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• W2968597918 abstract "Tumor necrosis factor (TNF) receptor associated factor-2 (TRAF2) knockout cells were generated to investigate the role of TRAF2 in signaling by TNFR1 and the CD95-type death receptors (DR) TRAILR1/2 and CD95. To prevent negative selection effects arising from the increased cell death sensitivity of TRAF2-deficient cells, cell lines were used for the generation of the TRAF2 knockout (KO) variants that were protected from DR-induced apoptosis downstream of caspase-8 activation. As already described in the literature, TRAF2 KO cells displayed enhanced constitutive alternative NFκB signaling and reduced TNFR1-induced activation of the classical NFκB pathway. There was furthermore a significant but only partial reduction in CD95-type DR-induced upregulation of the proinflammatory NFκB-regulated cytokine interleukin-8 (IL8), which could be reversed by reexpression of TRAF2. In contrast, expression of the TRAF2-related TRAF1 protein failed to functionally restore TRAF2 deficiency. TRAF2-deficiency resulted furthermore in enhanced procaspase-8 processing by DRs but this surprisingly came along with a reduction in net caspase-8 activity. In sum our data argues i) for a non-obligate promoting function of TRAF2 in proinflammatory DR signaling and ii) a yet not recognized stabilizing effect of TRAF2 on caspase-8 activity." @default.
• W2968597918 created "2019-08-22" @default.
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• W2968597918 date "2019-08-29" @default.
• W2968597918 modified "2023-10-02" @default.
• W2968597918 title "TRAF2 Controls Death Receptor-Induced Caspase-8 Processing and Facilitates Proinflammatory Signaling" @default.
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• W2968597918 doi "https://doi.org/10.3389/fimmu.2019.02024" @default.
• W2968597918 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6727177" @default.
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• W2968597918 hasPublicationYear "2019" @default.
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