Fig. 1.

Main molecular mechanisms linking PLSCR1 protein to apoptotic and autophagic processes. A Transient receptor potential canonical 5 (TRPC5) Ca²⁺ channel directly interacts with PLSCR1 and through Ca²⁺ influx activates it, promoting phosphatidylserine (PS) exposure on the outer leaflet of the cell membrane. B PLSCR1 favours p53-dependent apoptosis by association with the protein onzin, the resulting inhibition of Mdm2 phosphorylation/activation by Akt, and thus preserving p53 from proteasome degradation. C The ability of PLSCR1 to bind the complex ATG5/ATG12 complex, replacing the third member ATG16L, inhibits the elongation of the phagophore and autophagosome generation blocking the autophagic process. When autophagy plays an anti-apoptotic role through this mechanism, PLSCR1 promotes programmed cell death