IL-17 RE Antibody (944904) [Alexa Fluor® 700] Summary
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Immunogen
Mouse myeloma cell line NSO-derived recombinant mouse IL-17 RE
Met1-His414
Accession # Q8BH06
Met1-His414
Accession # Q8BH06
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Specificity
Detects mouse IL-17 RE in direct ELISAs.
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Isotype
IgG1
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Clonality
Monoclonal
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Host
Rat
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Applications/Dilutions
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Dilutions
- Flow Cytometry 0.25-1 ug/10^6 cells
Packaging, Storage & Formulations
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Storage
Store the unopened product at 2 – 8 °C. Do not use past expiration date.
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Buffer
Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for IL-17 RE Antibody (944904) [Alexa Fluor® 700]
- 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).
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).
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
product targets : Ribosomal S17 Kinase (RSK) inhibitors