Recruitment of activated IRF-3 and CBP/p300 to herpes simplex virus ICP0 nuclear foci: Potential role in blocking IFN-beta induction.
about
Different strains of Theiler's murine encephalomyelitis virus antagonize different sites in the type I interferon pathwayHerpes simplex virus-infected cell protein 0 blocks the silencing of viral DNA by dissociating histone deacetylases from the CoREST-REST complexHistone modifications induced by a family of bacterial toxinsProduction of immunogenic West Nile virus-like particles using a herpes simplex virus 1 recombinant vectorInterferon induction by RNA viruses and antagonism by viral pathogensToll-like receptors in antiviral innate immunityDengue Virus Control of Type I IFN Responses: A History of Manipulation and ControlThe nitric oxide pathway provides innate antiviral protection in conjunction with the type I interferon pathway in fibroblastsIFI16 restricts HSV-1 replication by accumulating on the hsv-1 genome, repressing HSV-1 gene expression, and directly or indirectly modulating histone modificationsVaricella-zoster virus immediate-early protein ORF61 abrogates the IRF3-mediated innate immune response through degradation of activated IRF3Role of chromatin during herpesvirus infections.Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responsesThe stability of herpes simplex virus 1 ICP0 early after infection is defined by the RING finger and the UL13 protein kinase.Self protection from anti-viral responses--Ro52 promotes degradation of the transcription factor IRF7 downstream of the viral Toll-Like receptors.ICP0 inhibits the decrease of HSV amplicon-mediated transgene expression.Structural insights into interferon regulatory factor activation.The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.Varicella-zoster virus immediate-early protein 62 blocks interferon regulatory factor 3 (IRF3) phosphorylation at key serine residues: a novel mechanism of IRF3 inhibition among herpesvirusesInterferon regulatory factor 3-dependent pathways are critical for control of herpes simplex virus type 1 central nervous system infection.Herpes simplex virus immediate-early ICP0 protein inhibits Toll-like receptor 2-dependent inflammatory responses and NF-kappaB signalingNuclear IFI16 induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 proteinIdentification of TRIM27 as a novel degradation target of herpes simplex virus 1 ICP0.The differential mobilization of histones H3.1 and H3.3 by herpes simplex virus 1 relates histone dynamics to the assembly of viral chromatinMicrobial strategies for antagonizing Toll-like-receptor signal transduction.Functions of the cytoplasmic RNA sensors RIG-I and MDA-5: key regulators of innate immunity.Innate and adaptive immune responses to herpes simplex virusThe virion host shutoff protein of herpes simplex virus 1 blocks the replication-independent activation of NF-κB in dendritic cells in the absence of type I interferon signaling.A Rhesus Rhadinovirus Viral Interferon (IFN) Regulatory Factor Is Virion Associated and Inhibits the Early IFN Antiviral Response.Interactions of the Antiviral Factor Interferon Gamma-Inducible Protein 16 (IFI16) Mediate Immune Signaling and Herpes Simplex Virus-1 ImmunosuppressionMammalian alphaherpesvirus miRNAs.HSV ICP0 recruits USP7 to modulate TLR-mediated innate responseICP27 protein encoded by bovine herpesvirus type 1 (bICP27) interferes with promoter activity of the bovine genes encoding beta interferon 1 (IFN-β1) and IFN-β3.The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases.Expression of gamma interferon-dependent genes is blocked independently by virion host shutoff RNase and by US3 protein kinaseN-terminal phosphorylation sites of herpes simplex virus 1 ICP0 differentially regulate its activities and enhance viral replication.DNA sensing-independent inhibition of herpes simplex virus 1 replication by DAI/ZBP1Function of RIG-I-like receptors in antiviral innate immunity.Recognition of herpesviruses by the innate immune systemControl of TANK-binding kinase 1-mediated signaling by the gamma(1)34.5 protein of herpes simplex virus 1
P2860
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P2860
Recruitment of activated IRF-3 and CBP/p300 to herpes simplex virus ICP0 nuclear foci: Potential role in blocking IFN-beta induction.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@ast
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@en
type
label
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@ast
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@en
prefLabel
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@ast
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@en
P2093
P2860
P1433
P1476
Recruitment of activated IRF-3 ...... n blocking IFN-beta induction.
@en
P2093
David M Knipe
Gregory T Melroe
Lindsey Silva
Priscilla A Schaffer
P2860
P304
P356
10.1016/J.VIROL.2006.10.028
P407
P577
2006-11-28T00:00:00Z