ArticleCell2009
Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation.
Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,427 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
1,427 citing papers in PubMed, 2,374 citations in OpenAlex.
- Biological consequences of Z-nucleic acid sensing by ZBP1 and ADAR1.RNA biology · 2026Review
- E3 ubiquitin ligase-mediated necroptosis: regulatory mechanisms and therapeutic implication in cancer.Molecular biology reports · 2026Review
- Death domain-mediated higher-order oligomerization of RIPK1 drives TNF-induced signaling.Cell death and differentiation · 2026Article
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Mechanisms, regulation and clinical relevance of necroptosis.Nature reviews. Molecular cell biology · 2026Review
- HERC4-mediated ubiquitination licenses RIPK1 to initiate TNF-induced cell death.Nature structural & molecular biology · 2026Article
- Article
- Evaluation of receptor-interacting protein kinases (RIP1 and RIP3) in the therapeutic effect of thymoquinone against rat testis ischemia/reperfusion.Molecular and cellular biochemistry · 2026Article
- Review
- UL45 of Human Cytomegalovirus Promotes Macrophage Survival and Modulates RIPK3-Associated Cell Death.Viruses · 2026Article
- Z-Nucleic Acid-Binding Protein (ZBP)1 (DAI/DLM1) Regulation in Antiviral Cell Death Pathways.Pathogens (Basel, Switzerland) · 2026Review
- Study on the Therapeutic Effects of Ginsenoside Rh2 in Asthma Improvement.International journal of molecular sciences · 2026Article
- Assessment of Aggregation- and Condensation-Prone Regions of Proteins Involved in Neurodegenerative, Neurological and Mental-State Diseases.Biomolecules · 2026Article
- Phagocytosis of necroptotic cells optimizes type 1 conventional dendritic cells for induction of a cytotoxic T-cell response.Cell death and differentiation · 2026Article
- Long non-coding RNAs: Emerging regulators of diverse programmed cell death pathways in neurons.Neural regeneration research · 2026Article
- Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Role of PANoptosis in the development of gastric immunity and related gastric mucosal disease (Review).Molecular medicine reports · 2026Review
- The kinase domain of RIPK3 tunes its scaffolding functions.Cell death and differentiation · 2026Article
- On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026Review
- Alkalization of the intracellular pH reprograms TNF-α signaling from inflammatory NF-κB activation to tumoricidal RIP kinase-dependent necroptosis in cancer cells.Acta pharmacologica Sinica · 2026Article
1,367 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Programmed necrosis is a form of caspase-independent cell death whose molecular regulation is poorly understood. The kinase RIP1 is crucial for programmed necrosis, but also mediates activation of the prosurvival transcription factor NF-kappaB. We postulated that additional molecules are required to specifically activate programmed necrosis. Using a RNA interference screen, we identified the kinase RIP3 as a crucial activator for programmed necrosis induced by TNF and during virus infection. RIP3 regulates necrosis-specific RIP1 phosphorylation. The phosphorylation of RIP1 and RIP3 stabilizes their association within the pronecrotic complex, activates the pronecrotic kinase activity, and triggers downstream reactive oxygen species production. The pronecrotic RIP1-RIP3 complex is induced during vaccinia virus infection. Consequently, RIP3(-/-) mice exhibited severely impaired virus-induced tissue necrosis, inflammation, and control of viral replication. Our findings suggest that RIP3 controls programmed necrosis by initiating the pronecrotic kinase cascade, and that this is necessary for the inflammatory response against virus infections.
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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.