ArticleCell death & disease2018
Nuclear-accumulated SQSTM1/p62-based ALIS act as microdomains sensing cellular stresses and triggering oxidative stress-induced parthanatos.
Article in Cell death & disease, 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, 45 citations in OpenAlex.
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- AMPK Limits MNNG-Induced Parthanatos by Inhibiting BH3-Only Protein Bim.International journal of molecular sciences · 2025Article
- Elaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling.iScience · 2025Article
- Calorie restriction in radiation-exposed mice affects the expression of autophagy-related protein p62.BMC cancer · 2025Article
- Truncated LKB1 nonenzymatically enhances Fas-induced apoptosis by acting as a surrogate of Smac.Cell death discovery · 2025Article
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
- Temporal transcriptomic atlas reveals sequential engagement of classical and emerging regulated cell death pathways during PRRSV infection.Frontiers in veterinary science · 2025Article
- Fundamentals of redox regulation in biology.Nature reviews. Molecular cell biology · 2024Review
- The E3 Ubiquitin Protein Ligase LINCR Amplifies the TLR-Mediated Signals through Direct Degradation of MKP1.Cells · 2024Article
- Aggregability of the SQSTM1/p62-based aggresome-like induced structures determines the sensitivity to parthanatos.Cell death discovery · 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
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- The Distinct Roles of LKB1 and AMPK in p53-Dependent Apoptosis Induced by Cisplatin.International journal of molecular sciences · 2022Article
- p62 Promotes the Mitochondrial Localization of p53 through Its UBA Domain and Participates in Regulating the Sensitivity of Ovarian Cancer Cells to Cisplatin.International journal of molecular sciences · 2022Article
- The polypeptide antibiotic polymyxin B acts as a pro-inflammatory irritant by preferentially targeting macrophages.The Journal of antibiotics · 2022Article
- The E3 Ubiquitin-Protein Ligase RNF4 Promotes TNF-α-Induced Cell Death Triggered by RIPK1.International journal of molecular sciences · 2021Article
- trans-Fatty acids promote p53-dependent apoptosis triggered by cisplatin-induced DNA interstrand crosslinks via the Nox-RIP1-ASK1-MAPK pathway.Scientific reports · 2021Article
- Gefitinib initiates sterile inflammation by promoting IL-1β and HMGB1 release via two distinct mechanisms.Cell death & disease · 2021Article
- TAK1 Mediates ROS Generation Triggered by the Specific Cephalosporins through Noncanonical Mechanisms.International journal of molecular sciences · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
Aggresome-like induced structures (ALIS) have been described as ubiquitinated protein-containing aggresomes transiently formed in response to various stresses. In this study, we provide evidence that ALIS composed of SQSTM1/p62 act as a key determinant of oxidative stress-induced parthanatos, which is newly discovered and distinct from regular programmed cell death. Interestingly, we first found that chemical stresses induced by particular chemical drugs, such as several cephalosporin antibiotics, cause oxidative stress-mediated parthanatos, accompanied by the ALIS formation. Blocking the ALIS formation potently suppressed the parthanatos, and p62 knockout cells exhibited the attenuated ALIS formation and high resistance to parthanatos. Moreover, we also found that the redox-sensing activity of p62 is required for nuclear accumulation of the p62-based ALIS, resulting in the induction of parthanatos. Together, our results demonstrate unexpected functions of p62 and ALIS as cell death mediators sensing oxidative stress, and thus uncover a novel mechanism whereby p62 mediates parthanatos.
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