ArticleProtein science : a publication of the Protein Society2024
The PB1 and the ZZ domain of the autophagy receptor p62/SQSTM1 regulate the interaction of p62/SQSTM1 with the autophagosome protein LC3B.
Article in Protein science : a publication of the Protein Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 18 citations in OpenAlex.
- Review
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- Clinical significance of SQSTM1 variants in ALS: report of p.Arg119Cys and literature review.Neurogenetics · 2026Review
- Paeonol's protective effects on H9C2 cells against hypoxia/ reoxygenation injury through the hypoxia-inducible factor 1-alpha/B-cell lymphoma-2/adenovirus E1B 19 kDa interacting protein 3 signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- A narrative review on the role of autophagy in male infertility-associated sperm abnormalities.Asian journal of andrology · 2026Review
- The oncogenic signalosome: SQSTM1/p62 as a master integrator of signaling, metabolism, and autophagy in cancer.Toxicological research · 2026Review
- Context-dependent NRF2 signaling in cancer: mechanisms and precision modulation.Molecular biology reports · 2026Review
- A single mutation in nonstructural protein 1 is critical for the adaptive evolution of influenza B virus.Nature communications · 2026Article
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- The multifaceted role of SQSTM1/p62 in disc degeneration: A master regulator of cellular stress responses.Biochemistry and biophysics reports · 2025Review
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Exogenous melatonin alleviates premature ovarian failure by regulating granulosa cell autophagy.NPJ Regenerative medicine · 2025Article
- Review
- Metformin Improves Palmitate-Induced Follicular Granulosa Cell Dysfunction by Activating ULK1-Mediated Autophagy.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- HNRNPH1 promotes autophagy to inhibit the development of lung adenocarcinoma via the HSP90AB1/MAP1LC3B axis.Respiratory research · 2025Article
- Genetic investigation of patients with autosomal recessive ataxia and identification of two novel variants in the SQSTM1 and SYNE1 genes.Human genome variation · 2024Article
- The PB1 and the ZZ domain of the autophagy receptor p62/SQSTM1 regulate the interaction of p62/SQSTM1 with the autophagosome protein LC3B.Protein science : a publication of the Protein Society · 2024Article
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13 authors at 2 institutions in 2 countries.
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Abstract
Autophagy is a highly conserved cellular process that allows degradation of large macromolecules. p62/SQSTM1 is a key adaptor protein that interacts both with material to be degraded and with LC3 at the autophagosome, enabling degradation of cargos such as protein aggregates, lipid droplets and damaged organelles by selective autophagy. Dysregulation of autophagy contributes to the pathogenesis of many diseases. In this study, we investigated if the interaction of p62/SQSTM1 with LC3B could be regulated. We purified full-length p62/SQSTM1 and established an in vitro assay that measures the interaction with LC3B. We used the assay to determine the role of the different domains of p62/SQSTM1 in the interaction with LC3B. We identified a mechanism of regulation of p62/SQSTM1 where the ZZ and the PB1 domains regulate the exposure of the LIR-sequence to enable or inhibit the interaction with LC3B. A mutation to mimic the phosphorylation of a site on the ZZ domain leads to increased interaction with LC3B. Also, a small compound that binds to the ZZ domain enhances interaction with LC3B. Dysregulation of these mechanisms in p62/SQSTM1 could have implications for diseases where autophagy is affected. In conclusion, our study highlights the regulated nature of p62/SQSTM1 and its ability to modulate the interaction with LC3B through a LIR-sequence Accessibility Mechanism (LAM). Furthermore, our findings suggest the potential for pharmacological modulation of the exposure of LIR, paving the way for future therapeutic strategies.
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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.