ArticleThe Journal of biological chemistry2014
Toll-like receptor-mediated down-regulation of the deubiquitinase cylindromatosis (CYLD) protects macrophages from necroptosis in wild-derived mice.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Molecular mechanisms of immune cell death in immunosenescence.Cell death and differentiation · 2025Review
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- CYLD in health and disease.Disease models & mechanisms · 2023Review
- The regulation of necroptosis by ubiquitylation.Apoptosis : an international journal on programmed cell death · 2022Review
- Skin manifestations of inborn errors of NF-κB.Frontiers in pediatrics · 2022Review
- Immunoprecipitation Strategies to Isolate RIPK1/RIPK3 Complexes in Mouse Macrophages.Current protocols · 2021Article
- Smac-mimetics reduce numbers and viability of human osteoclasts.Cell death discovery · 2021Article
- Rafting Down the Metastatic Cascade: The Role of Lipid Rafts in Cancer Metastasis, Cell Death, and Clinical Outcomes.Cancer research · 2021Review
- Toll-like receptors in sepsis-associated cytokine storm and their endogenous negative regulators as future immunomodulatory targets.International immunopharmacology · 2020Review
- Receptor-interacting protein kinase 2 (RIPK2) and nucleotide-binding oligomerization domain (NOD) cell signaling inhibitors based on a 3,5-diphenyl-2-aminopyridine scaffold.European journal of medicinal chemistry · 2020Article
- Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation.Cell reports · 2020Article
- Deubiquitinating Enzymes: A Critical Regulator of Mitosis.International journal of molecular sciences · 2019Review
- Constitutive interferon signaling maintains critical threshold of MLKL expression to license necroptosis.Cell death and differentiation · 2019Article
- Wild-derived mice: from genetic diversity to variation in immune responses.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Phenotypic screening identifies a new oxazolone inhibitor of necroptosis and neuroinflammation.Cell death discovery · 2018Article
- CYLD, A20 and OTULIN deubiquitinases in NF-κB signaling and cell death: so similar, yet so different.Cell death and differentiation · 2017Review
- Kinase Activities of RIPK1 and RIPK3 Can Direct IFN-β Synthesis Induced by Lipopolysaccharide.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Imiquimod has strain-dependent effects in mice and does not uniquely model human psoriasis.Genome medicine · 2017Article
- Activation of TNFR2 sensitizes macrophages for TNFR1-mediated necroptosis.Cell death & disease · 2016Article
- RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.Immunity · 2016Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Pathogen recognition by the innate immune system initiates the production of proinflammatory cytokines but can also lead to programmed host cell death. Necroptosis, a caspase-independent cell death pathway, can contribute to the host defense against pathogens or cause damage to host tissues. Receptor-interacting protein (RIP1) is a serine/threonine kinase that integrates inflammatory and necroptotic responses. To investigate the mechanisms of RIP1-mediated activation of immune cells, we established a genetic screen on the basis of RIP1-mediated necroptosis in wild-derived MOLF/EiJ mice, which diverged from classical laboratory mice over a million years ago. When compared with C57BL/6, MOLF/EiJ macrophages were resistant to RIP1-mediated necroptosis induced by Toll-like receptors. Using a forward genetic approach in a backcross panel of mice, we identified cylindromatosis (CYLD), a deubiquitinase known to act directly on RIP1 and promote necroptosis in TNF receptor signaling, as the gene conferring the trait. We demonstrate that CYLD is required for Toll-like receptor-induced necroptosis and describe a novel mechanism by which CYLD is down-regulated at the transcriptional level in MOLF/EiJ macrophages to confer protection from necroptosis.
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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.