Interactions between Autophagy Receptors and Ubiquitin-like Proteins Form the Molecular Basis for Selective Autophagy
pmid: 24462201
Interactions between Autophagy Receptors and Ubiquitin-like Proteins Form the Molecular Basis for Selective Autophagy
Selective autophagy ensures recognition and removal of various cytosolic cargoes. Hence, aggregated proteins, damaged organelles, or pathogens are enclosed into the double-membrane vesicle, the autophagosome, and delivered to the lysosome for degradation. This process is mediated by selective autophagy receptors, such as p62/SQSTM1. These proteins recognize autophagic cargo and, via binding to small ubiquitin-like modifiers (UBLs)--Atg8/LC3/GABARAPs and ATG5--mediate formation of selective autophagosomes. Recently, it was found that UBLs can directly engage the autophagosome nucleation machinery. Here, we review recent findings on selective autophagy and propose a model for selective autophagosome formation in close proximity to cargo.
- The Arctic University of Norway Norway
- Merck (Germany) Germany
- Goethe University Frankfurt Germany
Models, Molecular, Ubiquitination, Cell Biology, Models, Biological, Autophagy, Peroxisomes, Molecular Biology, Ubiquitins, Signal Transduction
Models, Molecular, Ubiquitination, Cell Biology, Models, Biological, Autophagy, Peroxisomes, Molecular Biology, Ubiquitins, Signal Transduction
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