Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
about
ICP0 dismantles microtubule networks in herpes simplex virus-infected cellsThe DNA-damage response in human biology and diseaseA viral E3 ligase targets RNF8 and RNF168 to control histone ubiquitination and DNA damage responsesHSV-1 ICP0: paving the way for viral replicationICP0 inhibits the decrease of HSV amplicon-mediated transgene expression.HSV-1 ICP0: An E3 Ubiquitin Ligase That Counteracts Host Intrinsic and Innate ImmunityAvian reovirus nonstructural protein p17-induced G(2)/M cell cycle arrest and host cellular protein translation shutoff involve activation of p53-dependent pathways.Human herpesvirus 6 suppresses T cell proliferation through induction of cell cycle arrest in infected cells in the G2/M phase.Activation of checkpoint kinase 2 is critical for herpes simplex virus type 1 replication in corneal epitheliumActivation of H2AX and ATM in varicella-zoster virus (VZV)-infected cells is associated with expression of specific VZV genesViral E3 ubiquitin ligase-mediated degradation of a cellular E3: viral mimicry of a cellular phosphorylation mark targets the RNF8 FHA domain.Viral manipulation of DNA repair and cell cycle checkpointsInhibition of ataxia telangiectasia mutated (ATM) kinase suppresses herpes simplex virus type 1 (HSV-1) keratitis.Cell Cycle-Dependent Expression of Adeno-Associated Virus 2 (AAV2) Rep in Coinfections with Herpes Simplex Virus 1 (HSV-1) Gives Rise to a Mosaic of Cells Replicating either AAV2 or HSV-1.An Intrinsically Disordered Region of the DNA Repair Protein Nbs1 Is a Species-Specific Barrier to Herpes Simplex Virus 1 in Primates.H2AX phosphorylation and DNA damage kinase activity are dispensable for herpes simplex virus replication.Initiation of lytic DNA replication in Epstein-Barr virus: search for a common family mechanism.Therapeutic targeting of chemoresistant and recurrent glioblastoma stem cells with a proapoptotic variant of oncolytic herpes simplex virus.Physical interaction between the herpes simplex virus type 1 exonuclease, UL12, and the DNA double-strand break-sensing MRN complex.Dynamic Proteomics of Herpes Simplex Virus Infection.
P2860
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P2860
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
description
2008 nî lūn-bûn
@nan
2008 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@ast
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@en
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@nl
type
label
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@ast
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@en
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@nl
prefLabel
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@ast
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@en
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@nl
P2093
P2860
P1433
P1476
Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth
@en
P2093
David M Krisky
Joseph C Glorioso
Justus B Cohen
Kiflai Bein
Rajasekaran Baskaran
P2860
P356
10.1016/J.VIROL.2008.01.038
P407
P50
P577
2008-05-25T00:00:00Z