Mouse IL-17RA/IL-17R Biotinylated Antibody
Mouse IL-17RA/IL-17R Biotinylated Antibody Summary
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
IL-17 R, also known as IL-17 RA, is a 120 kDa type I transmembrane glycoprotein protein that plays a central role in inflammatory responses (1-3). Mature mouse
IL‑17 R consists of a 291 amino acid (aa) extracellular domain, a 21 aa transmembrane segment, and a 521 aa cytoplasmic domain (4). The cytoplasmic domain contains a region homologous to the TIR domain of the TLR/IL-1 R family (5). Mouse IL-17 R shares 84% and 72% aa sequence identity with rat and human IL-17 R, respectively. Within the extracellular domain, it shares 18-25% sequence identity with mouse IL-17 RB, C, D, and E. While the expression of IL-17 is restricted to activated T cells, IL-17 R exhibits a broad tissue distribution (4). Even in the absence of ligand, IL-17 R exists on the cell surface as a multimer (6). IL-17 R can bind IL-17 but must associate with IL-17 RC to transduce signals (7, 8). Interestingly, human IL-17 R does not appear to form productive complexes with mouse IL-17 RC (8). The IL-17 R can also signal in response to IL-17F (9). IL-17 R ligation promotes T cell activation and the production of IL-6, G-CSF, SCF, and multiple pro‑inflammatory chemokines (4, 7, 9, 10). IL-17A and IL-17F synergize with TNF-alpha in the induction of CXCL1, G-CSF, and IL-6 (9, 11). This effect requires the presence of both TNF RI and TNF RII (9). IL-17 interactions with IL-17 R also inhibit the TNF-alpha induced upregulation of fibroblast CCL5 and VCAM-1 (11). CCL5 and VCAM-1 induced effects are differentially sensitive to blockade with IL-17 R specific antibodies, suggesting that IL-17 R triggers divergent intracellular signals (11). In vivo, IL‑17 R activity is important for increased generation of neutrophils and their recruitment to sites of inflammation (10, 12, 13). IL-17 R is required for host defense against microbial infection and for the progression of arthritis from inflammation to destructive joint erosion (10, 13).
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- Schnyder, B. et al. (2005) Cytokine 31:191.
- Tan, W. et al. (2006) J. Immunol. 176:6186.
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Citation for Mouse IL-17RA/IL-17R Biotinylated Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
1 Citation: Showing 1 - 1
DAP12 signaling directly augments proproliferative cytokine stimulation of NK cells during viral infections.
Authors: French AR, Sjolin H, Kim S, Koka R, Yang L, Young DA, Cerboni C, Tomasello E, Ma A, Vivier E, Karre K, Yokoyama WM
J. Immunol., 2006-10-15;177(8):4981-90.
Sample Types: Whole Cells
Applications: Flow Cytometry
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