ArticleiScience2021
PLK1-mediated S369 phosphorylation of RIPK3 during G2 and M phases enables its ripoptosome incorporation and activity.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- ISG15 negatively regulates RIPK3-mediated cell death and viral pathogenesis.Cell reports · 2026Article
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- ROCK1 promotes B cell differentiation and proteostasis under stress through the heme-regulated proteins, BACH2 and HRI.JCI insight · 2025Article
- Necroptosis-Related Gene Signature Predicts Prognosis in Patients with Advanced Ovarian Cancer.Cancers · 2025Article
- An immunohistochemical atlas of necroptotic pathway expression.EMBO molecular medicine · 2024Article
- Interplay between Cell Death and Cell Proliferation Reveals New Strategies for Cancer Therapy.International journal of molecular sciences · 2022Review
- Necroptosis as a Novel Facet of Mitotic Catastrophe.International journal of molecular sciences · 2022Article
- Establishment of a Necroptosis-Related Prognostic Signature to Reveal Immune Infiltration and Predict Drug Sensitivity in Hepatocellular Carcinoma.Frontiers in genetics · 2022Article
- Present and Future Perspective on PLK1 Inhibition in Cancer Treatment.Frontiers in oncology · 2022Review
- Identification of a Necroptosis-Related Prognostic Index and Associated Regulatory Axis in Kidney Renal Clear Cell Carcinoma.International journal of general medicine · 2022Article
- RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Receptor-interacting protein kinase 3 executes a form of regulated necrosis called necroptosis. Upon induction of an altered conformation by chemical inhibitors or via mutations in its kinase site, RIPK3 associates with a multiprotein complex called the ripoptosome-a signaling platform containing FADD, RIPK1, caspase 8, and cFLIP-and becomes decisive in the execution of apoptosis. Surprisingly, in contexts not completely understood, the ripoptosome itself cleaves RIPK3, highlighting an apparent conundrum on how RIPK3 fulfills its role via the complex responsible for its own degradation. Recently, ripoptosome assembly was found to occur in mitosis where we found elevated RIPK3 levels. We now report that PLK1 directly associates with RIPK3 and phosphorylates it at S369 as cells enter mitosis. G2/M phase RIPK3 has pro-apoptotic activity but upon release from ripoptosome, can trigger necroptosis. Taken together, phosphorylation of RIPK3 at S369 prevents its ripoptosome-mediated cleavage thereby retaining its pro-death activity during mitosis.
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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.