Human IL-36Ra/IL-1F5 Alexa Fluor® 594-conjugated Antibody Summary
Met1-Asp155
Accession # Q9UBH0
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
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Preparation and Storage
Background: IL-36Ra/IL-1F5
Human interleukin 1 family member #5 [IL-1F5; also named FIL-1δ (delta), IL-1HY1, IL-1H3, and IL-1L1] is a member of the IL-1 family of proteins (1‑5). IL-1 family members include IL-1 beta, IL-1 alpha, IL-1ra, IL-18, and IL-1F5 - IL-1F10 (6). All family members show a 12 beta -strand, beta -trefoil configuration, and all family members are believed to have arisen from a common ancestral gene that underwent multiple duplications (6). The human IL-1F5 gene is in closest proximity to the gene for IL-1ra and is likely a relatively recent duplication of the IL-1ra gene (2, 3). IL-1F5 is synthesized as a 155 amino acid (aa) protein that contains no signal sequence, no prosegment and no potential N-linked glycosylation site(s) (2‑5). Nevertheless, it appears to be secreted as a 17 kDa monomer (5). There is an alternate start site that potentially gives rise to an alternate splice form (5). The translated product, however, has a premature stop codon, resulting in a truncated 16 aa peptide. Human to mouse, full length IL-1F5 has 90% aa identity. Within the family, IL-1F5 is 50% aa identical to IL-1ra, and 32%, 31%, 35%, 37%, 32%, and 42% aa identical to IL‑1 beta, IL-1F6, F7, F8, F9, and F10, respectively. Cells reported to express IL-1F5 include monocytes, B cells, dendritic cells/Langerhans cells, keratinocytes, and gastric fundus Parietal and Chief cells (1, 7). The receptor for IL-1F5 has not been positively identified. Indirect evidence suggests it is IL-1 Rrp2 and/or IL‑1 RAcP (8). In either case, activity association with receptor binding is also unclear. It was initially reported to be an antagonist of IL-1F9 activity (4, 6). This would be consistent with its hypothesized relationship to IL-1ra. Studies, however, find IL-1F5 antagonist activity difficult to demonstrate (8).
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