PLSCR3 (phospholipid scramblase 3) may mediate accelerated ATP-independent bidirectional transbilayer migration of phospholipids upon binding calcium ions that results in a loss of phospholipid asymmetry in the plasma membrane. May play a central role in the initiation of fibrin clot formation, in the activation of mast cells and in the recognition of apoptotic and injured cells by the reticuloendothelial system. Members of this family, PLS1 and PLS3 are both substrates of Protein kinase C (PKC) delta and are phosphorylated by PKC-delta during apoptosis. PKC-delta translocates to mitochondria during apoptosis and phosphorylates PLS3. Overexpression of PLS3 in the HEK293 cells enhanced apoptosis induced by UV-irradiation.