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Taken together, mitophagy plays a dual role in iron-dependent cell death: under physiological states or the early stages of pathogenesis, including the development of oxidative stress, mitophagy degrades damaged mitochondria through negative feedback signaling, preventing ROS generation and hindering the initiation of iron-dependent cell death
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The mechanisms for this selection are largely undetermined, but different mutations at glycine-12 result in altered GTP hydrolysis mediated by KRAS, differential engagement of effector proteins and signalling 7–10
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