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Ubiquitination at the mitochondria in neuronal health and disease.
Covill-Cooke, Christian; Howden, Jack H; Birsa, Nicol; Kittler, Josef T.
Afiliação
  • Covill-Cooke C; Neuroscience, Physiology and Pharmacology Department, University College London, Gower Street, London, WC1E 6BT, UK; MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London, WC1E 6BT, UK.
  • Howden JH; Neuroscience, Physiology and Pharmacology Department, University College London, Gower Street, London, WC1E 6BT, UK.
  • Birsa N; UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
  • Kittler JT; Neuroscience, Physiology and Pharmacology Department, University College London, Gower Street, London, WC1E 6BT, UK. Electronic address: j.kittler@ucl.ac.uk.
Neurochem Int ; 117: 55-64, 2018 07.
Article em En | MEDLINE | ID: mdl-28711655
The preservation of mitochondrial function is of particular importance in neurons given the high energy requirements of action potential propagation and synaptic transmission. Indeed, disruptions in mitochondrial dynamics and quality control are linked to cellular pathology in neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Here, we will discuss the role of ubiquitination by the E3 ligases: Parkin, MARCH5 and Mul1, and how they regulate mitochondrial homeostasis. Furthermore, given the role of Parkin and Mul1 in the formation of mitochondria-derived vesicles we give an overview of this area of mitochondrial homeostasis. We highlight how through the activity of these enzymes and MDV formation, multiple facets of mitochondrial biology can be regulated, ensuring the functionality of the mitochondrial network thus preserving neuronal health.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / Ubiquitinação / Mitocôndrias / Neurônios Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / Ubiquitinação / Mitocôndrias / Neurônios Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article