Preconditioning Involves Selective Mitophagy Mediated by Parkin and p62/SQSTM1
Published 2011 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Preconditioning Involves Selective Mitophagy Mediated by Parkin and p62/SQSTM1
Authors
Keywords
-
Journal
PLoS One
Volume 6, Issue 6, Pages e20975
Publisher
Public Library of Science (PLoS)
Online
2011-06-18
DOI
10.1371/journal.pone.0020975
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy
- (2011) Nickie C. Chan et al. HUMAN MOLECULAR GENETICS
- Mitochondrial dynamics, cell death and the pathogenesis of Parkinson’s disease
- (2010) Hansruedi Büeler APOPTOSIS
- PINK1/Parkin direct mitochondria to autophagy
- (2010) Cristofol Vives-Bauza et al. Autophagy
- Cyclophilin D is required for mitochondrial removal by autophagy in cardiac cells
- (2010) Raquel S. Carreira et al. Autophagy
- p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both
- (2010) Derek Narendra et al. Autophagy
- Juvenile Exposure to Anthracyclines Impairs Cardiac Progenitor Cell Function and Vascularization Resulting in Greater Susceptibility to Stress-Induced Myocardial Injury in Adult Mice
- (2010) Chengqun Huang et al. CIRCULATION
- Hold Me Tight
- (2010) Monte S. Willis et al. CIRCULATION
- Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy
- (2010) Matthew E. Gegg et al. HUMAN MOLECULAR GENETICS
- Nix Is Critical to Two Distinct Phases of Mitophagy, Reactive Oxygen Species-mediated Autophagy Induction and Parkin-Ubiquitin-p62-mediated Mitochondrial Priming
- (2010) Wen-Xing Ding et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy
- (2010) Noriyuki Matsuda et al. JOURNAL OF CELL BIOLOGY
- PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
- (2010) Sven Geisler et al. NATURE CELL BIOLOGY
- The Mitochondrial Fusion-Promoting Factor Mitofusin Is a Substrate of the PINK1/Parkin Pathway
- (2010) Angela C. Poole et al. PLoS One
- Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin
- (2010) E. Ziviani et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Autophagy Induced by Ischemic Preconditioning is Essential for Cardioprotection
- (2010) Chengqun Huang et al. Journal of Cardiovascular Translational Research
- PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
- (2010) Derek P. Narendra et al. PLOS BIOLOGY
- Parkin-induced mitophagy in the pathogenesis of Parkinson disease
- (2009) Derek Narendra et al. Autophagy
- The mitochondrial permeability transition pore as a target for preconditioning and postconditioning
- (2009) Derek J. Hausenloy et al. BASIC RESEARCH IN CARDIOLOGY
- PINK1-dependent recruitment of Parkin to mitochondria in mitophagy
- (2009) C. Vives-Bauza et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection
- (2008) Hua Yuan et al. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
- Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
- (2008) Derek Narendra et al. JOURNAL OF CELL BIOLOGY
- Autophagy fights disease through cellular self-digestion
- (2008) Noboru Mizushima et al. NATURE
- A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy
- (2008) I. H. Lee et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationCreate your own webinar
Interested in hosting your own webinar? Check the schedule and propose your idea to the Peeref Content Team.
Create Now