Recombinant Mouse IL-17RE Fc Chimera Protein, CF Summary
Details of Functionality
Measured by its binding ability in a functional ELISA. When Recombinant Mouse IL-17 RE Fc Chimera is immobilized at 2 μg/mL (100 μL/well), the concentration of Recombinant Mouse IL‑17C (Catalog # 2306-ML) that produces 50% of the optimal binding response is approximately 0.4-2.4 ng/mL.
Source
Mouse myeloma cell line, NS0-derived mouse IL-17 RE protein
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
61 kDa (monomer). Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
65-70 kDa, reducing conditions
Publications
Read Publication using 7997-MR in the following applications:
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS.
Purity
>95%, by SDS-PAGE with silver staining
Reconstitution Instructions
Reconstitute at 100 μg/mL in PBS.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Mouse IL-17RE Fc Chimera Protein, CF
IL-17 RE
IL-17 receptor E
IL17RE
IL-17RE
Il25r
interleukin 17 receptor E
Background
Interleukin‑17 Receptor E (IL‑17 RE) is an approximately 70 kDa (predicted) transmembrane protein in the family of IL‑17 receptors. IL‑17 RE is required for mediating the pro‑inflammatory and homeostatic actions of IL‑17C in the skin and mucosa (1, 2). Mature mouse IL‑17 RE consists of a 391 amino acid (aa) extracellular domain, a 21 aa transmembrane segment, and a 202 aa cytoplasmic domain with one SEFIR/TIR domain (3). Within aa 115‑414, mouse IL‑17 RE shares 79% and 90% aa sequence identity with human and rat IL‑17 RE, respectively. Alternative splicing of mouse IL‑17 RE generates additional isoforms with either 201 aa or 326 aa N‑terminal deletions or deletion/substitution of the transmembrane segment (3). IL‑17 RE is expressed on keratinocytes, mucosal epithelial cells, Th17 cells, and gamma /δ T cells (4, 5). It associates with the widely expressed IL‑17 RA to form a heterodimeric receptor for IL-17C (4‑6). IL-17C binds to IL‑17 RE with high affinity and to IL‑17 RA with low affinity (4, 5). IL‑17C expression is induced by inflammatory stimulation in colon and airway epithelial cells, keratinocytes, CD4+ T cells, macrophages, and dendritic cells (4, 6, 7‑9). It is up‑regulated in various chronic inflammatory diseases including psoriasis, cystic fibrosis, and chronic obstructive pulmonary disease (COPD) (7, 8, 10). IL‑17 RE is reciprocally down‑regulated in psoriatic lesions (10). The interaction of IL‑17C with IL‑17 RE promotes mucosal immunity through the induction of anti‑bacterial peptides and pro‑inflammatory cytokines and chemokines (4, 6, 8, 9). IL‑17C action supports the integrity of the colon epithelium following infection induced damage (4, 6, 11) but also contributes to psoriatic skin thickening and the progression of arthritis (4, 8, 9). IL‑17C is additionally up‑regulated in Th17 cell dependent autoimmunity (5). In this setting, it exacerbates disease severity by inducing Th17 cell production of IL‑17A, IL‑17F, IL‑22, CCR6, and CCL20 (5). The up‑regulation of IL‑17 RE in hepatocellular carcinoma is associated with poor prognosis (12).
Pappu, R. et al. (2012) Trends Immunol. 33:343.
Rubino, S.J. et al. (2012) Trends Immunol. 33:112.
Li, T.S. et al. (2006) Cell. Signal. 18:1287.
Ramirez-Carrozzi, V. et al. (2011) Nat. Immunol. 12:1159.
Chang, S.H. et al. (2011) Immunity 35:611.
Song, X. et al. (2011) Nat. Immunol. 12:1151.
Pfeifer, P. et al. (2013) Am. J. Respir. Cell Mol. Biol. 48:415.
Johnston, A. et al. (2013) J. Immunol. 190:2252.
Yamaguchi, Y. et al. (2007) J. Immunol. 179:7128.
Johansen, C. et al. (2009) Br. J. Dermatol. 160:319.
Reynolds, J.M. et al. (2012) J. Immunol. 189:4226.
Liao, R. et al. (2013) J. Exp. Clin. Cancer Res. 32:3.
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