CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes

Figure 4 Increased resistance and induction of anti-apoptotic genes in CYLD^-/- PMH after death receptor triggering. A: Freshly isolated PMH were treated for 24 h with increasing concentrations of tumor necrosis factor (TNF)-α and (B) Jo2 in combination with actinomycin D (ActD) as well as with (C) SuperFasLigand (SFL) as indicated; D: Western blot analysis of caspase activation in WT and CYLD^-/- PMH after 4 h TNF-α/ActD, Jo2/ActD and SFL treatment with the indicated concentrations; E: Western blot analysis of WT and CYLD^-/- PMH for nuclear factor (NF)-κB dependent gene expression after TNF-α (left panel) and Jo2 (right panel) treatment. ^bP < 0.01, WT vs CYLD^-/-; ^dP < 0.01, WT vs CYLD^-/-.