Fig. 10. Model for PMA-induced apoptosis involving the signal from the RhoA/ROCK pathway. During PMA treatment, a concurrent signal from LPA or serum upregulates the RhoA/ROCK/MLC phosphorylation pathway, which cooperates with the PMA/PKC signal to generate a membrane contraction force that leads to activation of caspase-8 and -10. In this model, we propose that additional pathways including blocking myosin phosphatase by PKC-mediated upregulation of CPI, the negative control on MLC phosphorylation by cell adhesion, and the subsequent death-receptor-dependent or -independent pathway for activation of caspases-8 and -10, interplay with RhoA/ROCK pathway in PMA-induced apoptosis. Dashed lines represent the pathways that remain to be verified.

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