ArticleThe Journal of biological chemistry2016
Structural and Functional Attributes of the Interleukin-36 Receptor.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed.
- Anti-Inflammatory Cytokine Signatures in Primary Glaucoma Subtypes: Diagnostic and Pathophysiological Insights From IL-36Ra, IL-37, and IL-38.Journal of ophthalmology · 2026Article
- Review
- Discovery of selective low molecular weight interleukin-36 receptor antagonists by encoded library technologies.Nature communications · 2025Article
- Key Interleukins in Inflammatory Bowel Disease-A Review of Recent Studies.International journal of molecular sciences · 2024Review
- Exploring the role of IL-1β in inflammatory bowel disease pathogenesis.Frontiers in medicine · 2024Review
- Correlations between IL-36 family cytokines in peripheral blood and subjective and objective assessment results in patients with allergic rhinitis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- New insights on IL‑36 in intestinal inflammation and colorectal cancer (Review).Experimental and therapeutic medicine · 2023Review
- Assessment of the Pharmacokinetics and Safety of Spesolimab, a Humanised Anti-interleukin-36 Receptor Monoclonal Antibody, in Healthy Non-Japanese and Japanese Subjects: Results from Phase I Clinical Studies.Clinical pharmacokinetics · 2022Article
- IL-1RAP, a Key Therapeutic Target in Cancer.International journal of molecular sciences · 2022Review
- Clinical relevance and therapeutic potential of IL-38 in immune and non-immune-related disordersEuropean cytokine network · 2022Review
- Targeting IL-36 improves age-related coronary microcirculatory dysfunction and attenuates myocardial ischemia/reperfusion injury in mice.JCI insight · 2022Article
- Prognostic tools and candidate drugs based on plasma proteomics of patients with severe COVID-19 complications.Nature communications · 2022Article
- IL-36 is Closely Related to Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022Article
- IL-36α and Lipopolysaccharide Cooperatively Induce Autophagy by Triggering Pro-Autophagic Biased Signaling.Biomedicines · 2021Article
- Molecular Pathogenesis of Psoriasis and Biomarkers Reflecting Disease Activity.Journal of clinical medicine · 2021Review
- Article
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- Interleukin-36: Structure, Signaling and Function.Advances in experimental medicine and biology · 2021Review
- Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases.Frontiers in immunology · 2021Review
- Interleukin-36 Cytokine/Receptor Signaling: A New Target for Tissue Fibrosis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transduction by the IL-36 receptor (IL-36R) is linked to several human diseases. However, the structure and function of the IL-36R is not well understood. A molecular model of the IL-36R complex was generated and a cell-based reporter assay was established to assess the signal transduction of recombinant subunits of the IL-36R. Mutational analyses and functional assays have identified residues of the receptor subunit IL-1Rrp2 needed for cytokine recognition, stable protein expression, disulfide bond formation and glycosylation that are critical for signal transduction. We also observed that, overexpression of ectodomain (ECD) of Il-1Rrp2 or IL-1RAcP exhibited dominant-negative effect on IL-36R signaling. The presence of IL-36 cytokine significantly increased the interaction of IL-1Rrp2 ECD with the co-receptor IL-1RAcP. Finally, we found that single nucleotide polymorphism A471T in the Toll-interleukin 1 receptor domain (TIR) of the IL-1Rrp2 that is present in ∼2% of the human population, down-regulated IL-36R signaling by a decrease of interaction with IL-1RAcP.
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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.