Apoptotic stress (300 nM, 5 h) or CCCP (10 μ M, 24 h) did not induce quantifiable mitochondrial translocation of parkin and showed a trend for decreased TOM20 that was not statistically significant, while both treatments also increased apoptotic markers ( Figures 1c and d ).
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Inhibition of apoptotic Bax translocation to the mitochondria is a central function of parkin.
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