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Fig. 7. Steps in ER-stress-induced apoptosis and communication of this signaling event from the ER to the mitochondria by the PKC ${delta}$ -Abl complex. Several steps in the transduction of ER stress signaling leading to apoptosis have been identified. (Step 1) ER stress triggers translocation of PKC ${delta}$ to the ER where it binds to Abl and is (directly or indirectly) phosphorylatedon tyrosine residues by Abl. (Step 2) The PKC ${delta}$ -Abl complex translocates to mitochondria in a process that depends on PKC ${delta}$ catalytic activity. Abl is required for PKC ${delta}$ translocation to the mitochondria and, vice versa, PKC ${delta}$ is required for Abl translocation to this organelle. (Step 3) PKC ${delta}$ -Abl complex activates JNK-mediated mitochondrium-dependent apoptotic cascade. The PKC ${delta}$ -specific peptide inhibitor ${delta}$ V1-1, inhibits PKC ${delta}$ translocation to the ER and the subsequent interaction of PKC ${delta}$ and Abl, thereby suppressing ER-stress-mediated apoptosis. Rottlerin, an inhibitor of PKC ${delta}$ catalytic activity, blocks the translocation of PKC ${delta}$ -Abl complex to mitochondria and, thus, inhibits ER-stress-induced mitochondrium-dependent apoptosis.

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