Abstract
Macroautophagy/autophagy is a conserved lysosomal degradation system that breaks down intracellular material through the formation of double-membrane autophagosomes in eukaryotic cells. Cargo receptors have been shown to play essential roles in capturing and delivering specific substrates into phagophores, the precursors to autophagosomes, for degradation. However, the detailed mechanism underlying selective recognition of the substrates for autophagic degradation remains poorly understood. Recently, we have revealed that IFN (interferon)-induced BST2 recruits the E3 ubiquitin ligase MARCH8 to catalyze the K27-linked ubiquitination of MAVS for CALCOCO2-directed autophagic degradation, hence inhibiting DDX58-mediated type I interferon signaling through a negative feedback loop.
Keywords:
BST2; CALCOCO2; MAVS; selective autophagy; type I interferon; ubiquitination.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / metabolism*
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Antigens, CD / metabolism*
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Autophagosomes / metabolism
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Autophagy*
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Cell Line
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DEAD Box Protein 58 / metabolism*
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Feedback, Physiological
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GPI-Linked Proteins / metabolism
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Humans
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Interferon Type I / metabolism*
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Nuclear Proteins / metabolism*
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Proteolysis*
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RNA Virus Infections / immunology
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Receptors, Immunologic
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Ubiquitin-Protein Ligases / metabolism*
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Ubiquitination
Substances
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Adaptor Proteins, Signal Transducing
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Antigens, CD
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BST2 protein, human
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CALCOCO2 protein, human
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GPI-Linked Proteins
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Interferon Type I
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MAVS protein, human
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Nuclear Proteins
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Receptors, Immunologic
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MARCHF8 protein, human
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Ubiquitin-Protein Ligases
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RIGI protein, human
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DEAD Box Protein 58
Grants and funding
This work was supported by National Key Basic Research Program of China (2015CB859800), National Natural Science Foundation of China (31522018, 91629101, 31700760), and Guangzhou Science and Technology Project (201605030012).