Establishment of B-cell lines latently infected with reactivation-competent murine gammaherpesvirus 68 provides evidence for viral alteration of a DNA damage-signaling cascade.
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Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the HostGammaherpesvirus-driven plasma cell differentiation regulates virus reactivation from latently infected B lymphocytes.An in vitro system for studying murid herpesvirus-4 latency and reactivation.Virus-encoded microRNAs facilitate gammaherpesvirus latency and pathogenesis in vivoMurine gammaherpesvirus 68 LANA is essential for virus reactivation from splenocytes but not long-term carriage of viral genome.The murine gammaherpesvirus immediate-early Rta synergizes with IRF4, targeting expression of the viral M1 superantigen to plasma cellsMurine gamma-herpesvirus immortalization of fetal liver-derived B cells requires both the viral cyclin D homolog and latency-associated nuclear antigenViral latency and its regulation: lessons from the gamma-herpesviruses.Activation of NF-κB via endosomal Toll-like receptor 7 (TLR7) or TLR9 suppresses murine herpesvirus 68 reactivation.A gammaherpesvirus cooperates with interferon-alpha/beta-induced IRF2 to halt viral replication, control reactivation, and minimize host lethality.Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.Tiled microarray identification of novel viral transcript structures and distinct transcriptional profiles during two modes of productive murine gammaherpesvirus 68 infection.Amplification of JNK signaling is necessary to complete the murine gammaherpesvirus 68 lytic replication cycle.Alternatively initiated gene 50/RTA transcripts expressed during murine and human gammaherpesvirus reactivation from latencyEfficient infection of a human B cell line with cell-free Kaposi's sarcoma-associated herpesvirus.Is murine gammaherpesvirus-68 (MHV-68) a suitable immunotoxicological model for examining immunomodulatory drug-associated viral recrudescence?Genipin as a novel chemical activator of EBV lytic cycle.RTA Occupancy of the Origin of Lytic Replication during Murine Gammaherpesvirus 68 Reactivation from B Cell Latency.CTCF and Sp1 interact with the Murine gammaherpesvirus 68 internal repeat elements.The de novo methyltransferases DNMT3a and DNMT3b target the murine gammaherpesvirus immediate-early gene 50 promoter during establishment of latency.Lack of heparan sulfate expression in B-cell lines: implications for Kaposi's sarcoma-associated herpesvirus and murine gammaherpesvirus 68 infectionsMurine gammaherpesvirus-68 (MHV-68) is not horizontally transmitted amongst laboratory mice by cage contact.Signaling through Toll-like receptors induces murine gammaherpesvirus 68 reactivation in vivo.Regulation of gammaherpesvirus lytic replication by endoplasmic reticulum stress-induced transcription factors ATF4 and CHOP.
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P2860
Establishment of B-cell lines latently infected with reactivation-competent murine gammaherpesvirus 68 provides evidence for viral alteration of a DNA damage-signaling cascade.
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2008 nî lūn-bûn
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2008年の論文
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2008年論文
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2008年論文
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2008年論文
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2008年論文
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2008年論文
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Establishment of B-cell lines ...... DNA damage-signaling cascade.
@ast
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@en
type
label
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@ast
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@en
prefLabel
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@ast
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@en
P2860
P356
P1433
P1476
Establishment of B-cell lines ...... DNA damage-signaling cascade.
@en
P2093
J Craig Forrest
Samuel H Speck
P2860
P304
P356
10.1128/JVI.02689-07
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P577
2008-05-21T00:00:00Z