>80%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
18 kDa. 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
19-25 kDa, reducing conditions
Publications
Read Publication using 8949-IL/CF 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, -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in HCl with Trehalose.
Purity
>80%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 100 μg/mL in 4 mM HCl.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Rat IL-17E Protein, CF
IL17E
IL-17E
IL25
IL-25
interleukin 25
Interleukin-17E
interleukin-25
Background
The Interleukin-17 (IL-17) family of proteins are immunoregulatory cytokines that share a conserved cysteine-rich region. IL-17E, which is also known as IL-25, promotes Th2-biased immune responses. This is in contrast to other IL-17 family members which promote Th1- and Th17-biased inflammation. IL-25 is an important mediator of allergic reactions and protection against intestinal parasites (1, 2). Mature rat IL-25 shares 80% and 91% amino acid sequence identity with mouse and human IL-25, respectively (3, 4). During helminth infections and allergic reactions, IL-25 is locally up-regulated in intestinal and airway epithelial cells, atopic dermatitis skin lesions, and local Th2 cells, eosinophils, and basophils (4-9). It binds to IL-17 RB but also requires IL-17 RA to exert its activity (3, 8, 10). IL-25 acts on a variety of cell types which respond with increased production of Th2 cytokines (e.g. IL-4, IL-5, IL-13) and reduced production of Th1 and Th17 cytokines (e.g. IFN-gamma , IL-12, IL-23, IL-17A, IL-17F) (4-6, 8, 9, 11-15). Airway IL-25 can be activated by MMP-7, a protease that is up-regulated in airway epithelium in response to allergen exposure (16). Cleaved IL-25 shows enhanced binding to IL-17 RB and stronger induction of Th2 cytokines (16). The Th2 cytokines, in turn, trigger expansion of Th2 memory cells and anti-inflammatory M2 macrophages, increased eosinophil mobilization and activation, and dendritic cell migration (4, 6, 9, 13). These actions promote protective anti-helminth immune responses (4, 5) as well as allergic inflammation and airway hyperreactivity (11). The IL-25 induced suppression of Th1 and Th17 cytokines limits Th17 cell expansion and disease pathology in autoimmunity and colitis (12, 15). IL-25 also promotes vascular endothelial cell proliferation and assembly into tubular structures (7). It supports the integrity of the blood-brain barrier and limits CD4+ T cell infiltration into the brain (17).
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