Mitochondrial processing peptidase regulates PINK1 processing, import and Parkin recruitment

By Andrew W Greene, Karl Grenier, M. Aguileta, Stephanie Muise, R. Farazifard, M. E. Haque, H. McBride, David S. Park, Edward A. Fon. EMBO Reports, 2012

700 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/01f8dc234331c8ae36efbf369161394314115253

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. R. Youle
2. Edward A. Fon
3. Gian-Luca McLelland
4. H. McBride
5. M. Lazarou
6. Koji Yamano
7. B. Padman
8. T. Nguyen

In Genetics

1. Kentaro Tomii

In Molecular Biology

1. M. Lazarou
2. H. McBride
3. Edward A. Fon
4. Gian-Luca McLelland
5. R. Youle
6. B. Padman
7. T. Nguyen
8. Koji Yamano

Citations in the corpus

• PINK1 is degraded through the N-end rule pathway (2013, background): “Furthermore, PINK1(1-155)-YFP, a mutant with an N-end stabilizing residue was stably localized in the cytosol (Fig.”
• Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control (2014, methodology): “…paradigm, PINK1, a serine/threonine kinase, globally accumulates on depolarized mitochondria and recruits parkin from the cytosol to mitochondria in a manner dependent upon PINK1 phosphorylation activity (Narendra et al, 2008, 2010; Matsuda et al, 2010; Vives-Bauza et al, 2010; Greene et al, 2012).”
• MitoFates: Improved Prediction of Mitochondrial Targeting Sequences and Their Cleavage Sites (2015, background): “important event implicated in efficient protein import (18) and”
• 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.”
• Deciphering the Molecular Signals of PINK1/Parkin Mitophagy. (2016, background): “At the IMM, PINK1 is initially processed by matrix processing peptidase (MPP), which removes PINK1's N-terminal mitochondrial targeting signal [80].”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, unknown): “PINK1 seems to be imported via the TOM/TIM23 complexes at the outer/ inner mitochondrial membrane in a membrane potential-dependent manner for cleaving off its MTS by the mitochondrial processing protease (Greene et al , 2012).”
• A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, background): “During import, PINK1 is first cleaved by the 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;…”