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A general model for the role of PUS10 in apoptosis. Our study revealed caspase-3-mediated translocation of PUS10 from nucleus to mitochondria (thick lines) with concurrent release of cytochrome c and SMAC, and a reciprocal increase in caspase-3 activity. Release of cytochrome c could increase caspase-3 activity through the apoptosome and caspase-9 pathway and SMAC released from the mitochondria could sequester XIAP, thus removing inhibition of caspase-3 activity
