p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both

By Derek P. Narendra, L. A. Kane, David N. Hauser, I. Fearnley, R. Youle. Autophagy, 2010

782 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a880b51a85d29d5ee96c766fdf2757efa3b6feb3

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Citations in the corpus

Autophagy: Renovation of Cells and Tissues (2011, background): “When mitochondria are damaged and depolarized, PINK1 becomes stabilized and recruits Parkin to the damaged mitochondria (Matsuda et al., 2010; Narendra et al., 2008; Narendra et al., 2010a; Vives-Bauza et al., 2010).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “…import and processing by PARL is inhibited, leading to the integration of PINK1 into the outer mitochondrial membrane, which is a prerequisite to recruit parkin for the induction of mitophagy (Jin et al , 2010; Matsuda et al , 2010; Narendra et al , 2010b; Meissner et al , 2011) (see below).”
Ubiquitination and selective autophagy (2012, background): “ubiquitinated mitochondria and promotes mitochondrial ‘clumping’, several conflicting reports show that p62 is not responsible for parkin-mediated mitophagy and that VDAC1 is dispensable for both.(79) Concordantly, translocation of Parkin to uncoupled mitochondria and also its induction seems to be ”
Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “The cellular localization of Pink1 is controversial, with proposed locations including the intermembrane space of mitochondria or the outer mitochondrial membrane (Silvestri et al. , 2005 ; Zhou et al. , 2008 ; Narendra et al. , 2010b ).”
Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy (2011, background): “However, p62 appears to be involved in controlling mitochondrial distribution and is not essential for degradation of mitochondria (17,18).”
Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin (2012, background): “In healthy mitochondria, PINK1 levels are kept low through membrane potential dependent import and constitutive turn over (Jin et al., 2010; Narendra et al., 2010b).”
The PINK1-PARKIN mitochondrial ubiquitylation pathway drives a program of TBK1 activation and recruitment of OPTN and NDP52 to promote mitophagy (2015, background): “Early studies suggested that SQSTM1 is responsible for directing damaged mitochondria to the autophagosome (Geisler et al., 2010), but subsequent work revealed that SQSTM1 is required for aggregation of damaged mitochondria but not for mitophagy itself (Narendra et al., 2010).”
PINK1- and Parkin-mediated mitophagy at a glance (2012, background): “…Parkin ubiquitylates numerous outer mitochondrial membrane (OMM) proteins, which in turn recruit other proteins to mitochondria to initiate mitophagy (Chan et al., 2011; Geisler et al., 2010a; Lee et al., 2010b; Narendra et al., 2010a; Tanaka et al., 2010; Yoshii et al., 2011) (see Poster).”
Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization (2013, background): “These include the autophagy adaptor p62, previously linked with mitochondrial clustering after damage 24 , as well as TBC1D15 and DNML1, which are known to interact with FIS1 to regulate fission-fusion cycles.”
The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “However, the requirement of VDAC ubiquitination for mitophagy could not be replicated in a different study.(46) In fact, it is possible that the mere presence of high levels of ubiquitin on the mitochondrial surface, rather than ubiquitination of a particular substrate, is sufficient for induction o”
Phosphorylation of p62 activates the Keap1-Nrf2 pathway during selective autophagy. (2013, background): “, 2005), damaged mitochondria (Narendra et al., 2010), and endosomes ruptured by invasive microbes (Dupont et al.”