Figure 1
From: Inhibition of apoptotic Bax translocation to the mitochondria is a central function of parkin
Primary brain-derived cells demonstrate a muted mitophagic response, but show a parkin-dependent sensitivity to apoptosis. Mouse or rat primary cortical neurons isolated at E18 were treated with 300 nM staurosporine or 10 μM carbonylcyanide-3-chlorophenylhydrazone (CCCP) for stated times. (a) Cytosolic fractions from WT or parkin KO mouse cortical neurons were treated with DMSO, staurosporine (Sts) for 6 h or CCCP for 24 h and probed for parkin and apoptotic markers, and (b) the mitochondrial fractions were analyzed for mitochondrial protein levels. Hash (#) indicates a non-specific band. For quantification, band intensities of proteins in the cytosolic fractions were normalized to WT, and the mitochondrial proteins were normalized to the control (DMSO). (c) WT rat cortical neurons were treated with DMSO, CCCP or staurosporine for times listed and probed for parkin, apoptotic markers and (d) mitochondrial proteins. For quantification, band intensities of proteins from cytosolic and mitochondrial fractions were normalized to vehicle (DMSO). All bars represent mean±S.E.M., n=3. Asterisks indicate significant differences compared with WT or control (P<0.05)
