Human Syndecan-1/CD138 Alexa Fluor® 594-conjugated Antibody
Human Syndecan-1/CD138 Alexa Fluor® 594-conjugated Antibody Summary
Gln18-Glu251
Accession # NP_002988
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
- 12 months from date of receipt, 2 to 8 °C as supplied.
Background: Syndecan-1/CD138
Syndecan-1, designated CD138, is a dimeric type I transmembrane (TM) protein that belongs to the syndecan family of Type 1 transmembrane proteins (1, 2). The four syndecan family members are major carriers of heparan sulfate (HS) and chondroitin sulfate glycosaminoglycans (GAGs) that have different expression patterns and extracellular sequences. Syndecan-1 forms weak non-covalent homodimers, or heterodimers with Syndecan-2 or -3, through interactions of the transmembrane domain (3). It is synthesized as a 310 amino acid (aa) precursor with a 17 aa signal sequence, a 234 aa extracellular domain (ECD) that includes three closely-spaced consensus Ser-Gly HS attachment sites near the N-terminus, a 25 aa TM segment, and a 34 aa cytoplasmic region that includes a PDZ binding motif with a tyrosine phosphorylation site. The ECD is variably modified by GAGs, producing molecular weights of 120-200 kDa for native Syndecan-1. Soluble forms are shed via proteolytic cleavage. Human Syndecan-1 ECD shares 65-71% aa identity with the ECD of rat, mouse, canine, equine and bovine Syndecan-1. Syndecan-1 shows highest expression on epithelial cells such as keratinocytes, and terminally differentiated B cells such as plasma cells (4, 5). It aids wound healing in skin, cornea, and heart following myocardial infarction by promoting re-epithelialization, migration, and collagen deposition (4-8). It binds chemokines, creating chemotactic gradients when shed, but also binds and modulates integrins to control the influx of leukocytes (5, 7, 9). The net effect is to allow, but limit, inflammation. In myeloma and other cancers, shedding of Syndecan-1 can facilitate growth, angiogenesis and metastasis (10-12). Growth factors, such as FGFs and HGF, bind GAG chains and use Syndecan-1 as a coreceptor (12, 13). The GAG chains may also be used by a variety of viruses and bacteria for cell adhesion and uptake (4).
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- Ojeh, N. et al. (2008) J. Invest. Dermatol. 128:26.
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- Derksen, P.W.B. et al. (2002) Blood 99:1405.
- Su, G. et al. (2007) J. Biol. Chem. 282:14906.
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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