ArticleNature communications2018
RIP2 filament formation is required for NOD2 dependent NF-κB signalling.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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Who cites it
44 citing papers in PubMed, 93 citations in OpenAlex.
- Identification of Cellular Senescence-Related Hub Genes in Rheumatoid Arthritis from Bioinformatics Analysis Through Machine Learning up to Verifications in Mouse Macrophages and Tests in Patients.International journal of molecular sciences · 2026Article
- Structural and dynamic basis of NOD2 tandem CARD association and NOD1/2-RIP2 signaling complexes.PLoS computational biology · 2026Article
- Inactivation of NF-κB and MAPKs confers the potent therapeutic effect of carboxyamidotriazole on Blau syndrome.Arthritis research & therapy · 2026Article
- RNA stability: a novel perspective on gene regulatory networks in bovine mastitis.BMC genomics · 2025Article
- Nucleotide-Binding Oligomerization Domain 2 in Signaling, Immunity, and Mycobacterial Infection.Immunity, inflammation and disease · 2025Review
- Article
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Apaf-1 is an evolutionarily conserved DNA sensor that switches the cell fate between apoptosis and inflammation.Cell discovery · 2025Article
- Current advances on RIPK2 and its inhibitors in pathological processes: a comprehensive review.Frontiers in molecular neuroscience · 2025Review
- Ripks and Neuroinflammation.Molecular neurobiology · 2024Review
- NOD1 and NOD2: Essential Monitoring Partners in the Innate Immune System.Current issues in molecular biology · 2024Review
- NOD2 attenuates osteoarthritis via reprogramming the activation of synovial macrophages.Arthritis research & therapy · 2023Article
- Analysis of alternative splicing in chicken macrophages transfected with overexpression/knockdown ofAnimal biotechnology · 2023Article
- A Bacterial Quorum Sensing Regulated Protease Inhibits Host Immune Responses by Cleaving Death Domains of Innate Immune Adaptors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Design, synthesis and biological evaluation of 4-aminoquinoline derivatives as receptor-interacting protein kinase 2 (RIPK2) inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Structure shows that the BIR2 domain of E3 ligase XIAP binds across the RIPK2 kinase dimer interface.Life science alliance · 2023Article
- Macrophage DCLK1 promotes obesity-induced cardiomyopathy via activating RIP2/TAK1 signaling pathway.Cell death & disease · 2023Article
- Multifaceted roles and regulation of nucleotide-binding oligomerization domain containing proteins.Frontiers in immunology · 2023Review
- Selective autophagy of RIPosomes maintains innate immune homeostasis during bacterial infection.The EMBO journal · 2022Article
- Review
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the innate immune pattern recognition receptor NOD2 by the bacterial muramyl-dipeptide peptidoglycan fragment triggers recruitment of the downstream adaptor kinase RIP2, eventually leading to NF-κB activation and proinflammatory cytokine production. Here we show that full-length RIP2 can form long filaments mediated by its caspase recruitment domain (CARD), in common with other innate immune adaptor proteins. We further show that the NOD2 tandem CARDs bind to one end of the RIP2 CARD filament, suggesting a mechanism for polar filament nucleation by activated NOD2. We combine X-ray crystallography, solid-state NMR and high-resolution cryo-electron microscopy to determine the atomic structure of the helical RIP2 CARD filament, which reveals the intermolecular interactions that stabilize the assembly. Using structure-guided mutagenesis, we demonstrate the importance of RIP2 polymerization for the activation of NF-κB signalling by NOD2. Our results could be of use to develop new pharmacological strategies to treat inflammatory diseases characterised by aberrant NOD2 signalling.
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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.