ArticleFrontiers in cell and developmental biology2019
TRADD Mediates RIPK1-Independent Necroptosis Induced by Tumor Necrosis Factor.
Article in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Interaction between p-AMPK and RIPK3 reveals a mechanism by which AdipoAI suppresses necroptosis to attenuate periodontitis.Journal of translational medicine · 2026Article
- The RIPK3 Inhibitor GSK872 Attenuates Inflammation and Necroptosis via Modulation of the JNK Signaling Pathway in LPS-Stimulated Microglia.Biomolecules & therapeutics · 2026Article
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- Targeted Induction of Cancer Cell Necroptosis Potentiates Anti-PD-1 Immunotherapy via CD80 Activation.International journal of biological sciences · 2026Article
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- The Dual Role of TRADD in Liver Disease: From Cell Death Regulation to Inflammatory Microenvironment Remodeling.International journal of molecular sciences · 2025Review
- Inflammation and cancer cell survival: TRAF2 as a key player.Cell death & disease · 2025Review
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- TRADD-mediated pyroptosis contributes to diabetic cardiomyopathy.Acta pharmacologica Sinica · 2025Article
- Article
- Necroptosis-based glioblastoma prognostic subtypes: implications for TME remodeling and therapy response.Annals of medicine · 2024Article
- Significance of Necroptosis in Cartilage Degeneration.Biomolecules · 2024Review
- Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages.PLoS pathogens · 2024Article
- A RIPK1-specific PROTAC degrader achieves potent antitumor activity by enhancing immunogenic cell death.Immunity · 2024Article
- Necroptosis induced by ruthenium (II) complexes as mitochondrial disruptors.Cell death discovery · 2024Article
- Cellular heterogeneity in TNF/TNFR1 signalling: live cell imaging of cell fate decisions in single cells.Cell death & disease · 2024Review
- Genome, Metabolism, or Immunity: Which Is the Primary Decider of Pancreatic Cancer Fate through Non-Apoptotic Cell Death?Biomedicines · 2023Review
- Downregulation of BIRC2 hinders the progression of rheumatoid arthritis through regulating TRADD.Immunity, inflammation and disease · 2023Article
- HSP70 attenuates neuronal necroptosis through the HSP90α-RIPK3 pathway following neuronal trauma.Molecular biology reports · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a programmed necrotic cell death, necroptosis has the intrinsic initiators, including receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed-lineage kinase domain-like protein (MLKL), which combine to form necroptotic signaling pathway and mediate necroptosis induced by various necroptotic stimuli, such as tumor necrosis factor (TNF). Although chemical inhibition of RIPK1 blocks TNF-induced necroptosis, genetic elimination of RIPK1 does not suppress but facilitate necroptosis triggered by TNF. Moreover, RIPK3 has been reported to mediate the RIPK1-independent necroptosis, but the involved mechanism is unclear. In this study, we found that TRADD was essential for TNF-induced necroptosis in RIPK1-knockdown L929 and HT-22 cells. Mechanistic study demonstrated that TRADD bound RIPK3 to form new protein complex, which then promoted RIPK3 phosphorylation via facilitating RIPK3 oligomerization, leading to RIPK3-MLKL signaling pathway activation. Therefore, TRADD acted as a partner of RIPK3 to initiate necroptosis in RIPK1-knockdown L929 and HT-22 cells in response to TNF stimulation. In addition, TRADD was critical for the accumulation of reactive oxygen species (ROS), which contributed to RIPK1-independent necroptosis triggered by TNF. Collectively, our data demonstrate that TRADD acts as the new target protein for TNF-induced RIPK3 activation and the subsequent necroptosis in a RIPK1-independent manner.
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