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Tethering ATG16L1 or LC3 induces targeted autophagic degradation of protein aggregates and mitochondria.
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ID: paper-37424101
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Tethering ATG16L1 or LC3 induces targeted autophagic degradation of protein aggregates and mitochondria.
["Mei L", "Chen X", "Wei F", "Huang X", "Liu L", "Yao J", "Chen J", "Luo X", "Wang Z", "Yang A"]
Abstract
Proteolysis-targeting chimeras (PROTACs) based on the ubiquitin-proteasome system have made great progress in the field of drug discovery. There is mounting evidence that the accumulation of aggregation-prone proteins or malfunctioning organelles is associated with the occurrence of various age-related neurodegenerative disorders and cancers. However, PROTACs are inefficient for the degradation of such large targets due to the narrow entrance channel of the proteasome. Macroautophagy (hereafter ...
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