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.
about
The p127 subunit (DDB1) of the UV-DNA damage repair binding protein is essential for the targeted degradation of STAT1 by the V protein of the paramyxovirus simian virus 5Identification of a cis-acting element required for shunt-mediated translational initiation of the Sendai virus Y proteins.Complete genome sequence and pathogenicity of two swine parainfluenzavirus 3 isolates from pigs in the United States.Conserved charged amino acids within Sendai virus C protein play multiple roles in the evasion of innate immune responsesMumps virus V protein antagonizes interferon without the complete degradation of STAT1.Identification of paramyxovirus V protein residues essential for STAT protein degradation and promotion of virus replication.AIP1/Alix is a binding partner of Sendai virus C protein and facilitates virus budding.Human parainfluenza virus type 4 is incapable of evading the interferon-induced antiviral effectRinderpest virus phosphoprotein gene is a major determinant of species-specific pathogenicityThe 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 proteinThe amino-terminal extensions of the longer Sendai virus C proteins modulate pY701-Stat1 and bulk Stat1 levels independently of interferon signaling.Paramyxovirus accessory proteins as interferon antagonists.Clustered basic amino acids of the small sendai virus C protein Y1 are critical to its RAN GTPase-mediated nuclear localization.Viruses and the type I interferon antiviral system: induction and evasion.Characterization of the amino acid residues of sendai virus C protein that are critically involved in its interferon antagonism and RNA synthesis down-regulation.Expression of the Sendai (murine parainfluenza) virus C protein alleviates restriction of measles virus growth in mouse cells.Antagonism of innate immunity by paramyxovirus accessory proteins.Overproduction of double-stranded RNA in vesicular stomatitis virus-infected cells activates a constitutive cell-type-specific antiviral responseImportance of the anti-interferon capacity of Sendai virus C protein for pathogenicity in mice.Structural Basis of the Inhibition of STAT1 Activity by Sendai Virus C Protein.An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis.A short peptide at the amino terminus of the Sendai virus C protein acts as an independent element that induces STAT1 instability.Human parainfluenza virus type 2 V protein inhibits genome replication by binding to the L protein: possible role in promoting viral fitness.Studies on the paramyxovirus accessory genes by reverse genetics in the Sendai virus-mouse system.N-terminally truncated C protein, CNDelta25, of human parainfluenza virus type 3 is a potent inhibitor of viral replication.Paramyxovirus Glycoproteins and the Membrane Fusion Process.Newcastle disease virus (NDV)-based assay demonstrates interferon-antagonist activity for the NDV V protein and the Nipah virus V, W, and C proteinsThe STAT2 activation process is a crucial target of Sendai virus C protein for the blockade of alpha interferon signalingDegradation of STAT1 and STAT2 by the V proteins of simian virus 5 and human parainfluenza virus type 2, respectively: consequences for virus replication in the presence of alpha/beta and gamma interferons.The matrix protein of measles virus regulates viral RNA synthesis and assembly by interacting with the nucleocapsid protein.The RIG-I/MAVS signaling pathway in cancer cell-selective apoptosis.Measles virus circumvents the host interferon response by different actions of the C and V proteins.Sendai virus C protein impairs both phosphorylation and dephosphorylation processes of Stat1.Suppression of thermotolerance in mumps virus-infected cells is caused by lack of HSP27 induction contributed by STAT-1.Recombinant Sendai virus vectors for activated T lymphocytes.Intracellular processing of the Sendai virus C' protein leads to the generation of a Y protein module: structure-functional implications.Inhibition of the gamma interferon response by a Sendai virus C protein mutant with no STAT1-binding ability.
P2860
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P2860
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.
description
2001 nî lūn-bûn
@nan
2001 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@ast
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@en
type
label
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@ast
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@en
prefLabel
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@ast
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@en
P2093
P2860
P1433
P1476
Y2, the smallest of the Sendai ...... nhibiting viral RNA synthesis.
@en
P2093
P2860
P304
P356
10.1128/JVI.75.8.3802-3810.2001
P577
2001-04-01T00:00:00Z