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注意:仅列出部分参考文献,下载原文获取全部文献信息。Depletion of CoREST Does Not Improve the Replication of ICP0 Null Mutant Herpes Simplex Virus Type 1
Roger D. Everett
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Regulation of ICP0-Null Mutant Herpes Simplex Virus Type 1 Infection by ND10 Components ATRX and hDaxx
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Herpes Simplex Virus Type 1 Regulatory Protein ICP0 Aids Infection in Cells with a Preinduced Interferon Response but Does Not Impede Interferon-Induced Gene Induction
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Promyelocytic leukemia-nuclear body proteins: herpesvirus enemies, accomplices, or both?
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STAT-1- and IRF-3-dependent pathways are not essential for repression of ICP0-null mutant herpes simplex virus type 1 in human fibroblasts
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Herpes Simplex Virus Type 1 ICP0 Phosphorylation Mutants Impair the E3 Ubiquitin Ligase Activity of ICP0 in a Cell Type-Dependent Manner
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Replication of ICP0-Null mutant herpes simplex virus type 1 is restricted by both PML and Sp100
Roger D. Everett et al.
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Herpes simplex virus type 1 genomes are associated with ND10 nuclear substructures in quiescently infected human fibroblasts
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Bright/ARID3A contributes to chromatin accessibility of the immunoglobulin heavy chain enhancer
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Evidence that the herpes simplex virus type 1 ICPO protein does not initiate reactivation from latency in vivo
R. L. Thompson et al.
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Differential role of Sp100 isoforms in interferon-mediated repression of herpes simplex virus type 1 immediate-early protein expression
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PML contributes to a cellular mechanism of repression of herpes simplex virus type 1 infection that is inactivated by ICP0
Roger D. Everett et al.
JOURNAL OF VIROLOGY (2006)
A regulated nucleocytoplasmic shuttle contributes to Bright's function as a transcriptional activator of immunoglobulin genes
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Daxx: death or survival protein?
P Salomoni et al.
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Nomenclature of the ARID family of DNA-binding proteins
D Wilsker et al.
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ND10 components relocate to sites associated with herpes simplex virus type 1 nucleoprotein complexes during virus infection
RD Everett et al.
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Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor bright
J Rajaiya et al.
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Role of ICP0 in the strategy of conquest of the host cell by herpes simplex virus 1
R Hagglund et al.
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Visualization by live-cell microscopy of disruption of ND10 during herpes simplex virus type 1 infection
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E2FBP1/hDril1 modulates cell growth through downregulation of promyelocytic leukemia bodies
Y Fukuyo et al.
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Real time PCR for monitoring regulation of host gene expression in herpes simplex virus type 1-infected human diploid cells
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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 proteins
P Lopez et al.
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A functional screen identifies hDRIL1 as an oncogene that rescues RAS-induced senescence
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Requirements for the nuclear-cytoplasmic translocation of infected-cell protein 0 of herpes simplex virus 1
P Lopez et al.
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ICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency
WP Halford et al.
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Role of cyclin D3 in the biology of herpes simplex virus 1 ICP0
C Van Sant et al.
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The transcription factor, Bright, and immunoglobulin heavy chain expression
CF Webb
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The transcription factor Bright associates with Bruton's tyrosine kinase, the defective protein in immunodeficiency disease
CF Webb et al.
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Alphaherpesvirus proteins related to herpes simplex virus type 1 ICP0 affect cellular structures and proteins
J Parkinson et al.
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Activation of the IκB kinase complex by TRAF6 requires a dimeric ubiquitin-conjugating enzyme complex and a unique polyubiquitin chain
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PML regulates p53 acetylation and premature senescence induced by oncogenic Ras
M Pearson et al.
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Properties and assembly mechanisms of ND10, PML bodies, or PODs
GG Maul et al.
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