FIGURE 7. Ablation of jnk2 but not jnk1 inhibits caspase-8 activation, Bid cleavage, and mitochondrial cytochrome c release.

A, the cytosolic protein fraction was isolated from the livers of wild-type (+/+) and jnk2 knock-out (−/−) mice that were untreated or treated with GalN/LPS for 6 h. Samples were immunoblotted with antibodies against caspase-8, Bid, and β-actin. The top two panels represent different exposures of the same caspase-8 immunoblot. B, levels of capsase-8 activity in untreated control (Con) and 5-h GalN/LPS-treated wild-type (WT) and jnk2^−/− animals (*, p < 0.02 compared with wild-type mice). C, immunoblots of cytosolic protein fractions from untreated or 6-h GalN/LPS-treated wild-type and jnk1^−/− mice for caspase-8, Bid, and β-actin. D and E, mitochondrial protein fractions were isolated from the same livers as for the cytosolic fractions from wild-type, jnk2 (D), and jnk1 (E) knock-out mice and immunoblotted with antibodies against Bid, cytochrome c (cyto c), and cytochrome oxidase (cyto ox). F, total hepatic protein was isolated from wild-type (+/+) or jnk2 (−/−) knock-out mice that were untreated or treated with GalN/LPS for the indicated number of hours. Western blot analysis was performed with antibodies directed against TRAF-2, c-FLIP, Bax, Bad, phospho-Bad (P-Bad), Bcl-X_L, cellular inhibitor of apoptosis 1 (cIAP1) and 2 (cIAP2), and β-actin. Arrows in A, C, D, and E indicate procaspase-8 and its p43 cleavage product, full size Bid and its cleaved form tBid, and the extra long (EL) and long (L) forms of Bim. Findings are representative of three independent experiments.