Epstein-Barr virus lytic replication elicits ATM checkpoint signal transduction while providing an S-phase-like cellular environment.
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Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replicationTORC2, a coactivator of cAMP-response element-binding protein, promotes Epstein-Barr virus reactivation from latency through interaction with viral BZLF1 proteinDNA damage signaling and p53-dependent senescence after prolonged beta-interferon stimulationAsynchronous progression through the lytic cascade and variations in intracellular viral loads revealed by high-throughput single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection.The structure and regulation of Cullin 2 based E3 ubiquitin ligases and their biological functionsThe DNA damage response induced by infection with human cytomegalovirus and other virusesModulation of DNA damage and repair pathways by human tumour virusesPhosphoproteomic analyses reveal signaling pathways that facilitate lytic gammaherpesvirus replicationThe Adenovirus E4orf4 Protein Provides a Novel Mechanism for Inhibition of the DNA Damage ResponseIdentification of Novel Small Organic Compounds with Diverse Structures for the Induction of Epstein-Barr Virus (EBV) Lytic Cycle in EBV-Positive Epithelial MalignanciesNuclear accumulation of the papillomavirus E1 helicase blocks S-phase progression and triggers an ATM-dependent DNA damage responseThe papillomavirus E1 helicase activates a cellular DNA damage response in viral replication fociMislocalization of the MRN complex prevents ATR signaling during adenovirus infection.Viral oncogene-induced DNA damage response is activated in Kaposi sarcoma tumorigenesis.Homologous recombinational repair factors are recruited and loaded onto the viral DNA genome in Epstein-Barr virus replication compartments.Degradation of phosphorylated p53 by viral protein-ECS E3 ligase complex.Chromatin at the intersection of viral infection and DNA damageNoise cancellation: viral fine tuning of the cellular environment for its own genome replication.Activation and repression of Epstein-Barr Virus and Kaposi's sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acidsHepatitis C virus NS5B protein delays s phase progression in human hepatocyte-derived cells by relocalizing cyclin-dependent kinase 2-interacting protein (CINP).Avian reovirus nonstructural protein p17-induced G(2)/M cell cycle arrest and host cellular protein translation shutoff involve activation of p53-dependent pathways.Epstein-Barr virus BGLF4 kinase retards cellular S-phase progression and induces chromosomal abnormality.Human cytomegalovirus inhibits a DNA damage response by mislocalizing checkpoint proteinsAn ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cellsViral carcinogenesis: factors inducing DNA damage and virus integrationHuman herpesvirus 6 suppresses T cell proliferation through induction of cell cycle arrest in infected cells in the G2/M phase.Phosphorylation of MCM4 at sites inactivating DNA helicase activity of the MCM4-MCM6-MCM7 complex during Epstein-Barr virus productive replication.A novel mechanism inducing genome instability in Kaposi's sarcoma-associated herpesvirus infected cells.Cell cycle modulation by Marek's disease virus: the tegument protein VP22 triggers S-phase arrest and DNA damage in proliferating cells.Gammaherpesvirus gene expression and DNA synthesis are facilitated by viral protein kinase and histone variant H2AX.DNA Damage Signaling Is Induced in the Absence of Epstein-Barr Virus (EBV) Lytic DNA Replication and in Response to Expression of ZEBRA.Conserved herpesvirus kinases target the DNA damage response pathway and TIP60 histone acetyltransferase to promote virus replication.Proteomic profiling of the human cytomegalovirus UL35 gene products reveals a role for UL35 in the DNA repair responseThe lytic phase of epstein-barr virus requires a viral genome with 5-methylcytosine residues in CpG sites.Epstein-Barr virus BGLF4 kinase induces premature chromosome condensation through activation of condensin and topoisomerase II.Gamma-herpesvirus kinase actively initiates a DNA damage response by inducing phosphorylation of H2AX to foster viral replicationCoordinate regulation of DNA damage and type I interferon responses imposes an antiviral state that attenuates mouse gammaherpesvirus type 68 replication in primary macrophages.Enhanced phosphorylation of transcription factor sp1 in response to herpes simplex virus type 1 infection is dependent on the ataxia telangiectasia-mutated proteinEstablishment & characterization of lymphoblastoid cell lines from patients with multiple primary neoplasms in the upper aero-digestive tract & healthy individuals.Chloroquine triggers Epstein-Barr virus replication through phosphorylation of KAP1/TRIM28 in Burkitt lymphoma cells
P2860
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P2860
Epstein-Barr virus lytic replication elicits ATM checkpoint signal transduction while providing an S-phase-like cellular environment.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh
2004年學術文章
@zh-hant
name
Epstein-Barr virus lytic repli ...... ase-like cellular environment.
@en
type
label
Epstein-Barr virus lytic repli ...... ase-like cellular environment.
@en
prefLabel
Epstein-Barr virus lytic repli ...... ase-like cellular environment.
@en
P2093
P2860
P356
P1476
Epstein-Barr virus lytic repli ...... ase-like cellular environment.
@en
P2093
Ayumi Kudoh
Hiroki Isomura
Lumin Zhang
Masatoshi Fujita
Noriko Shirata
Tatsuya Tsurumi
Tohru Daikoku
Yukihiro Nishiyama
Yutaka Sugaya
P2860
P304
P356
10.1074/JBC.M411405200
P407
P577
2004-12-15T00:00:00Z