Critical role of mitochondrial ubiquitination and the OPTN–ATG9A axis in mitophagy

• Published in: The Journal of cell biology Vol. 219; no. 9; p. 1
• Main Authors: Yamano, Koji, Kikuchi, Reika, Kojima, Waka, Hayashida, Ryota, Koyano, Fumika, Kawawaki, Junko, Shoda, Takuji, Demizu, Yosuke, Naito, Mikihiko, Tanaka, Keiji, Matsuda, Noriyuki
• Format: Journal Article
• Language: English
• Published: United States Rockefeller University Press 07.09.2020
• Subjects: Activation; Adapters; Adaptor proteins; Animals; Autophagy; Autophagy - physiology; Autophagy-Related Proteins - metabolism; Binding; Biochemistry; Carrier Proteins - metabolism; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Cells, Cultured; Fluorescence; HCT116 Cells; HEK293 Cells; HeLa Cells; Humans; Mammals - metabolism; Mammals - physiology; Membrane Proteins - metabolism; Membrane Transport Proteins - metabolism; Mitochondria; Mitochondria - metabolism; Mitochondria - physiology; Mitophagy; Mitophagy - physiology; Movement disorders; Neurodegenerative diseases; Organelles; Parkin protein; Parkinson's disease; Phagocytosis; Protein Kinases - metabolism; Proteins; PTEN-induced putative kinase; Ubiquitin; Ubiquitin - metabolism; Ubiquitin-Protein Ligases - metabolism; Ubiquitination; Ubiquitination - physiology; Vesicular Transport Proteins - metabolism

Damaged mitochondria are selectively eliminated in a process called mitophagy. Parkin and PINK1, proteins mutated in Parkinson’s disease, amplify ubiquitin signals on damaged mitochondria with the subsequent activation of autophagic machinery. Autophagy adaptors are thought to link ubiquitinated mit...