ArticleThe Journal of biological chemistry2010
TILRR, a novel IL-1RI co-receptor, potentiates MyD88 recruitment to control Ras-dependent amplification of NF-kappaB.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- The Effect of Heparin and Other Exogenous Glycosaminoglycans (GAGs) in Reducing IL-1β-Induced Pro-Inflammatory Cytokine IL-8 and IL-6 mRNA Expression and the Potential Role for Reducing Inflammation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Host genetic susceptibility underlying SARS-CoV-2-associated Multisystem Inflammatory Syndrome in Brazilian Children.Molecular medicine (Cambridge, Mass.) · 2022Article
- Natural Immunity against HIV-1: Progression of Understanding after Association Studies.Viruses · 2022Review
- TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Toll-like Interleukin -1 Receptor Regulator (TILRR) Protein, a Major Modulator of Inflammation, is Expressed in Normal Human and Macaque Tissues and PBMCs.Journal of inflammation research · 2022Article
- Integrated Bioinformatics IdentifiesApplied bionics and biomechanics · 2022Article
- The Potential Role of FREM1 and Its Isoform TILRR in HIV-1 Acquisition through Mediating Inflammation.International journal of molecular sciences · 2021Review
- TILRR (Toll-like Interleukin-1 Receptor Regulator), an Important Modulator of Inflammatory Responsive Genes, is Circulating in the Blood.Journal of inflammation research · 2021Article
- Article
- TILRR Promotes Migration of Immune Cells Through Induction of Soluble Inflammatory Mediators.Frontiers in cell and developmental biology · 2020Article
- Distinct Binding Interactions of αBiophysical journal · 2019Article
- Toll-like Interleukin 1 Receptor Regulator Is an Important Modulator of Inflammation Responsive Genes.Frontiers in immunology · 2019Article
- The IL-1RI Co-Receptor TILRR (JACC. Basic to translational science · 2017Article
- TILRR Steers Interleukin-1 Signaling: Co-Receptor Provides Context and a Therapeutic Target.JACC. Basic to translational science · 2017Article
- Statistical Techniques Complement UML When Developing Domain Models of Complex Dynamical Biosystems.PloS one · 2016Article
- Activated IL-1RI Signaling Pathway Induces Th17 Cell DifferentiationFrontiers in immunology · 2016Article
- Article
- The chicken IL-1 family: evolution in the context of the studied vertebrate lineage.Immunogenetics · 2014Review
- Deficiency of FRAS1-related extracellular matrix 1 (FREM1) causes congenital diaphragmatic hernia in humans and mice.Human molecular genetics · 2013Article
- A genetic polymorphism of FREM1 is associated with resistance against HIV infection in the Pumwani sex worker cohort.Journal of virology · 2012Article
Corrections and comments
- Correction · 2010-06-04Error in Image ·
- Erratum issued
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Host defense against infection is induced by Toll-like and interleukin (IL)-1 receptors, and controlled by the transcription factor NF-kappaB. Our earlier studies have shown that IL-1 activation impacts cytoskeletal structure and that IL-1 receptor (IL-1RI) function is substrate-dependent. Here we identify a novel regulatory component, TILRR, which amplifies activation of IL-1RI and coordinates IL-1-induced control with mechanotransduction. We show that TILRR is a highly conserved and widely expressed enhancer of IL-1-regulated inflammatory responses and, further, that it is a membrane-bound glycosylated protein with sequence homology to members of the FRAS-1 family. We demonstrate that TILRR is recruited to the IL-1 receptor complex and magnifies signal amplification by increasing receptor expression and ligand binding. In addition, we show that the consequent potentiation of NF-kappaB is controlled through IL-1RI-associated signaling components in coordination with activation of the Ras GTPase. Using mutagenesis, we demonstrate that TILRR function is dependent on association with its signaling partner and, further, that formation of the TILRR-containing IL-1RI complex imparts enhanced association of the MyD88 adapter during ligand-induced activation of NF-kappaB. We conclude that TILRR is an IL-1RI co-receptor, which associates with the signaling receptor complex to enhance recruitment of MyD88 and control Ras-dependent amplification of NF-kappaB and inflammatory responses.
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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.