Mouse IL-17D Alexa Fluor® 488-conjugated Antibody Summary
Ala25-Arg205
Accession # NP_665836
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-17D
The Interleukin 17 (IL-17) family proteins, comprising six members (IL-17, IL-17B through IL-17F), are secreted, structurally related proteins that share a conserved cysteine-knot fold near the C-terminus, but have considerable sequence divergence at the N‑terminus (1, 2, 6). With the exception of IL-17B, which exists as a non‑covalently linked dimer, all IL-17 family members are disulfide-linked dimers (3). IL-17 family proteins are pro-inflammatory cytokines that induce local cytokine production and are involved in the regulation of immune functions (1, 2, 6). Two receptors (IL-17 R, and IL-17B R), which are activated by IL-17 family members, have been identified. In addition, at least three additional orphan type I transmembrane receptors with homology to IL-17 R, including IL-17 RL (IL-17 RC), IL-17 RD, and IL-17 RE, have also been reported (1‑6). Mouse IL-17D is synthesized as a 205 amino acid (aa) precursor that contains a putative 24 aa signal peptide and a 181 aa mature segment. The mature region contains two potential N-linked glycosylation sites and eight cysteines, four of which are involved in the formation of a modified cysteine-knot motif (5). The molecule is reported to exist as a 53 kDa disulfide-linked homodimer (2, 5). Given that its predicted homodimeric molecular weight is 40 kDa, the molecule is presumably glycosylated. In the mature region, mouse IL-17D is 88% aa identical to human IL-17D. There is less than 30% aa identity between mouse IL-17D and other members of the mouse IL-17 family. IL-17D is expressed in skeletal muscle, adipose tissue, fetal liver, and heart, plus resting CD4+ T cells and CD19+ B cells (1). R&D Systems has shown IL-17D binding to a mouse IL-17 R/Fc construct in a functional ELISA. IL-17D is known to induce the production of IL-8, IL-6 and GM-CSF (5).
- Aggarwal, S. and A.L. Gurney (2002) J. Leukoc. Biol. 71:1.
- Moseley, T.A. et al. (2003) Cytokine & Growth Factor Rev. 14:155.
- Hymowitz, S.G. et al. (2001) EMBO J. 20:5332.
- Haudenschild, D. et al. (2002) J. Biol. Chem. 277:4309.
- Starnes, T. et al. (2002) J. Immunol. 169:642.
- Kolls, J.K. and A. Linden (2004) Immunity 21:467.
Product Datasheets
Product Specific Notices
This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.
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