Human EMR2 Alexa Fluor® 488-conjugated Antibody Summary
Accession # AAI27006
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.
Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
EMR2 (EGF-like module-containing mucin-like receptor 2; designated CD312) is a glycoprotein belonging to the EGF-TM7 family of adhesion-type class B 7‑transmembrane (TM) receptors. EGF-like sequences within long extracellular N-termini, and a GPS (G-protein proteolytic site) domain are characteristic of this family, which is mainly expressed on cells of the immune system (1, 2). The human EMR2 cDNA encodes an 823 amino acid (aa) protein with five EGF-like domains within the first 250 aa, followed by a mucin-like stalk, a GPS domain (aa 479‑530) and a 7‑TM sequence (aa 531‑785). The GPS domain is the site of autocatalytic cleavage, forming two cleaved portions that remain non-covalently attached as a heterodimer (1, 3). Of the first 290 aa of human EMR2, 284 aa (97%) are identical with family member CD97, likely due to gene duplication (2). The portion of human EMR2 N-terminal to the GPS domain (aa 1‑478) shares 64%, 59%, 48% and 45% aa identity with corresponding regions of canine EMR2, equine EMR2, mouse CD97 and rat CD97, respectively. Alternate splicing of EMR2 creates isoforms that contain 2‑5 EGF-like domains. Only the 5-EGF form contains EGF4, which is necessary for calcium-dependent binding of the EMR2/CD97 ligand, chondroitin sulfate (CS) (2, 4‑6). None of the isoforms engage the CD97 ligand, CD55 (DAF). EMR2 is restricted to myeloid cells (1, 2). EMR2 expression increases as monocytes differentiate into macrophages, and decreases with differentiation into dendritic cells (5). Activation increases neutrophil EMR2 expression (5). EMR2 localizes to the leading edge of migrating neutrophils and plays an important role in migration, adhesion and superoxide production (7). It is also thought to facilitate specific interaction of myeloid cells with peripheral B lymphocytes which express CS (6).
- Kwakkenbos, M.J. et al. (2004) Immunogenetics 55:655.
- Lin, H.-H. et al. (2000) Genomics 67:188.
- Lin, H.-H. et al. (2004) J. Biol. Chem. 279:31823.
- Stacey, M. et al. (2003) Blood 102:2916.
- Chang G.-W. et al. (2007) Biochem. Biophys. Res. Commun. 353:133.
- Kwakkenbos, M.J. et al. (2005) J. Leukoc. Biol. 77:112.
- Yona, S. et al. (2008) FASEB J. 22:741.
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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