IL-1F8, Recombinant, Mouse, aa31-183 (IL-36 beta, Interleukin-36 beta, Interleukin-1 Family Member 8, Il36b, Fil1e, Il1f8)

Mouse interleukin-36 beta [IL-36B; previously IL-1F8, FIL-1H (eta) and IL-1H2] is a member of the IL-1 family of proteins that includes IL-1B, IL-1A, IL-1ra, IL-18, IL-36Ra/IL-1F5, IL-36A/IL-1F6, IL-37/IL-1F7, IL-36G/IL-1F9 and IL-1F10. All family members show a 12 B-stranded B-trefoil configuration, share up to 50% aa sequence identity, and are believed to have arisen from a common ancestral gene. Although two alternatively spliced transcript variants for human IL-36B/IL-1F8 have been described, to date, only one mouse IL-36B/IL-1F8 isoform is known. Mouse IL-36B/IL-1F8 is synthesized as a 183aa protein that contains no signal sequence, no prosegment and no potential N-linked glycosylation site(s). Mouse IL-36B/IL-1F8 shares 61% and 74% aa identity with human IL-36B isoform 2 and rat IL-36B, respectively. IL-36B 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. The receptor for IL-36 proteins is IL-1 Rrp2, with IL-1 RAcP as a coreceptor. Antagonism of IL-36 proteins by IL-36Ra, which also binds IL-1 Rrp2, has been shown by some investigators. Skin keratinocytes express highest levels of IL-36 proteins and their receptors, followed by epithelia in the esophagus, trachea and bronchae. IL-36B expression is increased in psoriatic skin and may play a role in pathogenesis of psoriasis. IL-36B is also expressed in resting and activated monocytes and B cells, synovial fibroblasts, neurons and glia, and is detectable in plasma and body fluids. IL-36B, along with IL-36A and IL-3G, is up-regulated by IL-A and TNF-A in keratinocytes, and has been shown to activate NF-kB and MAPK signaling pathways in an IL-1 Rrp2-dependent manner. Full-length recombinant IL-36 proteins appear less active than their endogenous counterparts, but trimming of the N-termini enhances their activity.\n\nSource:\nRecombinant corresponding to aa31-183 from mouse IL-36 beta, expressed in E.coli.\n\nMolecular Weight:\n~17.4kD\n\nBiological Activity:\nMeasured by its ability to induce IL-6 secretion by NIH/3T3 mouse embryonic fibroblasts. The ED50 for this effect is typically 1-6mg/ml.\n\nEndotoxin: ~1EU/1ug (LAL)\n\nStorage and Stability:\nLyophilized powder may be stored at -20 degrees C. Stable for 12 months at -20 degrees C. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Reconstituted product is stable for 3 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

I7663-24Y

Size

10ug

Form

Supplied as a lyophilized powder in Tris-HCl, EDTA, sodium chloride, TCEP. BSA free. Reconstitute with 10mM Tris-HCl, pH 8.0 to 0.1mg/ml.

Purity

~95% (SDS-PAGE)

References

1. Smith, D.E. et al. (2000) J. Biol. Chem. 275:1169. 2. Kumar, S. et al. (2000) J. Biol. Chem. 275:10308. 3. Nicklin, M.J.H. et al. (2002) Genomics 79:718. 4. Dunn, E. et al. (2001) Trends Immunol. 22:533. 5. Dinarello, C. et al. (2010) Nat. Immunol. 11:973. 6.Barksby, H.E. et al. (2007) Clin. Exp. Immunol. 149:217. 7. Towne, J.E. et al. (2004) J. Biol. Chem. 279:13677. 8. Johnston, A. et al. (2011) J. Immunol. 186:2613. 9. Magne, D. et al. (2005) Arthritis Res. Ther. 8:R80. 10. van Asseldonk, E.J.P. et al. (2010) Obesity 18:2234. 11. Wang, P. et al. (2005) Cytokine 29:245. 12. Blumberg, H. et al. (2010) J. Immunol. 185:4354.