Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin

By Atsushi Tanaka, Megan M. Cleland, Shan Xu, Derek P. Narendra, D. Suen, M. Karbowski, R. Youle. Journal of Cell Biology, 2010

1,356 citations recorded by the source corpus.

The Parkin ubiquitin ligase marks the mitofusins Mfn1 and Mfn2 for proteasome-dependent degradation, promoting disposal of damaged mitochondria by preventing their fusion with healthy organelles.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/ded264605f355088d43819f6f41324da7e017f54

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Citations in the corpus

The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin.”
Mitochondrial Cristae: Where Beauty Meets Functionality. (2016, background): “For example, Mitofusin 2 is ubiquitinated by the E3 Ub-ligase Parkin [77,78] and phosphorylated by c-Jun N terminal kinase (JNK) [79].”
The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “In this process, parkin ubiquitinates multiple mitochondrial substrates, including proteins involved in mitochondrial fusion [303, 304], leading to their degradation by the UPS and mitophagy [305].”
Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control (2014, methodology): “In the time-course experiment, cells were treated with DMSO, 25 lM antimycin A, 25 lM antimycin A and 10 lM oligomycin, 25 lM antimycin A and 50 lM EUK134, and 20 lM CCCP for the indicated time prior to fixation.”
Ubiquitination and selective autophagy (2012, background): “By selective degradation of mitofusin, Parkin can inhibit re-fusion of mitochondria.(84) Recognition of damaged mitochondria for selective removal can be initiated by integral mitochondrial membrane proteins.”
The Roles of PINK1, Parkin and Mitochondrial Fidelity in Parkinson's Disease (2015, background): “appears to be necessary for mitophagy (Chan et al., 2011; Tanaka et al., 2010).”
Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “In addition, p97, an AAA + ATPase, also accumulates on mitochondria in a Parkin-dependent manner to promote the degradation of outer mitochondrial membrane proteins and mitophagy (Tanaka et al. , 2010 ).”
Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy (2011, background): “Inhibition of either p97 or the proteasome also blocks mitophagy, but it is unclear whether this effect is due to the prevention of mitofusin degradation (32).”
Autophagy: Renovation of Cells and Tissues (2011, background): “Parkin can induce degradation of a broad range of mitochondrial outer membrane proteins, such as mitofusin 1/2 and Tom20 (Chan et al., 2011; Tanaka et al., 2010; Yoshii et al., 2011), which may also be important for mitochondrial quality control.”
Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization (2013, background): “1,5,6,7,8,10,11 The MOM porin proteins VDAC1/2/3 are also ubiquitylated by PARKIN, and are required for PARKIN localization on mitochondria through a poorly understood mechanism.”
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, positive): “PARK2 translocates to damaged mitochondria and ubiquitinates a wide range of outer membrane proteins including VDAC1, MFN1/2 and TOMM20/TOM20.(755,761,762,787) This results in the preferential degradation of mitochondrial outer membrane proteins by the proteasome, while inner membrane proteins and m”