PMC:4157140 / 27049-28082 JSONTXT

{"project":"2_test","denotations":[{"id":"25175347-21194381-2048466","span":{"begin":894,"end":896},"obj":"21194381"},{"id":"25175347-16738327-2048467","span":{"begin":1031,"end":1033},"obj":"16738327"}],"text":"Oxidative challenge with H2O2 of APOPT1-HA-expressing recombinant fibroblasts led to a prolonged increase in the amount of the mature protein species, suggesting a role for APOPT1 in mitochondrial anti-ROS defense mechanisms. In order to further test this hypothesis, we showed that APOPT1-deficient fibroblasts from individual S2 produce more ROS, whereas overexpression of wild-type APOPT1 leads to a reduction of ROS. We hypothesize that APOPT1 is induced by and plays a protective role under oxidative stress conditions, but it must be otherwise eliminated in standard conditions, at least in cultured cells. A similar mechanism has been demonstrated for other proteins acting at checkpoints in mitochondrial execution pathways, for example PINK1, which is eliminated in bioenergetically proficient mitochondria, but is stabilized by the dissipation of the mitochondrial membrane potential.27 In addition, an analogous mechanism applies to other important metabolic switch systems, such as the hypoxia program induced by HIF-1.28"}