Mouse Integrin alpha 10 Alexa Fluor® 405-conjugated Antibody Summary
Phe23-Thr1119 (Integrin alpha 10) and Gln21-Asp728 (Integrin beta 1)
Accession # NP_001289400.1 (Integrin alpha 10) and P09055 (Integrin beta 1)
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.
Background: Integrin alpha 10
Integrin alpha 10 beta 1 is one of twelve integrin family adhesion receptors that share the beta 1 subunit (1‑3). The non‑covalent heterodimer of 160 kDa alpha 11 and 130 kDa beta 1/CD29 type I transmembrane glycoprotein subunits is expressed mainly on chondrocytes within cartilage, but also in fibrous connective tissues such as heart valves and ligaments (3, 4). The alpha 10 extracellular domain (ECD) contains an I (inserted) domain which includes the ligand binding site (2, 3, 5). The beta 1 ECD contains a vWFA domain, which participates in binding. Each subunit then has a transmembrane sequence and a short cytoplasmic tail. The dimer is folded when it is least active. Divalent cations and intracellular (inside‑out) signaling convert it to its most active, extended and open conformation (1, 2). The 1100 amino acid (aa) mouse alpha 10 extracellular domain (ECD) shares 96% aa sequence identity with rat and 88‑89% with human, rabbit, porcine, canine and bovine alpha 10, while the 708 aa mouse beta 1 ECD shares 98% aa identity with rat and 93‑94% with human, bovine, porcine, ovine, canine and feline beta 1. A potential mouse alpha 10 splice variant diverges at aa 1039 and is terminated prematurely. If translated, this variant would result in a secreted protein (6). I domain‑containing beta 1 integrins alpha 1 beta 1, alpha 2 beta 1, alpha 10 beta 1 and alpha 11 beta 1 all bind collagens; all but alpha 11 beta 1 also bind laminins (5, 7, 8). During cartilage differentiation, alpha 10 beta 1 is thought to be the main integrin binding type II and IX cartilage collagens (3‑5, 7‑10). However, deletion of mouse alpha 10 causes a mild phenotype including slightly shortened bones and narrowed hypertrophic zones, indicating that another collagen‑binding integrin, likely alpha 2 beta 1, may compensate for alpha 10 beta 1 functions (11). Migration of melanoma cells has been noted to correlate with alpha 10 beta 1 expression (12).
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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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