PINK1 is degraded through the N-end rule pathway

By Koji Yamano, R. Youle. Autophagy, 2013

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The mitophagy pathway and its implications in human diseases (2023, background): “27,28 When mitochondria are damaged (e.g., depolarization of the mitochondrial membrane), the adenine nucleotide translocator (ANT) complex inhibits the translocation of PINK1 to TIM23 by interacting with TIM44, a well-known regulator of TIM23 polypeptide import.”
A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, background): “…matrix processing peptidases and PARL (Jin et al, 2010; Greene et al, 2012); however, almost all of the cleaved PINK1 is then released from the import channel and degraded in the cytosol through the N-end rule proteolytic pathway (Kondapalli et al, 2012; Lazarou et al, 2012; Yamano & Youle, 2013).”
The Roles of PINK1, Parkin and Mitochondrial Fidelity in Parkinson's Disease (2015, background): “PARL cleavage releases the N-terminal-deleted PINK1 into the cytosol where the N-terminal phenylalanine generated by the proteolysis is identified by the N-degron type 2 E3 ubiquitin ligases, according to the N-end rule, and degraded by the ubiquitin proteasome system (Yamano and Youle, 2013).”
Deciphering the Molecular Signals of PINK1/Parkin Mitophagy. (2016, background): “The F104 residue exposes PINK1 as an N-end rule substrate and leads to rapid degradation of PINK1 in the cytosol by the ubiquitin proteasome system [84].”