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

Figure 3 Increased nuclear factor-κB activation in CYLD^-/- mice and analysis of other survival signaling pathways. A: Nuclear factor (NF)-κB transcription factor activation. Assays were performed in triplicates and are representative of two independent experiments. Values represent the mean ± SD; B: Western blot analysis of liver lysates for NF-κB subunits; C: Western blot analysis of liver lysates for p-inhibitor of NF-κB (IκB)-α and IκB-α from untreated (upper), D-GalN/lipopolysaccharide (LPS) (middle) and Jo2 treated (lower panel) WT and CYLD^-/- mice; D: Quantitative real-time polymerase chain reaction (upper panel) and Western blot (lower panel) analysis of NF-κB regulated genes. Mean ± SD are presented; E: Representative immunohistological stainings of RelA in liver sections of D-GalN/LPS and Jo2 treated WT and CYLD^-/- mice (Scale bar: 40 μm); F: Western blot analysis of liver lysates for NF-κB subunits after D-GalN/LPS (left panel) and Jo2 (right panel) injection in WT and CYLD^-/- mice; G: Analysis of survival related pathway activation in untreated (left panels), D-GalN/LPS (middle panels) and Jo2 (right panels) treated WT and CYLD^-/- mice by Western blotting of p-Akt/Akt, p-ERK/ERK and p-JNK/JNK. ^aP < 0.05, WT vs CYLD^-/-; ^bP < 0.01, WT vs CYLD^-/-; ^dP < 0.01, WT vs CYLD^-/-.