Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
about
Hendra and Nipah viruses: different and dangerous.Comparison of predicted amino acid sequences of measles virus strains in the Edmonston vaccine lineage.Identification of paramyxovirus V protein residues essential for STAT protein degradation and promotion of virus replication.Y2, the smallest of the Sendai virus C proteins, is fully capable of both counteracting the antiviral action of interferons and inhibiting viral RNA synthesis.Alteration of Sendai virus morphogenesis and nucleocapsid incorporation due to mutation of cysteine residues of the matrix proteinThe amino-terminal half of Sendai virus C protein is not responsible for either counteracting the antiviral action of interferons or down-regulating viral RNA synthesisC-terminal region of STAT-1alpha is not necessary for its ubiquitination and degradation caused by mumps virus V proteinParamyxovirus accessory proteins as interferon antagonists.Mutations in influenza virus M1 CCHH, the putative zinc finger motif, cause attenuation in mice and protect mice against lethal influenza virus infection.Characterization of the amino acid residues of sendai virus C protein that are critically involved in its interferon antagonism and RNA synthesis down-regulation.Zinc binding activity of human metapneumovirus M2-1 protein is indispensable for viral replication and pathogenesis in vivo.Importance of the anti-interferon capacity of Sendai virus C protein for pathogenicity in mice.Inhibition of interferon regulatory factor 3 activation by paramyxovirus V protein.Studies on the paramyxovirus accessory genes by reverse genetics in the Sendai virus-mouse system.The interferon antagonistic activities of the V proteins from two strains of Newcastle disease virus correlate with their known virulence properties.Virulence of Newcastle disease virus: what is known so far?Paramyxovirus evasion of innate immunity: Diverse strategies for common targets.Neuraminidase inhibition of Dietary chlorogenic acids and derivatives - potential antivirals from dietary sources.Analysis of interaction of Sendai virus V protein and melanoma differentiation-associated gene 5.Newcastle disease virus (NDV)-based assay demonstrates interferon-antagonist activity for the NDV V protein and the Nipah virus V, W, and C proteinsEbola virus transcription activator VP30 is a zinc-binding protein.Newcastle disease virus V protein is associated with viral pathogenesis and functions as an alpha interferon antagonist.A zinc-binding region in Vif binds Cul5 and determines cullin selection.Structural analysis of the STAT1-STAT2 heterodimer revealed the mechanism of Sendai virus C protein-mediated blockade of type 1 interferon signaling.
P2860
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P2860
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
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2000年论文
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name
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@en
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@nl
type
label
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@en
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@nl
prefLabel
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@en
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@nl
P2093
P2860
P1433
P1476
Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.
@en
P2093
Fukuhara N
Kiyotani K
P2860
P304
P356
10.1128/JVI.74.17.7834-7841.2000
P407
P577
2000-09-01T00:00:00Z