A novel member of the interleukin 1 receptor (IL-1R) superfamily, SIGIRR (single Ig IL-1R-related molecule) was identified in mouse and human. Although it shows the typical conserved motifs that characterize the IL-1R and Toll superfamily, it is structurally and functionally distinct from both. SIGIRR has only one Ig domain in its extracellular portion whereas the IL-1R family contains three Ig folds. An unusually long cytoplasmic domain is reminiscent of the structure of drosophila Toll, yet the SIGIRR peptide sequence is more closely related to IL-1RI. The human SIGIRR gene maps to 11p15. 5 and thus is not located in the same cluster on chromosome 2 that is known to contain four members of the IL-1R family. It failed to bind to the known IL-1-family members and, when co-expressed with the IL-1RI, had no effect on the binding of IL-1 and on subsequent nuclear factor kappaB (NFkappaB) activation. A chimera, in which the SIGIRR intracellular domain was fused to the IL-1R extracellular domain, did not activate NFkappaB unlike similar fusion proteins of other IL-1R related molecules. We conclude that the SIGIRR protein represents a novel subtype of the IL-1R superfamily.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1006/cyto.1998.0452 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeting MyD88: Therapeutic mechanisms and potential applications of the specific inhibitor ST2825.
Inflamm Res
November 2023
Hengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China.
Background: Myeloid differentiation factor-88 (MyD88) is a crucial adapter protein that coordinates the innate immune response and establishes an adaptive immune response. The interaction of the Toll/Interleukin-1 receptor (IL-1R) superfamily with MyD88 triggers the activation of various signalling pathways such as nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), promoting the production of a variety of immune and inflammatory mediators and potentially driving the development of a variety of diseases.
Objective: This article will explore the therapeutic potential and mechanism of the MyD88-specific inhibitor ST2825 and describe its use in the treatment of several diseases.
A novel tumor necrosis factor receptor-associated factor 6 (TRAF6) gene from Macrobrachiumrosenbergii involved in antibacterial defense against Aeromonas hydrophila.
Fish Shellfish Immunol
September 2023
Department of Biology, Faculty of Science, Srinakharinwirot University, Bangkok, 10110, Thailand; Center of Excellence in Animal, Plant and Parasite Biotechnology (COE), Srinakharinwirot University, Bangkok, 10110, Thailand. Electronic address:
Tumor necrosis factor receptor-associated factor 6 (TRAF6) is an adapter protein that triggers downstream cascades mediated by both TNFR and the interleukin-1 receptor/Toll-like receptor (IL-1R/TLR) superfamily. TRAF6 is involved in various biological processes, including innate and adaptive immunity. In the present study, a homolog of TRAF6 from Macrobrachium rosenbergii (MrTRAF6) was identified and characterized.
View Article and Find Full Text PDFGenome-wide identification of TNF receptor-associated factors in Japanese flounder (Paralichthys olivaceus) and functional analysis of resistance to temperature and Edwardsiella tarda stress.
Fish Shellfish Immunol
July 2023
Key Laboratory of Aquacultural Biotechnology (Ningbo University), Ministry of Education, Ningbo, Zhejiang, China; National Engineering Research Laboratory of Marine Biotechnology and Engineering, Ningbo University, China; Collaborative Innovation Center for Zhejiang Marine High-efficiency and Healthy Aquaculture, Ningbo University, China; Key Laboratory of Marine Biotechnology of Zhejiang Province, Ningbo University, Ningbo, China; Key Laboratory of Green Mariculture (Co-construction By Ministry and Province), Ministry of Agriculture and Rural, Ningbo University, China. Electronic address:
Tumor necrosis factor receptor-associated factors (TRAFs), as the signaling mediators of the tumor necrosis factor (TNFR) superfamily, toll-like receptors (TLR) and interleukin-1 receptor (IL-1R) superfamily, can activate downstream signal transduction pathways and play an important role in the body's immune process. In this study, six TRAF genes, namely PoTRAF2a, PoTRAF2b, PoTRAF3, PoTRAF4, PoTRAF6 and PoTRAF7, were identified and annotated in Japanese flounder by using bioinformatics methods. Phylogenetic analysis confirmed that TRAF genes can be divided into seven groups.
View Article and Find Full Text PDFIL-1R8: A molecular brake of anti-tumor and anti-viral activity of NK cells and ILC.
Semin Immunol
March 2023
Translational Immunology Unit, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy. Electronic address:
Interleukin-1 receptor family members (ILRs) and Toll-Like Receptors (TLRs) play pivotal role in immunity and inflammation and are expressed by most cell types including cells of both the innate and adaptive immune system. In this context, IL-1 superfamily members are also important players in regulating function and differentiation of adaptive and innate lymphoid cells. This system is tightly regulated in order to avoid uncontrolled activation, which may lead to detrimental inflammation contributing to autoimmune or allergic responses.
View Article and Find Full Text PDFIL-17-induced dimerization of IL-17RA drives the formation of the IL-17 signalosome to potentiate signaling.
Cell Rep
October 2022
Novartis Institutes for BioMedical Research, Novartis Pharma AG, 4002 Basel, Switzerland. Electronic address:
Signaling through innate immune receptors such as the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily proceeds via the assembly of large membrane-proximal complexes or "signalosomes." Although structurally distinct, the IL-17 receptor family triggers cellular responses that are typical of innate immune receptors. The IL-17RA receptor subunit is shared by several members of the IL-17 family.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!