TRAF2 is a critical adaptor molecule for TNF receptors in inflammatory and immune signaling. Upon receptor engagement, TRAF2 is recruited to CD40 and translocates to lipid rafts in a RING finger-dependent process, whi...TRAF2 is a critical adaptor molecule for TNF receptors in inflammatory and immune signaling. Upon receptor engagement, TRAF2 is recruited to CD40 and translocates to lipid rafts in a RING finger-dependent process, which enables the activation of downstream kinases. TRAF1 can displace TRAF2 and CD40 from raft fractions, and it promotes the ability of TRAF2 to sustain signal activation. Replacement of the RING finger of TRAF2 with a raft-targeting signal restores JNK activation and association with the cytoskeletal protein Filamin, but not NF-KB activation. TRAF1-/-dendritic cells show attenuated展开更多
Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis acti...Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis activity via the NF κB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC) Methods A stable transfected cell line HNE2 LMP1 was established by introducing LMP1 cDNA into HNE2 cells Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis Apoptosis activity was observed through fluorescence staining Results LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis This induction could be blocked by antisense LMP1 Moreover, LMP1 mediated induction of a TRAF1 promoter driven reporter gene was significantly impaired when the κB site κB1 or κB5 was disrupted, whereas mutation of κB3 had only a minor effect on LMP1 dependent up regulation of the reporter gene Conclusion LMP1 induces TRAF1 expression and promotes its anti apoptosis activity via the NF κB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells展开更多
文摘TRAF2 is a critical adaptor molecule for TNF receptors in inflammatory and immune signaling. Upon receptor engagement, TRAF2 is recruited to CD40 and translocates to lipid rafts in a RING finger-dependent process, which enables the activation of downstream kinases. TRAF1 can displace TRAF2 and CD40 from raft fractions, and it promotes the ability of TRAF2 to sustain signal activation. Replacement of the RING finger of TRAF2 with a raft-targeting signal restores JNK activation and association with the cytoskeletal protein Filamin, but not NF-KB activation. TRAF1-/-dendritic cells show attenuated
基金StateKeyBasicResearchProgram FundamentalInvestigationonHumanCarcinogenesis (No .G19980 5 12 0 1) +1 种基金NationalScienceFundforDistinguishedYoungScholars (No .3 95 2 5 0 2 2 ) theNationalNaturalScienceFoundationofChina (No 3 0 10 0 0 0 5 )
文摘Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis activity via the NF κB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC) Methods A stable transfected cell line HNE2 LMP1 was established by introducing LMP1 cDNA into HNE2 cells Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis Apoptosis activity was observed through fluorescence staining Results LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis This induction could be blocked by antisense LMP1 Moreover, LMP1 mediated induction of a TRAF1 promoter driven reporter gene was significantly impaired when the κB site κB1 or κB5 was disrupted, whereas mutation of κB3 had only a minor effect on LMP1 dependent up regulation of the reporter gene Conclusion LMP1 induces TRAF1 expression and promotes its anti apoptosis activity via the NF κB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells
