I4026
Interleukin-17 from mouse
≥97% (SDS-PAGE), recombinant, expressed in E. coli, lyophilized powder, suitable for cell culture
Synonym(s):
CTLA-8, IL-17
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About This Item
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biological source
mouse
Quality Level
recombinant
expressed in E. coli
Assay
≥97% (SDS-PAGE)
form
lyophilized powder
mol wt
16.5 kDa
packaging
pkg of 25 μg
technique(s)
cell culture | mammalian: suitable
impurities
endotoxin, tested
UniProt accession no.
storage temp.
−20°C
Gene Information
mouse ... Il17a(16171)
Biochem/physiol Actions
IL-17 (interleukin-17) participates in the activation of nuclear factor-κB and mitogen-activated protein kinase pathways and CCAAT/enhancer-binding protein family of transcription factors, thereby regulating pro-inflammatory and antimicrobial genes. In rheumatoid arthritis, IL-17 is responsible for the inflammation as well as destruction of joints.
Interleukin 17 (IL-17), initially known as CTLA-8, is a T cell-expressed polypeptide that appears to be involved in the regulation of the hematopoietic system. IL-17 has been shown to induce IL-6, IL-8, and G-CSF production by fibroblasts; all of these cytokines have demonstrated effects on hematopoiesis.
Physical form
Lyophilized from a 0.2 μm filtered solution in 30% acetonitrile and 0.1% trifluoroacetic acid containing 1.25 mg of bovine serum albumin.
Analysis Note
The biological activity of mouse IL-17 is measured by its ability to induce IL-6 production using NIH/3T3 cells.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Tomoki Maekawa et al.
Nature communications, 6, 8272-8272 (2015-09-17)
Del-1 is an endothelial cell-secreted anti-inflammatory protein. In humans and mice, Del-1 expression is inversely related to that of IL-17, which inhibits Del-1 through hitherto unidentified mechanism(s). Here we show that IL-17 downregulates human endothelial cell expression of Del-1 by
Annica Andersson et al.
Clinical immunology (Orlando, Fla.), 161(2), 324-332 (2015-10-02)
Interleukin-17 (IL-17) drives inflammation and destruction of joints in rheumatoid arthritis (RA). The female sex hormone 17β-estradiol (E2) inhibits experimental arthritis. γδT cells are significant producers of IL-17, thus the aim of this study was to investigate if E2 influenced
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