycophorin A.

200 ed on the right-handed dimerization motif of glycophorin A.

201 the erythrocyte-specific cell surface marker glycophorin A.

202 surface is developed here and validated with glycophorin A.

203 sitive receptors to enter the RBCs, of which glycophorins A and B are the prominent ones.

204 of two classes of membrane protein, namely, glycophorin (a simple alpha-helical bundle) and OmpA (a

205 more than 30 healthy human donors of CD45(+)/glycophorin-A (GlyA)(+) cells.

206 and EBA175 and the host erythrocyte receptor Glycophorin-A (GYPA) has been implicated previously.

207 a2-3Gal displayed on the O-linked glycans of glycophorin-A (GYPA).

208 /DBMC; i.e., DBMC depleted of CD3, CD15, and glycophorin-A positive cells) and DBMC positively select

209 nger than 25 amino acids have been prepared: glycophorin-A, prion (110-137), and fibroblast growth fa

210 The glycophorins and an unknown trypsin sensitive factor are

211 aracterized sialic acid-containing receptors glycophorin B (GPB) and glycophorin C (GPC).

212 ompared the sequences of GPA and its homolog glycophorin B (GPB; which does not facilitate band 3 cel

213 alysis, we identified extensive variation in glycophorin B (GYPB) transcript levels in individuals fr

214 Using nulls lacking glycophorin A [En(a-)], glycophorin B (S-s-U-) or a combination of glycophorin A

215 To analyze the degree of dependence on glycophorin B for invasion by P. falciparum through the

216 The high degree of polymorphism in glycophorin B found in malaria-endemic regions suggests

217 ovide evidence from erythrocyte-binding that glycophorin B is a receptor for the P. falciparum protei

218 (Mk/Mk) we showed that erythrocytes lacking glycophorin B retain the ability to bind but a lack of g

219 strain of P. falciparum is not dependent on glycophorin B to invade through a trypsin-resistant path

220 In addition, glycophorin B(+) but not glycophorin B-null erythrocytes

221 2 of EBL-1, expressed on CHO-K1 cells, bound glycophorin B(+) but not glycophorin B-null erythrocytes

222 Rh30 and other Rh-related glycoproteins (LW, glycophorin B) in nonerythroid cells.

223 is trypsin-resistant pathway is dependent on glycophorin B, as P. falciparum strains invade trypsin-d

224 throid specific promoters we tested (GATA-1, glycophorin B, ferrochelatase, porphobilinogen deaminase

225 Other erythroid promoters (GATA-1, glycophorin B, ferrochelatase, porphobilinogen deaminase

226 . falciparum strains invade trypsin-digested glycophorin B-deficient erythrocytes at a highly reduced

227 owever, Indochina I invaded trypsin-digested glycophorin B-deficient erythrocytes at the same efficie

228 ion by 3D7, HB3, and Dd2 of trypsin-digested glycophorin B-deficient erythrocytes was further reduced

229 the P. falciparum 7G8 strain did not invade glycophorin B-deficient erythrocytes, a finding that was

230 Invasion was variably reduced in glycophorin B-deficient erythrocytes.

231 d Indochina I, on trypsin-treated normal and glycophorin B-deficient erythrocytes.

232 rum is able to invade erythrocytes through a glycophorin B-independent, trypsin-resistant pathway.

233 e of these strain, 7G8, also does not invade Glycophorin B-negative erythrocytes.

234 In addition, glycophorin B(+) but not glycophorin B-null erythrocytes adsorbed native EBL-1 fr

235 CHO-K1 cells, bound glycophorin B(+) but not glycophorin B-null erythrocytes.

236 xpanded in response to the high frequency of glycophorin B-null in the population.

237 the Congo have the highest gene frequency of glycophorin B-null in the world, raising the possibility

238 acid changes in the extracellular domain of glycophorin B.

239 The glycophorin/bilayer simulation supports the two-state mo

240 g sialic acid (Sia)-dependent recognition of glycophorins by merozoite erythrocyte-binding proteins,

241 erythrocyte-binding protein that recognizes Glycophorin C (GPC) on the red blood cell (RBC) surface

242 ignificantly enhanced the binding of 4.1R to glycophorin C (GPC), it inhibited the binding of 4.1R to

243 containing receptors glycophorin B (GPB) and glycophorin C (GPC).

244 etic stem cells further supports the role of glycophorin C as a receptor in P vivax rosette formation

245 analogous to the PDZ-domain protein p55 and glycophorin C at the erythrocyte membrane, a similar com

246 rythrocytes that express a truncated form of glycophorin C because it lacks exon 3.

247 We demonstrate that soluble glycophorin C completely blocks the binding of BAEBL (VS

248 is an obligate component of the protein 4.1-glycophorin C complex, which regulates the stability and

249 We conclude from these data that (i) glycophorin C contributes the primary anchoring site of

250 its attachment to the transmembrane protein glycophorin C creates a bridge between the protein netwo

251 N-linked oligosaccharide from the wild-type glycophorin C eliminates its ability to inhibit binding

252 re developed to genotype individuals for the glycophorin C exon 3 deletion associated with Melanesian

253 ax, and the Gerbich-negative modification of glycophorin C for Plasmodium falciparum.

254 N-linked oligosaccharide of Gerbich-negative glycophorin C has a markedly different composition than

255 Glycophorin C immunohistochemical analysis was useful to

256 ycophorin C, leading to reduced retention of glycophorin C in detergent-extracted spectrin/actin skel

257 its docking site on the cytoplasmic pole of glycophorin C is demonstrated to reduce the same protein

258 are present in normal or increased amounts, glycophorin C is missing and XK, Duffy, and Rh are much

259 e in addition to the classic protein 4.1-p55-glycophorin C linkage exists at the RBC junctional compl

260 spectrin and F-actin and with the band 3 and glycophorin C membrane proteins.

261 rum erythrocyte invasion ligand that engages glycophorin C on host erythrocytes during malaria infect

262 s been identified that specifically binds to glycophorin C on red blood cells.

263 o these induced clusters, whereas Band 3 and glycophorin C remain more homogeneously dispersed on the

264 We found that although glycophorin C sorts to reticulocytes normally, it distri

265 entify residues in the cytoplasmic domain of glycophorin C that are critical for its interaction with

266 laps the region of 4.1R involved in the p55, glycophorin C, and 4.1R ternary complex.

267 domains in the ternary complex between p55, glycophorin C, and protein 4.1.

268 omplex directly to the cytoplasmic domain of glycophorin C, but this bridging function has never been

269 9E10) epitope precedes the appearance of the glycophorin C, glycophorin A, and band III erythroid lin

270 all promote dissociation of protein 4.1 from glycophorin C, leading to reduced retention of glycophor

271 gene mutations, lack not only 4.1R but also glycophorin C, which links the cytoskeleton and bilayer.

272 is well established, the contribution of the glycophorin C-protein 4.1 bridge to red cell function re

273 regulating membrane cohesion, rupture of the glycophorin C-protein 4.1 interaction has little effect

274 2 linkages: band 3-ankyrin-beta-spectrin and glycophorin C-protein 4.1-beta-spectrin.(1-7) Although e

275 The band 3-ankyrin-spectrin bridge and the glycophorin C-protein 4.1-spectrin/actin bridge constitu

276 re, suggest that, although regulation of the glycophorin C-protein 4.1-spectrin/actin bridge likely o

277 dly different composition than the wild-type glycophorin C.

278 y for one BAEBL variant (VSTK) that binds to glycophorin C.

279 und for the fluid bilayer and network-linked glycophorin C.

280 tain protein 4.1, adducin, dematin, p55, and glycophorin C.

281 essor) do not bind the cytoplasmic domain of glycophorin C.

282 of the cytoplasmic domain of human erythroid glycophorin C.

283 igand that binds sialic acid on its receptor glycophorin C.

284 d in another erythrocyte, sialoglycoprotein (glycophorin C/D).

285 n fetuin, equine chorionic gonadotropin, and glycophorin can be analyzed in less than 50 min.

286 We find that HAs bound to sialates on glycophorin can participate in fusion as members of the

287 cid-containing oligosaccharides and O-linked glycophorin exhibits Procrit-level in vivo activity in m

288 We analyzed nucleotide diversity of the glycophorin gene family in 15 African populations with d

289 e the identification and analysis of a novel glycophorin He allele, GPHe(GL), which gives rise to the

290 The glycophorin helix dimer is a paradigm for the exploratio

291 The simulated glycophorin helix dimer is remarkably close in structure

292 hat a dynamic equilibrium exists between the glycophorin helix monomer and dimer within a bilayer.

293 esting a role of sialic acid and one or more glycophorins in the binding to a putative gamete recepto

294 to be so characterized was human erythrocyte glycophorin, in 1978.

295 or a more complex interaction involving the glycophorin peptide backbone, is the erythrocyte recepto

296 ropose that either the sialic acid moiety of glycophorins, predominantly glycophorin A, or a more com

297 d in recognizing antigens that correspond to glycophorins, rather than Band 3.

298 rocytes and to bind sialic acid presented on glycophorin, the cell surface molecule bound by type 3 r

299 rotein diffusive motion, that is, band 3 and glycophorin, through the membrane.

300 rin A to force dimerization or with a mutant glycophorin transmembrane domain to prevent dimerization