about
Antioxidant c-FLIP inhibits Fas ligand-induced NF-kB activation in a phosphatidylinositol 3-kinase/Akt-dependent mannerThe KSHV oncoprotein vFLIP contains a TRAF-interacting motif and requires TRAF2 and TRAF3 for signalling.Hepatitis B virus polymerase suppresses NF-κB signaling by inhibiting the activity of IKKs via interaction with Hsp90βElevated NF-kappaB responses and FLIP levels in leukemic but not normal lymphocytes: reduction by salicylate allows TNF-induced apoptosisMechanisms of Hsp90 regulationInterplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the HostThe activity of hsp90 alpha promoter is regulated by NF-kappa B transcription factorsFLIP and the death effector domain familyHsp90 inhibitors are efficacious against Kaposi Sarcoma by enhancing the degradation of the essential viral gene LANA, of the viral co-receptor EphA2 as well as other client proteinsProbing 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 SpectroscopyProtein-Protein Interactions Mediated by Helical Tertiary Structure Motifs.Host and viral proteins in the virion of Kaposi's sarcoma-associated herpesvirus.Murine gamma-herpesvirus 68 latency protein M2 binds to Vav signaling proteins and inhibits B-cell receptor-induced cell cycle arrest and apoptosis in WEHI-231 B cells.K13 blocks KSHV lytic replication and deregulates vIL6 and hIL6 expression: a model of lytic replication induced clonal selection in viral oncogenesis.Molecular biology of KSHV in relation to AIDS-associated oncogenesis.Kaposi Sarcoma Herpesvirus (KSHV) Latency-Associated Nuclear Antigen (LANA) recruits components of the MRN (Mre11-Rad50-NBS1) repair complex to modulate an innate immune signaling pathway and viral latencyKSHV and the pathogenesis of Kaposi sarcoma: listening to human biology and medicine.Constitutive NF-kappaB activation, normal Fas-induced apoptosis, and increased incidence of lymphoma in human herpes virus 8 K13 transgenic miceKSHV vCyclin counters the senescence/G1 arrest response triggered by NF-κB hyperactivation.Hsp90 and Hsp40/Erdj3 are required for the expression and anti-apoptotic function of KSHV K1Molecular 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.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.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.The human herpes virus 8-encoded viral FLICE-inhibitory protein induces cellular transformation via NF-kappaB activation.HIV/AIDS: epidemiology, pathophysiology, and treatment of Kaposi sarcoma-associated herpesvirus disease: Kaposi sarcoma, primary effusion lymphoma, and multicentric Castleman disease.Human tumor-associated viruses and new insights into the molecular mechanisms of cancer.Unraveling virus-induced lymphomagenesisKaposi sarcoma-associated herpesvirus-encoded viral FLICE inhibitory protein (vFLIP) K13 cooperates with Myc to promote lymphoma in mice.Kaposi sarcoma herpesvirus (KSHV) vFLIP oncoprotein induces B cell transdifferentiation and tumorigenesis in miceDiethyldithiocarbamate induces apoptosis in HHV-8-infected primary effusion lymphoma cells via inhibition of the NF-κB pathway.Inhibition of the NF-kappaB pathway by varicella-zoster virus in vitro and in human epidermal cells in vivo.KSHV LANA--the master regulator of KSHV latency.Immune evasion by Kaposi's sarcoma-associated herpesvirus.Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and ReactivationKaposi's sarcoma-associated herpesvirus vFLIP and human T cell lymphotropic virus type 1 Tax oncogenic proteins activate IkappaB kinase subunit gamma by different mechanisms independent of the physiological cytokine-induced pathwaysKSHV RTA abolishes NFκB responsive gene expression during lytic reactivation by targeting vFLIP for degradation via the proteasome.Molecular biology of Kaposi's sarcoma-associated herpesvirus and related oncogenesis
P2860
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P2860
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
KSHV vFLIP binds to IKK-gamma to activate IKK.
@en
KSHV vFLIP binds to IKK-gamma to activate IKK.
@nl
type
label
KSHV vFLIP binds to IKK-gamma to activate IKK.
@en
KSHV vFLIP binds to IKK-gamma to activate IKK.
@nl
prefLabel
KSHV vFLIP binds to IKK-gamma to activate IKK.
@en
KSHV vFLIP binds to IKK-gamma to activate IKK.
@nl
P2093
P356
P1476
KSHV vFLIP binds to IKK-gamma to activate IKK.
@en
P2093
Chris Boshoff
Laurent Daviet
Mark Daniels
Mary Collins
Nigel Field
Steven Howell
Walter Low
P304
P356
10.1242/JCS.00691
P407
P577
2003-07-30T00:00:00Z