Recombinant Mouse IL-36 beta/IL-1F8 (aa 31-183) Protein
Recombinant Mouse IL-36 beta/IL-1F8 (aa 31-183) Protein Summary
Product Specifications
Ser31-Lys183
Analysis
Product Datasheets
Carrier Free
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
7060-ML
| Formulation | Lyophilized from a 0.2 μm filtered solution in MES, NaCl, TCEP, EDTA, CHAPS and PEG 8000 with BSA as a carrier protein. |
| Reconstitution | Reconstitute at 100 μg/mL in 10 mM Tris-HCl, pH 8.0. |
| Shipping | The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below. |
| Stability & Storage: | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
|
7060-ML/CF
| Formulation | Lyophilized from a 0.2 μm filtered solution in MES, NaCl, TCEP, EDTA, CHAPS and PEG 8000 with Trehalose. |
| Reconstitution | Reconstitute at 100 μg/mL in 10 mM Tris-HCl, pH 8.0. |
| Shipping | The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. |
| Stability & Storage: | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
|
Scientific Data
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Recombinant Mouse IL-36 beta /IL-1F8 (aa 31-183) (Catalog # 7060-ML) induces IL-6 secretion in the NIH‑3T3 mouse embryonic fibroblast cell line. The ED50 for this effect is 1-6 ng/mL.
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1 µg/lane of Recombinant Mouse IL-36 beta /IL-1F8 (aa 31-183) was resolved with SDS-PAGE under reducing (R) conditions and visualized by silver staining, showing a single band at 16 kDa.
Reconstitution Calculator
Background: IL-36 beta/IL-1F8
Mouse interleukin‑36 beta [IL-36 beta ; previously IL‑1F8, FIL‑1 eta (eta) and IL‑1H2] is a member of the IL‑1 family of proteins that includes IL‑1 beta, IL‑1 alpha, IL‑1ra, IL‑18, IL‑36Ra/IL‑1F5, IL‑36 alpha /IL‑1F6, IL‑37/IL‑1F7, IL‑36 gamma /IL‑1F9 and IL‑1F10 (1 ‑ 6). All family members show a 12 beta ‑stranded beta ‑trefoil configuration, share up to 50% amino acid (aa) sequence identity, and are believed to have arisen from a common ancestral gene (3, 4). Although two alternatively spliced transcript variants for human IL‑36 beta /IL‑1F8 have been described, to date, only one mouse IL‑36 beta /IL‑1F8 isoform is known (3). Mouse IL‑36 beta /IL‑1F8 is synthesized as a 183 amino acid (aa) protein that contains no signal sequence, no prosegment and no potential N‑linked glycosylation site(s) (1, 2). Mouse IL‑36 beta /IL‑1F8 shares 61% and 74% aa identity with human IL‑36 beta isoform 2 and rat IL‑36 beta, respectively. IL‑36 beta is agonistic, stimulating release of inflammatory mediators such as IL‑6 and IL‑8, and cytotoxic peptides such as beta-defensins 2 and 3 that aid in defense against microbial pathogens (7 ‑ 10). The receptor for IL-36 proteins is IL‑1 Rrp2, with IL‑1 RAcP as a coreceptor (7, 9). Antagonism of IL‑36 proteins by IL‑36Ra, which also binds IL‑1 Rrp2, has been shown by some investigators (5, 6). Skin keratinocytes express highest levels of IL‑36 proteins and their receptors, followed by epithelia in the esophagus, trachea and bronchae (7 ‑ 9). IL‑36 beta expression is increased in psoriatic skin and may play a role in pathogenesis of psoriasis (7, 8). IL‑36 beta is also expressed in resting and activated monocytes and B cells, synovial fibroblasts, neurons and glia, and is detectable in plasma and body fluids (1, 7, 9, 11). IL‑36 beta, along with IL‑36 alpha and IL‑36 gamma, is up‑regulated by IL‑1 alpha and TNF‑ alpha in keratinocytes, and has been shown to activate NF‑ kappa B and MAPK signaling pathways in an IL‑1 Rrp2‑dependent manner (7 ‑ 9). Full‑length recombinant IL‑36 proteins appear less active than their endogenous counterparts, but trimming of the N‑termini enhances their activity (9, 12).
- Smith, D.E. et al. (2000) J. Biol. Chem. 275:1169.
- Kumar, S. et al. (2000) J. Biol. Chem. 275:10308.
- Nicklin, M.J.H. et al. (2002) Genomics 79:718.
- Dunn, E. et al. (2001) Trends Immunol. 22:533.
- Dinarello, C. et al. (2010) Nat. Immunol. 11:973.
- Barksby, H.E. et al. (2007) Clin. Exp. Immunol. 149:217.
- Towne, J.E. et al. (2004) J. Biol. Chem. 279:13677.
- Johnston, A. et al. (2011) J. Immunol. 186:2613.
- Magne, D. et al. (2005) Arthritis Res. Ther. 8:R80.
- van Asseldonk, E.J.P. et al. (2010) Obesity 18:2234.
- Wang, P. et al. (2005) Cytokine 29:245.
- Blumberg, H. et al. (2010) J. Immunol. 185:4354.
Citation for Recombinant Mouse IL-36 beta/IL-1F8 (aa 31-183) Protein
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
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Psoriasiform dermatitis is driven by IL-36-mediated DC-keratinocyte crosstalk.
Authors: Tortola L, Rosenwald E, Abel B, Blumberg H, Schafer M, Coyle A, Renauld J, Werner S, Kisielow J, Kopf M
J Clin Invest, 2012-10-15;122(11):3965-76.
Species: Mouse
Sample Types: Whole Cells
Applications: Bioassay
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