ArticleAutophagy2019
TRIM16 governs the biogenesis and disposal of stress-induced protein aggregates to evade cytotoxicity: implication for neurodegeneration and cancer.
Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- TRIM16 mediates YAP1 K63-linked ubiquitination to alleviate sepsis-induced acute liver injury through YAP/Nrf2 axis in mice.Cell & bioscience · 2025Article
- Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.Biomolecules · 2025Review
- TRIM16 facilitates SIRT-1-dependent regulation of antioxidant response to alleviate age-related sarcopenia.Journal of cachexia, sarcopenia and muscle · 2024Article
- Degradation of NLRP3 by p62-dependent-autophagy improves cognitive function in Alzheimer's disease by maintaining the phagocytic function of microglia.CNS neuroscience & therapeutics · 2023Article
- Saikosaponin A protects against uremic toxin indole‑3 acetic acid‑induced damage to the myocardium.Molecular medicine reports · 2023Article
- Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy.International journal of molecular sciences · 2023Review
- Article
- An update on the bridging factors connecting autophagy and Nrf2 antioxidant pathway.Frontiers in cell and developmental biology · 2023Review
- Pan-cancer illumination of TRIM gene family reveals immunology regulation and potential therapeutic implications.Human genomics · 2022Article
- Potential Diets to Improve Mitochondrial Activity in Amyotrophic Lateral Sclerosis.Diseases (Basel, Switzerland) · 2022Review
- Manipulating autophagic degradation in human diseases: from mechanisms to interventions.Life medicine · 2022Review
- The Association of the BRAF-V600E Mutation with the Expression of the Molecular Markers in the Primary Tumor and Metastatic Tissue in Papillary Thyroid Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.Oxidative medicine and cellular longevity · 2021Review
- Proteotoxic Stress and Cell Death in Cancer Cells.Cancers · 2020Review
- Crosstalks between inflammasome and autophagy in cancer.Journal of hematology & oncology · 2020Review
- TRIM16 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells by Modulating CHIP-Mediated Degradation of RUNX2.Frontiers in cell and developmental biology · 2020Article
- Emerging Roles of Tripartite Motif-Containing Family Proteins (TRIMs) in Eliminating Misfolded Proteins.Frontiers in cell and developmental biology · 2020Review
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11 authors at 1 institution in 1 country.
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Abstract
The formation of protein aggregates is linked to several diseases collectively called proteinopathies. The mechanisms and the molecular players that control the turnover of protein aggregates are not well defined. We recently showed that TRIM16 acts as a key regulatory protein to control the biogenesis and degradation of protein aggregates. We show that TRIM16 interacts with, enhances K63-linked ubiquitination of, and stabilizes NFE2L2/NRF2 leading to its activation. The activated NFE2L2 upregulates the SQSTM1/p62 and ubiquitin pathway proteins, which interact with and ubiquitinate the misfolded proteins resulting in protein aggregate formation. TRIM16 is physically present around the protein aggregates and acts as a scaffold protein to recruit SQSTM1 and macroautophagy/autophagy initiation proteins for sequestration of the protein aggregates within autophagosomes, leading to their degradation. Hence, TRIM16 utilizes a two-pronged approach to safely dispose of the stress-induced misfolded proteins and protein aggregates, and protect cells from oxidative and proteotoxic stresses. This study could provide a framework for understanding the mechanisms of protein aggregate formation in neurodegeneration. The enhancement of TRIM16 activity could be a beneficial therapeutic approach in proteinopathies. On the flip side, cancer cells appear to hijack this machinery for their survival under stress conditions; hence, depleting TRIM16 could be a beneficial therapeutic strategy for treating cancer.
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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.