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Quality control of mitochondria: protection against neurodegeneration and ageing.
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Mitochondrial protein quality control systems in aging and disease.
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Mitochondrial dynamics in aging and disease.
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Mitochondria removal by autophagy.
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Mitochondrial dysfunction: mitochondrial diseases and pathways with a focus on neurodegeneration. Preface.
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Loss-of-function of human PINK1 results in mitochondrial pathology and can be rescued by parkin.
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Regulation of mitochondrial fusion and division.
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Functions and dysfunctions of mitochondrial dynamics.
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The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1.
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OPA1 cleavage depends on decreased mitochondrial ATP level and bivalent metals.
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Self-eating and self-killing: crosstalk between autophagy and apoptosis.
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Regulation of the mitochondrial dynamin-like protein Opa1 by proteolytic cleavage.
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OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L.
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Mitochondrial fusion protects against neurodegeneration in the cerebellum.
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OPA1 processing reconstituted in yeast depends on the subunit composition of the m-AAA protease in mitochondria.
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