Initiation of DNA replication within oriP is dispensable for stable replication of the latent Epstein-Barr virus chromosome after infection of established cell lines.
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Plasticity of DNA replication initiation in Epstein-Barr virus episomesKeeping it quiet: chromatin control of gammaherpesvirus latencyChromatin organization of gammaherpesvirus latent genomes.Cell cycle regulation of chromatin at an origin of DNA replicationThe replicator of the Epstein-Barr virus latent cycle origin of DNA replication, oriP, is composed of multiple functional elements.Establishment of latent Epstein-Barr virus infection and stable episomal maintenance in murine B-cell lines.The dyad symmetry element of Epstein-Barr virus is a dominant but dispensable replication origin.Human DNA replication initiation factors, ORC and MCM, associate with oriP of Epstein-Barr virus.Detection of Epstein-Barr virus genomes in peripheral blood B cells from solid-organ transplant recipients by fluorescence in situ hybridization.Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus.In search of the holy replicatorMolecular virology of Epstein-Barr virus.The plasmid replicon of Epstein-Barr virus: mechanistic insights into efficient, licensed, extrachromosomal replication in human cells.Identifying a property of origins of DNA synthesis required to support plasmids stably in human cells.Telomere repeat binding factors TRF1, TRF2, and hRAP1 modulate replication of Epstein-Barr virus OriPThe latency-associated nuclear antigen, a multifunctional protein central to Kaposi's sarcoma-associated herpesvirus latency.Replication of Epstein-Barr viral DNA.Timeless-dependent DNA replication-coupled recombination promotes Kaposi's Sarcoma-associated herpesvirus episome maintenance and terminal repeat stabilityEfficient replication of Epstein-Barr virus-derived plasmids requires tethering by EBNA1 to host chromosomes.Coupling of mitotic chromosome tethering and replication competence in epstein-barr virus-based plasmids.The replisome pausing factor Timeless is required for episomal maintenance of latent Epstein-Barr virus.Sequences adjacent to oriP improve the persistence of Epstein-Barr virus-based episomes in B cells.Activation of TRAF5 and TRAF6 signal cascades negatively regulates the latent replication origin of Epstein-Barr virus through p38 mitogen-activated protein kinase.The microRNAs of Epstein-Barr Virus are expressed at dramatically differing levels among cell lines.The minimal replicator element of the Kaposi's sarcoma-associated herpesvirus terminal repeat supports replication in a semiconservative and cell-cycle-dependent manner.The latent origin of replication of Epstein-Barr virus directs viral genomes to active regions of the nucleusBacterial artificial chromosomes establish replication timing and sub-nuclear compartment de novo as extra-chromosomal vectors.EBNA1: Oncogenic Activity, Immune Evasion and Biochemical Functions Provide Targets for Novel Therapeutic Strategies against Epstein-Barr Virus- Associated Cancers.
P2860
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P2860
Initiation of DNA replication within oriP is dispensable for stable replication of the latent Epstein-Barr virus chromosome after infection of established cell lines.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Initiation of DNA replication ...... ion of established cell lines.
@en
Initiation of DNA replication ...... ion of established cell lines.
@nl
type
label
Initiation of DNA replication ...... ion of established cell lines.
@en
Initiation of DNA replication ...... ion of established cell lines.
@nl
prefLabel
Initiation of DNA replication ...... ion of established cell lines.
@en
Initiation of DNA replication ...... ion of established cell lines.
@nl
P2093
P2860
P1433
P1476
Initiation of DNA replication ...... ion of established cell lines.
@en
P2093
C L Schildkraut
P2860
P304
P356
10.1128/JVI.74.18.8563-8574.2000
P407
P577
2000-09-01T00:00:00Z