IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
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Sequestration and inhibition of Daxx-mediated transcriptional repression by PMLCommon properties of nuclear body protein SP100 and TIF1alpha chromatin factor: role of SUMO modificationSp100 interacts with ETS-1 and stimulates its transcriptional activityEvidence for a role of the cellular ND10 protein PML in mediating intrinsic immunity against human cytomegalovirus infectionsDifferential role of Sp100 isoforms in interferon-mediated repression of herpes simplex virus type 1 immediate-early protein expressionMolecular characterization of NDP52, a novel protein of the nuclear domain 10, which is redistributed upon virus infection and interferon treatmentInteraction of SP100 with HP1 proteins: a link between the promyelocytic leukemia-associated nuclear bodies and the chromatin compartmentChromatin components as part of a putative transcriptional repressing complexEvidence for covalent modification of the nuclear dot-associated proteins PML and Sp100 by PIC1/SUMO-1Cellular localization, expression, and structure of the nuclear dot protein 52Human cytomegalovirus infection causes degradation of Sp100 proteins that suppress viral gene expressionViral immediate-early proteins abrogate the modification by SUMO-1 of PML and Sp100 proteins, correlating with nuclear body disruptionResistance to virus infection conferred by the interferon-induced promyelocytic leukemia proteinConjugation with the ubiquitin-related modifier SUMO-1 regulates the partitioning of PML within the nucleus.Inactivating a cellular intrinsic immune defense mediated by Daxx is the mechanism through which the human cytomegalovirus pp71 protein stimulates viral immediate-early gene expressionEpstein-Barr virus (EBV) SM protein induces and recruits cellular Sp110b to stabilize mRNAs and enhance EBV lytic gene expressionEstablishment of papillomavirus infection is enhanced by promyelocytic leukemia protein (PML) expressionArsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemiaCellular promyelocytic leukemia protein is an important dengue virus restriction factorH-1 parvovirus-associated replication bodies: a distinct virus-induced nuclear structure.Interactions of herpes simplex virus type 1 with ND10 and recruitment of PML to replication compartments.HSV-1 ICP0: An E3 Ubiquitin Ligase That Counteracts Host Intrinsic and Innate ImmunityPrimary biliary cirrhosis (PBC), PBC autoantibodies, and hepatic parameter abnormalities in a large population of systemic sclerosis patientsRegulation of Sp100A subnuclear localization and transcriptional function by EBNA-LP and interferon.Overexpression of promyelocytic leukemia protein precludes the dispersal of ND10 structures and has no effect on accumulation of infectious herpes simplex virus 1 or its proteinsPromyelocytic leukemia protein mediates interferon-based anti-herpes simplex virus 1 effectsReversible silencing of cytomegalovirus genomes by type I interferon governs virus latency.PML is induced by oncogenic ras and promotes premature senescenceKaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen and angiogenin interact with common host proteins, including annexin A2, which is essential for survival of latently infected cells.The Epstein-Barr virus-encoded nuclear antigen EBNA-5 accumulates in PML-containing bodies.The major immediate-early proteins IE1 and IE2 of human cytomegalovirus colocalize with and disrupt PML-associated nuclear bodies at very early times in infected permissive cells.PML nuclear bodies: assembly and oxidative stress-sensitive sumoylation.Identification of new autoantigens for primary biliary cirrhosis using human proteome microarrays.Human cytomegalovirus immediate early interaction with host nuclear structures: definition of an immediate transcript environment.Characterization of Recombinant Human Cytomegaloviruses Encoding IE1 Mutants L174P and 1-382 Reveals that Viral Targeting of PML Bodies Perturbs both Intrinsic and Innate Immune ResponsesA highly amplified mouse gene is homologous to the human interferon-responsive Sp100 gene encoding an autoantigen associated with nuclear dots.The interferon-induced antiviral protein PML (TRIM19) promotes the restriction and transcriptional silencing of lentiviruses in a context-specific, isoform-specific fashion.Sp100 provides intrinsic immunity against human papillomavirus infection.Promyelocytic leukemia-nuclear body proteins: herpesvirus enemies, accomplices, or both?Interplay between Herpesvirus Infection and Host Defense by PML Nuclear Bodies
P2860
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P2860
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
description
1992 nî lūn-bûn
@nan
1992 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1992 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
1992年の論文
@ja
1992年論文
@yue
1992年論文
@zh-hant
1992年論文
@zh-hk
1992年論文
@zh-mo
1992年論文
@zh-tw
1992年论文
@wuu
name
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@ast
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@en
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@nl
type
label
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@ast
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@en
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@nl
prefLabel
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@ast
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@en
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@nl
P2093
P1476
IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis.
@en
P2093
Grötzinger T
Guldner HH
Szostecki C
P304
P407
P577
1992-12-01T00:00:00Z