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1 infectivity by binding to the E2 (envelope) surface glycoprotein.
2 Clr-a as a disulfide-linked homodimeric cell surface glycoprotein.
3 tive metacyclic forms expressing the variant surface glycoprotein.
4 receptor-binding site on the haemagglutinin surface glycoprotein.
5 osomes, of pre-existing cell surface variant surface glycoprotein.
6 quence changes in the V3 region of the gp120 surface glycoprotein.
7 hatidylinositol-anchored (GPI-anchored) cell surface glycoprotein.
8 e third hypervariable (V3) loop of the HIV-1 surface glycoprotein.
9 contained mutations in the hr1 region of the surface glycoprotein.
10 on CTLs may be linked to reduced motility of surface glycoproteins.
11 rated into O-GlcNAcylated proteins over cell-surface glycoproteins.
12 e trafficking, activity, and localization of surface glycoproteins.
13 g, corroborating an increase in high mannose surface glycoproteins.
14 well-characterized antigenic changes in the surface glycoproteins.
15 ,6GlcNAc-branched N-glycans attached to cell surface glycoproteins.
16 masking glycan ligands on midgut epithelial surface glycoproteins.
17 ot motif found in multisubunit external cell surface glycoproteins.
18 rus (VSV) or Ross River virus (RRV) envelope surface glycoproteins.
19 ed alpha2,3 or alpha2,6 sialic acids on cell surface glycoproteins.
20 Here we report that CTB binds cell surface glycoproteins.
21 binding to terminally sialylated glycans on surface glycoproteins.
22 ee new anti-HIV aptamers targeting the viral surface glycoprotein 120 (gp120) were selected, synthesi
23 ntitrypanosomal drug, suramin, via invariant surface glycoprotein 75, and in the uptake of trypanosom
24 ce proteomes, being dominated by the variant surface glycoprotein (African) or mucins (American) resp
25 orption of an antibody specific for a virion surface glycoprotein allowed differentiation of MCMV fro
26 quence) gene family encodes eight large cell-surface glycoproteins (Als1-Als7 and Als9) that have adh
27 cyclophilin C or rotamase) to the CD147 cell surface glycoprotein (also known as extracellular matrix
28 orchestrated via the concerted action of two surface glycoproteins: an attachment protein called hema
29 t stage, enabling rapid recycling of variant surface glycoprotein and antibody clearance from the sur
31 the hemagglutinin (HA) or neuraminidase (NA) surface glycoprotein and other influenza virus proteins.
33 rophobic helical structures, from the HCV E2 surface glycoprotein and the CD81 protein, a major host
35 any cellular processes by oligomerizing cell surface glycoproteins and glycolipids into higher-order
36 iversity, and selection pressure between the surface glycoproteins and internal gene segments of avia
37 cine include the variability of the envelope surface glycoproteins and its high-density glycan shield
38 anism for regulation of the activity of cell-surface glycoproteins and likely contributes to maintena
39 ptamer conjugates against two different cell surface glycoproteins and show that these reagents are a
42 to date have incorporated the RSV fusion (F) surface glycoprotein, because the sequence of F is highl
45 nveloped viruses often require cleavage of a surface glycoprotein by a cellular endoprotease such as
47 We reported that removing a specific set of surface glycoproteins by ex vivo treatment with O-sialog
51 n MSC expression of the multifunctional cell surface glycoprotein CD44, a putative stem cell marker.
53 ding bovine submaxillary mucin and leukocyte surface glycoproteins CD45 and P-selectin glycoprotein l
58 hell in a rationally arranged fashion with a surface glycoprotein coated on to the surface and non-st
59 the viral polymerases and the hemagglutinin surface glycoprotein conferred respiratory droplet trans
61 ly active isoforms: a membrane-spanning cell surface glycoprotein (csCSF-1), a secreted proteoglycan
63 the lack of structural information about its surface glycoproteins E1 and E2, the two constituents of
67 ei results in derepression of silent variant surface glycoprotein ESs, as had previously been shown f
68 that is driven primarily by soluble variant surface glycoprotein exposure, and it may be that IFN-al
69 cell adhesion molecule (EpCAM) (CD326) is a surface glycoprotein expressed by invasive carcinomas an
70 ly protein basigin (EMMPRIN/CD147) is a cell surface glycoprotein expressed by tumor cells that stimu
71 cell adhesion molecule-2 (CEACAM2) is a cell-surface glycoprotein expressed on blood, epithelial, and
72 BAI1 (termed Vstat120) requires CD36, a cell surface glycoprotein expressed on microvascular endothel
74 crothrombocytopenic and had reduced platelet surface glycoprotein expression, including GPVI, alphaII
76 condly, knockdown of clathrin or the variant surface glycoprotein failed to perturb transcription.
77 rculating antibodies against the Ebola virus surface glycoprotein for more than a decade after infect
79 s bind GlcNAc-branched N-glycans attached to surface glycoproteins, forming a molecular lattice that
81 clonal antibodies using a set of recombinant surface glycoproteins from Reston, Tai Forest, Bundibugy
86 the Rhabdoviridae family, contains a single surface glycoprotein (G) that is responsible for attachm
87 endocytosis, a process mediated by the virus surface glycoprotein (G), but the cellular factors and p
90 ted a monoclonal antibody raised against CMV surface glycoprotein (gB) with gold nanoparticles (GNP)
92 ar stomatitis virus (serotype Indiana) whose surface glycoprotein gene was replaced by the Zaire Ebol
94 elomeric regions rich in life-stage-specific surface glycoprotein genes involved in pathogenesis.
95 anosome relies upon the silencing of variant surface glycoprotein genes that are found adjacent to te
96 criptional switching of subtelomeric variant surface glycoprotein genes, continues to operate indepen
97 d involves switches in expression of variant surface glycoprotein genes, which are co-transcribed wit
98 ere identified using antibodies against ANDV surface glycoproteins Gn and Gc to competitively elute a
100 s expressing the Ebola virus (Zaire species) surface glycoprotein (GP) alone or in combination with t
103 monoclonal antibodies (MAbs) that target the surface glycoprotein (GP) of Ebola virus (EBOV) are effe
106 a proinflammatory signature triggered by the surface glycoprotein (GP), which can be inhibited by blo
111 two amino acid changes, one within the virus surface glycoprotein (GP1: F260L) and the other within t
112 cleaved by cellular proteases to the mature surface glycoprotein gp120 and the transmembrane glycopr
114 hly variable and immunogenic region of HIV-1 surface glycoprotein gp120, and structural information a
116 Previous work has demonstrated that the surface glycoprotein (gp120) of human immunodeficiency v
117 of a transmembrane glycoprotein (gp41) and a surface glycoprotein (gp120), and forms trimers on the s
119 imeric complex of heterodimers composed of a surface glycoprotein, gp120, and a transmembrane compone
121 pathogenic and nonpathogenic members, whose surface glycoproteins (GPs) are characterized by differe
126 Influenza C viruses have only one major surface glycoprotein, HEF (hemagglutinin-esterase fusion
127 s and detailed molecular mechanisms of viral surface glycoprotein hemagglutinin (HA) binding with a b
129 o induce neutralizing antibodies against the surface glycoprotein hemagglutinin (HA) is the primary m
130 ified amino acids in antigenic site B of the surface glycoprotein hemagglutinin (HA) that explain the
131 nic properties are largely determined by the surface glycoprotein hemagglutinin (HA), and amino acid
132 n occurs through the binding formed by viral surface glycoprotein hemagglutinin and certain types of
133 differences, which generally agreed with the surface glycoprotein hemagglutinin esterase phylogeny, w
134 us and have been licensed for human use, the surface glycoproteins hemagglutinin (HA) and neuraminida
135 s with the cell surface is controlled by the surface glycoproteins hemagglutinin (HA) and neuraminida
136 l-mediated immunity, often against the viral surface glycoproteins hemagglutinin (HA) and neuraminida
137 e transmissibility is the interaction of the surface glycoproteins hemagglutinin (HA) and neuraminida
138 luenza virus induces antibodies to the viral surface glycoproteins hemagglutinin and neuraminidase, a
141 ody responses against the hemagglutinin (HA) surface glycoprotein; however, the diversity of HAs acro
142 infectious virus in the absence of their own surface glycoprotein if a suitable glycoprotein from a f
144 mulated with the trypanosome soluble variant surface glycoprotein in vitro and in macrophages taken f
145 le NST gene results in measurable defects in surface glycoproteins in different life cycle stages of
146 this question, we profiled the abundance of surface glycoproteins in WT and CRISPR-mediated GNPTAB(-
148 ect expression and functions of CD44, a cell-surface glycoprotein influencing immunologic, inflammato
149 ring with the endocytic transport of variant surface glycoprotein is a highly desirable strategy for
150 an EBOV vaccine candidate in which the viral surface glycoprotein is biomanufactured as a fusion to a
153 ies maintained a similar organization of the surface glycoproteins, matrix protein (M), M2-1, and the
154 nsional density maps show how the hantavirus surface glycoproteins, membrane, and ribonucleoprotein a
155 essing the hepatitis B virus middle envelope surface glycoprotein (MS) that induces strong MS-specifi
156 ic responses to Pneumocystis jirovecii major surface glycoprotein (Msg) antigen in African cohorts, o
157 ne responses to Pneumocystis jirovecii major surface glycoprotein (Msg) in individuals with human imm
161 t fragments that span the P. jirovecii major surface glycoprotein: MsgA (amino terminus), MsgB (middl
164 homophilic interaction mediated by the cell surface glycoprotein MUC18 (also known as melanoma cell
165 principal target for these drugs is a virus surface glycoprotein, neuraminidase, which facilitates t
166 cosylation of HA and the other two major IAV surface glycoproteins, neuraminidase (NA) and M2 ion cha
167 sion of the hemagglutinin-neuraminidase (HN) surface glycoprotein of human parainfluenza virus type 3
168 richia coli was able to solubilize the major surface glycoprotein of Pneumocystis, thus potentially f
172 stomatitis virus-based vaccine expressing a surface glycoprotein of Zaire Ebolavirus (rVSV-ZEBOV) is
173 ee adenovirus 3 (ChAd3) vaccine encoding the surface glycoprotein of Zaire ebolavirus (ZEBOV) to 60 h
177 al basis of the interaction of the two major surface glycoproteins of influenza A virus with their co
178 (NA) is a sialidase that is one of the major surface glycoproteins of influenza A viruses and the tar
181 ect energy utilization and synthesis of cell-surface glycoproteins or glycolipids involved in cell mo
182 tope on O-glycans linked to a leukocyte cell-surface glycoprotein, P-selectin Glycoprotein Ligand-1 (
183 requires the virus RING finger Z protein and surface glycoprotein precursor (GPC) and the correct pro
184 P) of the lymphocytic choriomeningitis virus surface glycoprotein precursor has several unique charac
185 ife cycle, beyond translocation of the viral surface glycoprotein precursor into the endoplasmic reti
186 timulated by direct Gal-1 engagement to cell surface glycoproteins, principally CD45, on activated Th
192 Here, we report the structure of the JUNV surface glycoprotein receptor-binding subunit (GP1) boun
194 vanced glycation end-products and other cell surface glycoprotein receptors on MDSC, signal through t
197 MHC-encoded butyrophilin, BTN2A1, is a cell surface glycoprotein related to the extended family of B
200 nv) and influenza hemagglutinin (HA) are the surface glycoproteins responsible for viral entry into h
201 ins and the glycan ligands presented on cell surface glycoproteins results in high-avidity binding th
202 of entry of HIV-1 pseudotyped with SARS-CoV surface glycoprotein S (SARS-S) but not that of HIV-1 ps
203 ainst axonal guidance cues, such as the cell surface glycoproteins Semaphorin 1a (Sema 1a) and Fascic
204 RPs, when administered intranasally, induced surface glycoprotein-specific virus neutralizing antibod
205 class I-related chain A (MICA) antigens are surface glycoproteins strongly implicated in innate immu
206 rom the FeLV-A prototype, FeLV-A/61E, in the surface glycoprotein (SU) and long terminal repeat (LTR)
209 A strong antiviral response to the viral surface glycoprotein (SU) was noted in both natural and
210 tions and, therefore, reduce the motility of surface glycoproteins, such as the T-cell receptor.
211 ce proteins, especially a unique and complex surface glycoprotein superfamily, as well as proteases a
212 c sugar composition of the parasites variant surface glycoprotein synthesized in cells incubated in 5
213 glycosyl phosphatidylinositol-anchored cell surface glycoprotein T-cadherin (encoded by Cdh13) prote
214 Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both ex
216 B, type I (SR-BI), is a homooligomeric cell surface glycoprotein that controls HDL structure and met
217 ound that antibodies to glycoprotein (g)B, a surface glycoprotein that has been developed as a HCMV v
219 the LIM-domain factors with axonin1, a cell surface glycoprotein that is a member of the immunoglobu
221 (TF) (CD142) is a 47 kDa transmembrane cell surface glycoprotein that triggers the extrinsic coagula
222 on protein PrP(C) is a Cu(2)(+)-binding cell surface glycoprotein that, when misfolded, is responsibl
223 driven by antigenic changes (drift) in viral surface glycoproteins that allow evasion from preexistin
224 , FRbeta and FRgamma) are cysteine-rich cell-surface glycoproteins that bind folate with high affinit
225 eptors (KIR) are structurally unrelated cell surface glycoproteins that evolved independently to func
226 sion molecules-A, -B, and -C (Jams) are cell surface glycoproteins that have been shown to play an im
227 rogrammed death ligand 1) and PD-L2 are cell-surface glycoproteins that interact with programmed deat
228 patibility (MHC) class II molecules are cell surface glycoproteins that present extracellular antigen
229 y specific carbohydrate moieties on specific surface glycoproteins that serve as receptors for typhoi
230 A and B influenza viruses contain two major surface glycoproteins: the hemagglutinin (HA) and the ne
231 nfluenza viruses bind by their hemagglutinin surface glycoprotein to sialic acid (N-acetylneuraminic
235 how that TIV, which is formulated to contain surface glycoproteins to induce serotype-specific antibo
238 ody that binds carbonic anhydrase IX, a cell surface glycoprotein ubiquitously expressed in clear cel
240 components are proteases, which cleave viral surface glycoproteins, unleashing them to refold in ways
243 ends upon switches in its protective Variant Surface Glycoprotein (VSG) coat by antigenic variation.
245 se by repeatedly replacing its dense variant surface glycoprotein (VSG) coat from its large genomic V
246 ckness, constantly changes its dense variant surface glycoprotein (VSG) coat to avoid elimination by
251 is protected by an essential coat of Variant Surface Glycoprotein (VSG) comprising approximately 10%
252 ut twenty telomeric bloodstream form Variant Surface Glycoprotein (VSG) expression sites (BESs), of w
253 of the RNA polymerase I transcribed variant surface glycoprotein (VSG) expression sites (ESs) of Try
254 tion is altered at telomere-proximal variant surface glycoprotein (VSG) expression sites (ESs), sugge
255 lation of telomere-proximal silenced variant surface glycoprotein (VSG) expression sites and procycli
256 in the human bloodstream, expresses variant surface glycoprotein (VSG) from 1 of 15 bloodstream expr
257 -I) to transcribe just one telomeric variant surface glycoprotein (VSG) gene at a time, producing sup
258 , Trypanosoma brucei transcribes its variant surface glycoprotein (VSG) gene expression sites (ESs) i
259 RNA polymerase I (Pol I)-transcribed variant surface glycoprotein (VSG) gene expression sites (ESs),
260 cated within the silent subtelomeric variant surface glycoprotein (VSG) gene expression sites, but no
261 rough DNA-repair processes involving Variant Surface Glycoprotein (VSG) gene rearrangements at subtel
262 ression of one of about 20 telomeric variant surface glycoprotein (VSG) gene-expression sites (ESs) w
263 pression and reversible silencing of variant surface glycoprotein (VSG) genes found adjacent to telom
265 rypanosoma brucei is used for moving variant surface glycoprotein (VSG) genes into expression sites d
266 s upon rearrangement of subtelomeric variant surface glycoprotein (VSG) genes to achieve antigenic va
267 expresses one of approximately 1500 variant surface glycoprotein (VSG) genes while multiplying in th
268 can trypanosomes possess hundreds of variant surface glycoprotein (VSG) genes, but only one is expres
269 ution of a massive archive of silent Variant Surface Glycoprotein (VSG) genes, which are activated by
275 at consists of ten million copies of variant surface glycoprotein (VSG) that is expressed from a sing
276 y switches its major surface antigen variant surface glycoprotein (VSG) to evade mammalian host immun
277 ssing its major surface antigen, the Variant Surface Glycoprotein (VSG), in a monoallelic manner.
278 lies on RNA Pol I for expressing the variant surface glycoprotein (VSG), the key protein in antigenic
284 directed homologous recombination of Variant Surface Glycoproteins (VSG) genes, most of which reside
285 on due to antigenic variation of the Variant Surface Glycoproteins (VSG) that coat parasites while th
286 eriodically replacing a monolayer of variant surface glycoproteins (VSG) that covers its cell surface
287 arly, defective glycosylation of the variant surface glycoprotein (VSG221) as well as the lysosomal m
288 he sequential expression of distinct variant surface glycoproteins (VSGs) at extremely high density o
292 n of bloodstream-form T. brucei, the variant surface glycoprotein, was unaffected in the TbGT8 mutant
295 ated by structurally diverse classes of cell-surface glycoproteins, which form homophilic or heteroph
297 leased from intracellular organelle and cell surface glycoproteins, while maintaining histopathology
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