Inaugural Article: Ubiquitin signals autophagic degradation of cytosolic proteins and peroxisomes

By P. Kim, D. Hailey, R. Mullen, Jennifer Lippincott-Schwartz. 2008

559 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/df37575675158bb990c95fd04ede010e0811428a

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Citations in the corpus

Regulation Mechanisms and Signaling Pathways of Autophagy (2009, background): “p62 directly binds both poly- or mono-ubiquitin via its ubiquitin-associated (UBA) domain and the mammalian Atg8 homolog, LC3 (microtubule-associated protein 1 light chain 3) (64,110), and links the ubiquitinated cargos to the autophagy machinery for autophagic degradation.”
Interactions between autophagy receptors and ubiquitin-like proteins form the molecular basis for selective autophagy. (2014, background): “Ub is a protein that is 76 amino acids long and highly conserved from yeast to man (reviewed in Kirkin and Dikic, 2007).”
Principles and Current Strategies for Targeting Autophagy for Cancer Treatment (2011, background): “This characteristic allows these adaptor proteins to bind both ubiquinated cargo and LC3, enabling tight sequestration of ubiquinated cargo by surrounding LC3containing membranes, with little cytosolic content included (26).”
Ubiquitination and selective autophagy (2012, background): “was sufficient for targeting them to autophagosomes in a p62-dependent manner.(96) The deubiquitination activity of Ubp3/Bre5 is crucial for selective autophagy of excess ribosomes.”
Mechanisms of Selective Autophagy (2016, unknown): “Indeed, while ubiquitination per se could be sufficient to render any cellular material a substrate for autophagy [71], the higher the local concentration of ubiquitin on a cytoplasmic material, the more efficient the recruitment of cargo receptors will be.”
Transcriptional Regulation by Nrf2 (2017, background): “These include p62, also known as sequestosome 1 (SQSTM1), a ubiquitinbinding protein that targets protein aggregates for degradation via the autophagic pathway (26, 76, 83, 90).”
Autophagy, Immunity, and Microbial Adaptations (2009, background): “Although it is not known whether these tag-receptor pairs are ubiquitously used to slate other targets, such as organelles, for autophagy, monoubiqutination has been shown to be sufficient to target an ectopically expressed cytoplasmic protein as well as peroxisomes for autophagic degradation (Kim e”
Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin (2012, background): “Discussion It is currently under debate whether PINK1-dependent phosphorylation of Parkin or another substrate drives mitochondrial translocation and activity of Parkin (Kim et al., 2008b; Narendra et al., 2010b; Sha et al., 2010; Vives-Bauza et al., 2010).”
p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both (2010, background): “Recently, it was shown that ubiquitin anchored to peroxisomes is sufficient to induce p62 recruitment and pexaphagy.(13) Similar to these findings, we observed that anchoring ubiquitin to mitochondria is sufficient to recruit p62 to mitochondria.”
The Nrf2 cell defence pathway: Keap1-dependent and -independent mechanisms of regulation. (2013, unknown): “[52,53].”
A role for ubiquitin in selective autophagy. (2009, background): “While monoUb-driven autophagy depends on p62 (Kim et al., 2008), low affinity of the p62 UBA domain toward monoUb (Kirkin et al., 2009; Long et al., 2008) suggests that other factors, such as substrate/ receptor oligomerization, will play a role in selective degradation of monoubiquitinated cargo…”
Exosomes: extracellular organelles important in intercellular communication. (2010, background): “[97] Kim PK, Hailey DW, Mullen RT, Lippincott-Schwartz J.”