ArticleBiochemical and biophysical research communications2018
PB1 and UBA domains of p62 are essential for aggresome-like induced structure formation.
Article in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Local autophagy impairment triggers brain-wide presynaptic remodeling and resilience.The EMBO journal · 2026Article
- DcR3 Suppresses Lipopolysaccharide-Induced Aggresome-like Structures in Macrophages via Inhibition of Reactive Oxygen Species and p38 MAPK.International journal of molecular sciences · 2026Article
- Molecular mechanisms underlying p62-dependent secretion of the Alzheimer-associated ubiquitin variant UBBProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of SQSTM1/p62 in regulating Mallory-Denk body in alcohol-associated liver disease.eGastroenterology · 2025Article
- Dual roles of AtNBR1 in regulating selective autophagyAutophagy · 2024Article
- Protein aggregation and biomolecular condensation in hypoxic environments (Review).International journal of molecular medicine · 2024Review
- TLR-mediated aggresome-like induced structures comprise antimicrobial peptides and attenuate intracellular bacterial survival.Molecular biology of the cell · 2024Article
- Conversion of methylmercury into inorganic mercury via organomercurial lyase (MerB) activates autophagy and aggresome formation.Scientific reports · 2023Article
- LLPS of SQSTM1/p62 and NBR1 as outcomes of lysosomal stress response limits cancer cell metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- SQSTM1/p62 and Hepatic Mallory-Denk Body Formation in Alcohol-Associated Liver Disease.The American journal of pathology · 2023Review
- Review
- Mechanistic insights into enhancement or inhibition of phase separation by different polyubiquitin chains.EMBO reports · 2022Article
- Autophagic sequestration of SQSTM1 disrupts the aggresome formation of ubiquitinated proteins during proteasome inhibition.Cell death & disease · 2022Article
- Residues TRetrovirology · 2021Article
- Different Roles of p62 (SQSTM1) Isoforms in Keratin-Related Protein Aggregation.International journal of molecular sciences · 2021Article
- Marliolide Derivative Induces Melanosome Degradation via Nrf2/p62-Mediated Autophagy.International journal of molecular sciences · 2021Article
- Inhibition of the proteasome and proteaphagy enhances apoptosis in FLT3-ITD-driven acute myeloid leukemia.FEBS open bio · 2021Article
- Fate and propagation of endogenously formed Tau aggregates in neuronal cells.EMBO molecular medicine · 2020Article
- Ubiquitin-Modulated Phase Separation of Shuttle Proteins: Does Condensate Formation Promote Protein Degradation?BioEssays : news and reviews in molecular, cellular and developmental biology · 2020Review
- Structure, dynamics and functions of UBQLNs: at the crossroads of protein quality control machinery.The Biochemical journal · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
ALIS are large, transient, cytosolic aggregates that serve as storage compartments for ubiquitin-tagged defective ribosomal products. We determined the importance of the protein p62 in the formation of ALIS and demonstrated that two domains of p62-PB1 and UBA-are essential for ALIS assembly. Those two major binding domains of p62, also known as sequestosome 1, were shown to play a critical role in the formation of autophagosomes or cytoplasmic aggregates. Specifically, the PB1 domain is essential for self-oligomerization, and the UBA domain allows p62 to bind to polyubiquitin chains or ubiquitinated proteins. After stimulation of RAW 264.7 macrophages with lipopolysaccharide, we observed a significant decrease in the number of cells with ALIS. Importantly, cells overexpressing either a PB1 mutant or UBA-deleted p62 construct also exhibited a substantially diminished number of cells containing ALIS. Since both p62 and ubiquitin are found in ALIS, we evaluated the dynamics of YFP-tagged p62 in ALIS. In contrast to the findings of a previous study that evaluated GFP-tagged ubiquitin motility in ALIS, we determined that YFP-tagged p62 has very limited mobility. Lastly, we determined that GST-tagged full-length p62 binds to Lys-63-linked polyubiquitin chains but not to Lys-48-linked chains. Overall, our findings provide insight on the essential role that p62, particularly its PB1 and UBA domains, has in the formation of ALIS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.