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1 1 (IFIT1) is the principal antiviral ISG for parainfluenza virus 5.
2 sequence, FPIV, important for the budding of parainfluenza virus 5.
3 NASEK was dispensable for viruses, including parainfluenza virus 5 and Coxsackie B virus, that enter
5 ructed chimeras containing the ectodomain of parainfluenza virus 5 F (PIV5 F) and either the MPER, th
6 Here we report the crystal structure of the parainfluenza virus 5 F protein in its prefusion conform
7 ess the functional role of the paramyxovirus parainfluenza virus 5 F protein TM domain, alanine scann
9 rystal structure of a fragment of the simian parainfluenza virus 5 fusion protein (SV5 F), revealing
10 , we show that the FP from the paramyxovirus parainfluenza virus 5 fusogenic protein, F, forms an N-t
11 ng globular head domain of the paramyxovirus parainfluenza virus 5 HN protein is entirely dispensable
12 usion activation, F activation involving the parainfluenza virus 5 HN stalk domain, and properties of
17 hat Cav-1 colocalizes with the paramyxovirus parainfluenza virus 5 (PIV-5) nucleocapsid (NP), matrix
20 Proline substitution in this region of HN of parainfluenza virus 5 (PIV5) and Newcastle disease virus
21 erent VLP production platforms, one based on parainfluenza virus 5 (PIV5) and the other based on Nipa
23 rmined the structure of the L-P complex from parainfluenza virus 5 (PIV5) at 4.3- angstrom resolution
24 In this work, we generated a recombinant parainfluenza virus 5 (PIV5) containing NP from H5N1 (A/
27 igh similarity to the structure of prefusion parainfluenza virus 5 (PIV5) F, with the main structural
28 Because only the prefusion structure of the parainfluenza virus 5 (PIV5) F-trimer is available, to s
29 MR spectroscopy, we show that the TMD of the parainfluenza virus 5 (PIV5) fusion protein adopts lipid
30 ucts were coexpressed with the nonhomologous parainfluenza virus 5 (PIV5) fusion protein, indicating
39 To investigate the role of NP protein in parainfluenza virus 5 (PIV5) particle formation, NP prot
40 ation of copyback DVGs readily occurs during parainfluenza virus 5 (PIV5) replication, but that their
42 serendipitously identified a viral mRNA from parainfluenza virus 5 (PIV5) that activates IFN expressi
44 quence variation of 16 different isolates of parainfluenza virus 5 (PIV5) that were isolated from a n
45 unable to be recognized by measles virus and parainfluenza virus 5 (PIV5) V proteins were tested in s
47 he threonine residue at position 286 of P of parainfluenza virus 5 (PIV5) was found phosphorylated.
48 The V proteins of measles virus (MV) and parainfluenza virus 5 (PIV5) were introduced into HFLC u
49 rotein (prefusion form) of the paramyxovirus parainfluenza virus 5 (PIV5) WR isolate was determined.
56 V), human parainfluenza virus 2 (hPIV2), and parainfluenza virus 5 (PIV5), all members of the genus R
59 y, papaverine also inhibited paramyxoviruses parainfluenza virus 5 (PIV5), human parainfluenza virus
60 that a porcine isolate of the paramyxovirus parainfluenza virus 5 (PIV5), known as SER, requires a l
63 hesis that complement (C')-mediated lysis of parainfluenza virus 5 (PIV5)-infected cells would differ
64 , and cellular immunogenicity of intranasal, parainfluenza virus 5 (PIV5)-vectored COVID-19 vaccine C
72 this study, we show that vaccination with a parainfluenza virus 5 recombinant vaccine candidate expr
74 sion (F) protein of the paramxyovirus simian parainfluenza virus 5 (SV5) promotes virus-cell and cell
75 on (F) protein from the paramyxovirus simian parainfluenza virus 5 (SV5) resulted in mutant F protein
76 ined the ability of the paramyxovirus simian parainfluenza virus 5 (SV5) to affect cell cycle progres
77 recently published prefusogenic structure of parainfluenza virus 5/SV5 F places CBF(2) in direct cont
78 ed "stalk exposure model" first proposed for parainfluenza virus 5 to other paramyxoviruses and propo