IndraLab

"Indeed, tBid initiates a CsA-sensitive process of cristae remodeling that increases cytochrome c availability in the intermembrane space, which is consistent with a PT-dependent facilitation of cytochrome c release even when the outer membrane is intact (Scorrano et al., xref , xref ); and Bax inhibits the mitochondrial inner membrane potassium channel Kv1.3 (Szabó et al., xref ), a proapoptotic effect that critically depends on Bax residue K128 and is abrogated by a K128E mutation, while an E158K mutation in antiapoptotic Bcl-xL (position 158 of Bcl-xL corresponds to position 128 of Bax) turns Bcl-xL into a proapoptotic protein (Szabó et al., xref )."

"We have previously shown that Kv1.3 is inhibited by Bax and contributes to a series of apoptotic events at the level of mitochondria (Szabò et al, xref ; Szabò et al, xref )."