The Sendai paramyxovirus accessory C proteins inhibit viral genome amplification in a promoter-specific fashion
about
Emerging roles for the influenza A virus nuclear export protein (NEP)NP and L proteins of lymphocytic choriomeningitis virus (LCMV) are sufficient for efficient transcription and replication of LCMV genomic RNA analogsThe paramyxovirus, Sendai virus, V protein encodes a luxury function required for viral pathogenesis.Initiation and regulation of paramyxovirus transcription and replicationConserved charged amino acids within Sendai virus C protein play multiple roles in the evasion of innate immune responsesSendai virus C proteins must interact directly with cellular components to interfere with interferon actionAltered growth characteristics of recombinant respiratory syncytial viruses which do not produce NS2 protein.A role for the Sendai virus P protein trimer in RNA synthesis.Recombinant measles viruses with mutations in the C, V, or F gene have altered growth phenotypes in vivo.The various Sendai virus C proteins are not functionally equivalent and exert both positive and negative effects on viral RNA accumulation during the course of infection.Mutations in the 5' trailer region of a respiratory syncytial virus minigenome which limit RNA replication to one step.Versatility of the accessory C proteins of Sendai virus: contribution to virus assembly as an additional role.Sendai virus C proteins counteract the interferon-mediated induction of an antiviral stateComparison of predicted amino acid sequences of measles virus strains in the Edmonston vaccine lineage.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.Transcription and RNA replication of tacaribe virus genome and antigenome analogs require N and L proteins: Z protein is an inhibitor of these processesAIP1/Alix is a binding partner of Sendai virus C protein and facilitates virus budding.Paramyxovirus assembly and budding: building particles that transmit infections.The NS1 protein of human respiratory syncytial virus is a potent inhibitor of minigenome transcription and RNA replicationInterplay between innate immunity and negative-strand RNA viruses: towards a rational modelThe amino-terminal half of Sendai virus C protein is not responsible for either counteracting the antiviral action of interferons or down-regulating viral RNA synthesisThe amino-terminal extensions of the longer Sendai virus C proteins modulate pY701-Stat1 and bulk Stat1 levels independently of interferon signaling.Clustered basic amino acids of the small sendai virus C protein Y1 are critical to its RAN GTPase-mediated nuclear localization.Given the opportunity, the Sendai virus RNA-dependent RNA polymerase could as well enter its template internally.Defective viral genomes arising in vivo provide critical danger signals for the triggering of lung antiviral immunityEvolution and structural organization of the C proteins of paramyxovirinae.Antagonism of innate immunity by paramyxovirus accessory proteins.Hendra and nipah infection: pathology, models and potential therapies.Emerging paramyxoviruses: molecular mechanisms and antiviral strategiesSuppression of the Sendai virus M protein through a novel short interfering RNA approach inhibits viral particle production but does not affect viral RNA synthesisInhibition of interferon regulatory factor 3 activation by paramyxovirus V protein.Novel Strategy to Control Transgene Expression Mediated by a Sendai Virus-Based Vector Using a Nonstructural C Protein and Endogenous MicroRNAs.Regulation of Viral RNA Synthesis by the V Protein of Parainfluenza Virus 5Active borna disease virus polymerase complex requires a distinct nucleoprotein-to-phosphoprotein ratio but no viral X proteinInhibition of Sendai virus genome replication due to promoter-increased selectivity: a possible role for the accessory C proteins.Human parainfluenza virus type 2 V protein inhibits genome replication by binding to the L protein: possible role in promoting viral fitness.Human parainfluenza virus type 1 C proteins are nonessential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in nonhuman primates.Sendai virus C protein plays a role in restricting PKR activation by limiting the generation of intracellular double-stranded RNA.Studies on the paramyxovirus accessory genes by reverse genetics in the Sendai virus-mouse system.Measles virus nonstructural C protein modulates viral RNA polymerase activity by interacting with host protein SHCBP1
P2860
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P2860
The Sendai paramyxovirus accessory C proteins inhibit viral genome amplification in a promoter-specific fashion
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
1996年论文
@zh
1996年论文
@zh-cn
name
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@ast
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@en
type
label
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@ast
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@en
prefLabel
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@ast
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@en
P2093
P2860
P1433
P1476
The Sendai paramyxovirus acces ...... in a promoter-specific fashion
@en
P2093
Kolakofsky D
Tapparel C
P2860
P304
P407
P577
1996-08-01T00:00:00Z