ArticleCell reports2016
MLKL and FADD Are Critical for Suppressing Progressive Lymphoproliferative Disease and Activating the NLRP3 Inflammasome.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 88 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Alveolar epithelial barrier disruption by FKBP5-mediated necroptosis aggravates lung injury.Respiratory research · 2026Article
- Caspase-8-mediated CYLD cleavage boosts LPS-induced endotoxic shock.Cell death and differentiation · 2026Article
- Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026Review
- Targeting kinases that regulate programmed cell death: a new therapeutic strategy for breast cancer.Journal of translational medicine · 2025Review
- Targeting alveolar epithelial cells with lipid micelle-encapsulated necroptosis inhibitors to alleviate acute lung injury.Communications biology · 2025Article
- Cooperation of TRADD- and RIPK1-dependent cell death pathways in maintaining intestinal homeostasis.Nature communications · 2025Article
- The research potential of A20 in psoriatic arthritis.Frontiers in immunology · 2025Review
- Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.International journal of molecular sciences · 2024Review
- MLKL promotes hepatocarcinogenesis through inhibition of AMPK-mediated autophagy.Cell death and differentiation · 2024Article
- FADD regulates adipose inflammation, adipogenesis, and adipocyte survival.Cell death discovery · 2024Article
- Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation.International journal of molecular sciences · 2024Review
- Hypoxic Preconditioning Attenuates Neuroinflammation via Inhibiting NF-κB/NLRP3 Axis Mediated by p-MLKL after Transient Global Cerebral Ischemia.Molecular neurobiology · 2024Article
- ABIN1 (Q478) is Required to Prevent Hematopoietic Deficiencies through Regulating Type I IFNs Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Excessive apoptosis of Rip1-deficient T cells leads to premature aging.EMBO reports · 2023Article
- Functions of the RIP kinase family members in the skin.Cellular and molecular life sciences : CMLS · 2023Review
- Targeting Endothelial Necroptosis Disrupts Profibrotic Endothelial-Hepatic Stellate Cells Crosstalk to Alleviate Liver Fibrosis in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2023Article
- The Impact of Curcumin on Immune Response: An Immunomodulatory Strategy to Treat Sepsis.International journal of molecular sciences · 2022Review
- Caspase-8 inactivation drives autophagy-dependent inflammasome activation in myeloid cells.Science advances · 2022Article
- LCK-Mediated RIPK3 Activation Controls Double-Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A-ERK Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
MLKL, a key component downstream of RIPK3, is suggested to be a terminal executor of necroptosis. Genetic studies have revealed that Ripk3 ablation rescues embryonic lethality in Fadd- or Caspase-8-deficient mice. Given that RIPK3 has also been implicated in non-necroptotic pathways including apoptosis and inflammatory signaling, it remains unclear whether the lethality in Fadd(-/-) mice is indeed caused by necropotosis. Here, we show that genetic deletion of Mlkl rescues the developmental defect in Fadd-deficient mice and that Fadd(-/-)Mlkl(-/-) mice are viable and fertile. Mlkl(-/-)Fadd(-/-) mice display significantly accelerated lymphoproliferative disease characterized by lymphadenopathy and splenomegaly when compared to Ripk3(-/-)Fadd(-/-) mice. Mlkl(-/-)Fadd(-/-) bone-marrow-derived macrophages and dendritic cells have impaired NLRP3 inflammasome activation associated with defects in ASC speck formation and NF-κB-dependent NLRP3 transcription. Our findings reveal that MLKL and FADD play critical roles in preventing lymphoproliferative disease and activating the NLRP3 inflammasome.
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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.