KSHV vFLIP is essential for the survival of infected lymphoma cells. - Wikidata - awgldk - TriplyDB

KSHV vFLIP is essential for the survival of infected lymphoma cells.

KSHV vFLIP is essential for the survival of infected lymphoma cells.

http://www.wikidata.org/entity/Q36399405

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The KSHV oncoprotein vFLIP contains a TRAF-interacting motif and requires TRAF2 and TRAF3 for signalling.Stimulation of c-Myc transcriptional activity by vIRF-3 of Kaposi sarcoma-associated herpesvirus The viral etiology of AIDS-associated malignancies KSHV-Mediated Angiogenesis in Tumor Progression Activation of DNA Damage Response Induced by the Kaposi's Sarcoma-Associated Herpes Virus Small molecules targeting viral RNA The Modulation of Apoptotic Pathways by Gammaherpesviruses KSHV Genome Replication and Maintenance Oncogenes and RNA splicing of human tumor viruses Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host Interference with the Autophagic Process as a Viral Strategy to Escape from the Immune Control: Lesson from Gamma Herpesviruses Recent advances on viral manipulation of NF-κB signaling pathway Viral control of mitochondrial apoptosis Azidothymidine Sensitizes Primary Effusion Lymphoma Cells to Kaposi Sarcoma-Associated Herpesvirus-Specific CD4+ T Cell Control and Inhibits vIRF3 Function Probing the Solution Structure of IκB Kinase (IKK) Subunit γ and Its Interaction with Kaposi Sarcoma-associated Herpes Virus Flice-interacting Protein and IKK Subunit β by EPR Spectroscopy Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma.KSHV infects a subset of human tonsillar B cells, driving proliferation and plasmablast differentiation.Histone deacetylase classes I and II regulate Kaposi's sarcoma-associated herpesvirus reactivation.Inhibition of NF-kappaB activation in vivo impairs establishment of gammaherpesvirus latency.K13 blocks KSHV lytic replication and deregulates vIL6 and hIL6 expression: a model of lytic replication induced clonal selection in viral oncogenesis.Integrated microarray and multiplex cytokine analyses of Kaposi's Sarcoma Associated Herpesvirus viral FLICE Inhibitory Protein K13 affected genes and cytokines in human blood vascular endothelial cells.Nucleophosmin phosphorylation by v-cyclin-CDK6 controls KSHV latency.Molecular biology of KSHV in relation to AIDS-associated oncogenesis.Recurrent genomic imbalances in primary effusion lymphomas.Newly emerging therapies targeting viral-related lymphomas.An Sp1 response element in the Kaposi's sarcoma-associated herpesvirus open reading frame 50 promoter mediates lytic cycle induction by butyrate Kaposi's sarcoma-associated herpesvirus-encoded viral FLICE inhibitory protein (vFLIP) K13 suppresses CXCR4 expression by upregulating miR-146a.KSHV and the pathogenesis of Kaposi sarcoma: listening to human biology and medicine.Caspase-7 cleavage of Kaposi sarcoma-associated herpesvirus ORF57 confers a cellular function against viral lytic gene expression.NEMO is essential for Kaposi's sarcoma-associated herpesvirus-encoded vFLIP K13-induced gene expression and protection against death receptor-induced cell death, and its N-terminal 251 residues are sufficient for this process.Constitutive NF-kappaB activation, normal Fas-induced apoptosis, and increased incidence of lymphoma in human herpes virus 8 K13 transgenic mice KSHV vCyclin counters the senescence/G1 arrest response triggered by NF-κB hyperactivation.Molecular biology of human herpesvirus 8: novel functions and virus-host interactions implicated in viral pathogenesis and replication.Viral latency and its regulation: lessons from the gamma-herpesviruses.Efficacy of bortezomib in a direct xenograft model of primary effusion lymphoma Viral FLIP enhances Wnt signaling downstream of stabilized beta-catenin, leading to control of cell growth.Kaposi's sarcoma associated herpesvirus encoded viral FLICE inhibitory protein K13 activates NF-κB pathway independent of TRAF6, TAK1 and LUBAC.A computational profiling of changes in gene expression and transcription factors induced by vFLIP K13 in primary effusion lymphoma Contribution of viral mimics of cellular genes to KSHV infection and disease.Functional analysis of Kaposi's sarcoma-associated herpesvirus vFLIP expression reveals a new mode of IRES-mediated translation.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

http://www.wikidata.org/entity/Q36399405

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年學術文章

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2004年學術文章

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2004年學術文章

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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KSHV vFLIP is essential for the survival of infected lymphoma cells.

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Journal of Experimental Medicine

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Ethel Cesarman

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Ilaria Guasparri

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Shannon A Keller

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P2860

Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations

Modulation of the NF-kappa B pathway by virally encoded death effector domains-containing proteins

Human herpesvirus 8 K1-associated nuclear factor-kappa B-dependent promoter activity: role in Kaposi's sarcoma inflammation?

Cellular FLICE-inhibitory protein splice variants inhibit different steps of caspase-8 activation at the CD95 death-inducing signaling complex

The long form of FLIP is an activator of caspase-8 at the Fas death-inducing signaling complex

Kaposi's sarcoma-associated herpesvirus-like DNA sequences in AIDS-related body-cavity-based lymphomas

Kinetics of Kaposi's sarcoma-associated herpesvirus gene expression.

Activation of NF-kappaB by the human herpesvirus 8 chemokine receptor ORF74: evidence for a paracrine model of Kaposi's sarcoma pathogenesis

Epstein-Barr virus-mediated B-cell proliferation is dependent upon latent membrane protein 1, which simulates an activated CD40 receptor

HHV-8 is associated with a plasmablastic variant of Castleman disease that is linked to HHV-8-positive plasmablastic lymphoma.

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