Figure 6.

Schematic model of the mechanism through which PINK1–Bcl-xL interaction could protect against cell death induced by mitochondrial depolarization. Mitochondrial depolarization induces cleavage of Bcl-xL at the aspartate 61 (D61). The resulting C-terminal fragment (ΔN-Bcl-xL) lacks the anti-apoptotic N-terminal BH4 domain and is a potent inducer of cell death. PINK1 phosphorylates the serine 62 (S62) of Bcl-xL, impairing cleavage at the adjacent D61 site. In this way, the BH4 domain of Bcl-xL is maintained and the full-length protein can exert its anti-apoptotic function