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1 y with moesin (membrane-organizing extension spike protein).
2 inant viruses were determined largely by the spike protein.
3 ion is mediated by the E1 subunit of the SFV spike protein.
4 S1) and fusion-inducing (S2) subunits of the spike protein.
5 s differing in a hypervariable region of the spike protein.
6 topes in the context of the full-length TGEV spike protein.
7 s prompted us to examine the cleavage of the spike protein.
8 pH-induced conformational changes in the SFV spike protein.
9 bited membrane fusion induced by the MHV JHM spike protein.
10 ect from infection with CoVs using the novel spike protein.
11 antibodies (MAbs) to the ectodomain of HKU1 spike protein.
12 eceptor-binding domain (RBD) of the MERS-CoV Spike protein.
13 proteins, VP6, and two domains from VP4, the spike protein.
14 erences in ground states of their respective spike proteins.
15 ed sites on acid-treated virions or isolated spike proteins.
16 llular processing of newly synthesized viral spike proteins.
17 d with affinities of the receptors for viral spike proteins.
18 tibodies specific for both bat and human CoV Spike proteins.
19 onvoluted extracted ion chromatograms of the spiked proteins.
20 litis replicon particles expressing MERS-CoV spike protein].
21 brane fusion reaction catalyzed by the virus spike protein, a complex containing E1 and E2 transmembr
22 sly undergoes genetic changes to its surface spike protein, a major target of neutralizing antibodies
23 lls in vitro with the murine hepatitis virus spike protein, a natural ligand for the N-domain of CEAC
24 its hACE2-dependent transduction by SARS-CoV spike protein, a successful application of the hot spot
26 he receptor-binding domain (RBD) of MERS-CoV spike protein and DPP4 was determined by crystallography
27 ned receptor-binding domain (RBD) on a viral spike protein and its host receptor, angiotensin-convert
28 y requires specific interactions between the spike protein and lipid rafts, probably during the virus
30 pread, attributed to determinants within the spike protein and possibly perpetuated by suboptimal CD8
31 eceptor-binding domain (RBD) of the MERS-CoV spike protein and thereby competitively blocks the bindi
32 hepatotropism of MHV-JHM depends not on the spike protein and viral entry but rather on a combinatio
34 ace biotinylation of newly synthesized virus spike proteins and retrieval of biotinylated virions usi
35 ectin from hosts, incorporated it into their spike protein, and evolved it into viral receptor-bindin
36 tes that consisted of the same protruding or spike protein antigens of the three viruses in two forma
38 ns recognize different receptors and how the spike proteins are regulated to undergo conformational t
39 annose-type glycans (HMTGs) decorating viral spike proteins are targets for virus neutralization.
40 nating disease, and our model identifies the spike protein as a therapeutic target to prevent axonal
42 y (ca. 70%) of Stx phages via conserved tail spike proteins associated with a short-tailed morphology
43 trigger conformational changes in the viral spike protein at 37 degrees C that facilitate virus entr
44 correlated with the continued degradation of spike proteins at all times of virus infection in sterol
46 hus, the data suggest that the domain of the spike protein between amino acids 417 and 547 is require
48 , inhibit cell infection, and cause envelope spike protein breakdown, including gp120 shedding and, f
49 that deletion of this 197-aa fragment in the spike protein can attenuate a highly virulent PEDV, but
51 urine ( approximately 1.5 muM total protein; spiked protein concentrations were 0.067% of the overall
52 gn for emerging CoVs should involve chimeric spike protein containing neutralizing epitopes from mult
53 e receptor-binding S1 subunit of coronavirus spike proteins contains two distinctive domains, the N-t
54 In contrast, at later times of infection, spike protein degradation was markedly reduced and effic
55 a, the receptor-binding S1 subunits of their spike proteins differ in primary, secondary, and tertiar
56 dding was unaffected by the stability of the spike protein dimer but was a function of the host cell.
61 myelinating strains of MHV, differing in the spike protein expressed, infect neurons and glial cells
62 y be correlated with the high specificity of spike proteins for such glycans expressed in the intesti
63 was able to detect differential abundance of spiked proteins for expected ratios >/=2, with comparabl
66 st the CD4 binding site (CD4bs) on the HIV-1 spike protein gp120 can show exceptional potency and bre
71 tides corresponding to sequences of SARS-CoV spike protein HR1 and HR2 regions and investigated the i
72 the structures and functions of coronavirus spike proteins, illustrating how the two S1 domains reco
74 ese findings identified a novel role for the spike protein in regulating the uncoating and delivery o
80 C (379-388) and A (521-531) epitopes of the spike protein inserted into the 987P major fimbrial subu
81 Proteolytic cleavage of the VP4 outer capsid spike protein into VP8* and VP5* proteins is required fo
85 at the receptor-binding domain (RBD) of HKU1 spike protein is located in the C domain, where the spik
86 ] and non-P[6] strains suggests that the VP4 spike protein is most likely one of the main reasons pre
91 inding to the target cell, the transmembrane spike protein might change conformation by association b
93 prefusion to postfusion conformation of the spike protein must be triggered, leading to membrane fus
95 with Z3A5, a monoclonal antibody against the spike protein of bovine coronavirus (BCV), on an indirec
98 acids, containing the 5B19 epitope from the spike protein of murine hepatitis virus (MHV) and giving
99 against this fragment recognized the native spike protein of SARS CoV in both monomeric and trimeric
101 rotein is located in the C domain, where the spike proteins of alpha-CoVs and beta-CoVs in groups B a
102 uman lung tissue and cleave and activate the spike proteins of the Middle East respiratory syndrome a
105 erential effects of certain mutations in the spike protein on 80R versus ACE2 binding, including esca
106 red in a murine model a range of recombinant spike protein or inactivated whole-virus vaccine candida
107 his study shows that formulation of SARS-CoV spike protein or inactivated whole-virus vaccines with n
108 osable with that of the tail-less phage PRD1 spike protein P5 and the adenovirus knob, domains that i
109 Modeling the binding energies of MERS-CoV spike protein RBD to DPP4 of human (susceptible) or hams
110 determined the crystal structure of NL63-CoV spike protein receptor-binding domain (RBD) complexed wi
111 these two critical functions of coronavirus spike proteins, receptor recognition and membrane fusion
112 roperties of genetically engineered isogenic spike protein recombinant demyelinating and nondemyelina
113 , and most significantly, identifies a novel spike protein region involved in the virus cholesterol r
115 nants which express either the wild-type JHM spike protein (RJHM) or spike containing the N514S mutat
117 studies indicate that SARS-coronavirus (CoV) spike protein (S protein) and its truncated fragments ar
119 Using synthetic biology, we engineered the spike protein (S) from a civet strain, SZ16, into our ep
120 nistration of BHPIV3 expressing the SARS-CoV spike protein (S) induced a high titer of SARS-CoV-neutr
124 rus enters cells through the activities of a spike protein (S) which has receptor-binding (S1) and me
126 d animals all had antibody responses against spike protein S1 fragment and T-cell responses against t
127 d SARS-CoV strain Urbani structural antigens spike protein S1 fragment, membrane protein, and nucleoc
128 lix bundle fusion core structure of MERS-CoV spike protein S2 subunit by X-ray crystallography and bi
129 evere acute respiratory syndrome coronavirus spike protein (SARS-CoV S) can be primed by a variety of
130 -free top-down quantitation strategies using spiked proteins, spectral counting, along with normalize
131 A monoclonal antibody (MAb) (Z3A5) against spike protein subunit of bovine coronavirus (BCV) reacte
133 Our results identify a region of the SFV E2 spike protein subunit that regulates the pH dependence o
134 rred by a single amino acid change in the E1 spike protein subunit, proline 226 to serine, that incre
136 gh neurovirulence is associated with the JHM spike protein, the protein responsible for attachment to
137 n group A, uses the galectin-like NTD in its spike protein to bind its receptor protein, while HCoV-O
140 rom the metastable, nonfusogenic form of the spike protein to the highly stable form involved in fusi
142 eutralizing antibody treatment or a MERS-CoV spike protein vaccine protected the engineered mice agai
143 istally located VP8* domain of the rotavirus spike protein VP4 (ref. 5) mediates such interactions.
146 rted the identification of the P type of the spike protein VP4 of four lapine rotavirus strains as be
148 us cell attachment protein, the outer capsid spike protein VP4, contains the sequence GDE(A) recogniz
150 h a series of intersubunit interactions, the spike protein (VP4) adopts a dimeric appearance above th
151 ntry by trypsin cleavage of the outer capsid spike protein, VP4, into a hemagglutinin, VP8*, and a me
156 t the VP5 cleavage fragment of the rotavirus spike protein, VP4, undergoes a foldback rearrangement t
160 this study, we demonstrated that the surface spike protein VP8* of the major P genotypes of human RVs
161 The distal portion of rotavirus (RV) VP4 spike protein (VP8*) is implicated in binding to cellula
163 peptide, and mutations in this domain of the spike protein were previously shown to shift the pH thre
165 RCV]) was mediated through the N but not the spike protein, whereas weaker cross-reactivity occurred
167 tion, consistent with the association of the spike protein with lipid rafts in the plasma membrane.
168 stribution for the functional domains of the spike proteins within the structure of wild-type Sindbis
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