ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Kinase Activities of RIPK1 and RIPK3 Can Direct IFN-β Synthesis Induced by Lipopolysaccharide.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 60 citations in OpenAlex.
- Necroptotic cell death consequences and disease relevance.Nature immunology · 2025Review
- STING and Nonnecroptotic MLKL-Mediated Mechanisms Improve Dendritic Cell Maturation and Killing of Cancer Cells.European journal of immunology · 2025Article
- Splicing QTL mapping in stimulated macrophages associates low-usage splice junctions with immune-mediated disease risk.Nature communications · 2025Article
- Inhibition of RIPK1 or RIPK3 kinase activity post ischemia-reperfusion reduces the development of chronic kidney injury.The Biochemical journal · 2025Article
- Activation of ZBP1/RIPK3/MLKL-Dependent Necroptosis by Pseudorabies Virus Restricts Viral Infection in BV2 Microglia Cells.Transboundary and emerging diseases · 2025Article
- RIPK3 impacts antibody generation in an induced model of murine lupus through mechanisms other than necroptosis and antigen presentation.Frontiers in immunology · 2025Article
- RIPK1 signaling pathways: implications for autoimmune and neuroinflammatory diseases.Frontiers in immunology · 2025Review
- Regulation of Zfp36 by ISGF3 and MK2 restricts the expression of inflammatory cytokines during necroptosis stimulation.Cell death & disease · 2024Article
- Inhibition of RIP1 improves immune reconstitution and reduces GVHD mortality while preserving graft-versus-leukemia effects.Science translational medicine · 2023Article
- Dichotomous roles of RIPK3 in regulating the IFN response and NLRP3 inflammasome in human monocytes.Journal of leukocyte biology · 2023Article
- RIPK3 promotes brain region-specific interferon signaling and restriction of tick-borne flavivirus infection.PLoS pathogens · 2023Article
- RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis.Virologica Sinica · 2023Article
- The Molecular Mechanisms of Neuroinflammation in Alzheimer's Disease, the Consequence of Neural Cell Death.International journal of molecular sciences · 2023Review
- Caspase-8 inhibition improves the outcome of bacterial infections in mice by promoting neutrophil activation.Cell reports. Medicine · 2023Article
- A necroptosis-independent function of RIPK3 promotes immune dysfunction and prevents control of chronic LCMV infection.Cell death & disease · 2023Article
- Neuroprotective Effects of Erinacine A on an Experimental Model of Traumatic Optic Neuropathy.International journal of molecular sciences · 2023Article
- High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease.Oxidative medicine and cellular longevity · 2023Article
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow CroakerAntibiotics (Basel, Switzerland) · 2021Article
- Review
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
The innate immune response is a central element of the initial defense against bacterial and viral pathogens. Macrophages are key innate immune cells that upon encountering pathogen-associated molecular patterns respond by producing cytokines, including IFN-β. In this study, we identify a novel role for RIPK1 and RIPK3, a pair of homologous serine/threonine kinases previously implicated in the regulation of necroptosis and pathologic tissue injury, in directing IFN-β production in macrophages. Using genetic and pharmacologic tools, we show that catalytic activity of RIPK1 directs IFN-β synthesis induced by LPS in mice. Additionally, we report that RIPK1 kinase-dependent IFN-β production may be elicited in an analogous fashion using LPS in bone marrow-derived macrophages upon inhibition of caspases. Notably, this regulation requires kinase activities of both RIPK1 and RIPK3, but not the necroptosis effector protein, MLKL. Mechanistically, we provide evidence that necrosome-like RIPK1 and RIPK3 aggregates facilitate canonical TRIF-dependent IFN-β production downstream of the LPS receptor TLR4. Intriguingly, we also show that RIPK1 and RIPK3 kinase-dependent synthesis of IFN-β is markedly induced by avirulent strains of Gram-negative bacteria,
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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.