Human Integrin alpha 2/CD49b Alexa Fluor® 647-conjugated Antibody
Human Integrin alpha 2/CD49b Alexa Fluor® 647-conjugated Antibody Summary
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
Background: Integrin alpha 2/CD49b
Integrin alpha 2 is one of twelve integrin family alpha subunits that share the beta 1 subunit (1‑3). Integrin alpha 2 beta 1 is the non-covalent heterodimer of 160 kDa alpha 2 (CD49b) and 130 kDa beta 1 (CD29) type I transmembrane glycoprotein subunits and is one of six very late antigens on activated T cells, designated VLA2 (3). The alpha 2 extracellular domain (ECD) contains an I (inserted) domain which includes the ligand binding site (2, 3). 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 1102 amino acid (aa) human alpha 2 extracellular domain (ECD) shares 83‑89% aa sequence identity with mouse, rat, canine, bovine and equine alpha 2. The 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, with alpha 2 beta 1 preferring collagens I‑III (4, 5). Platelet alpha 2 beta 1, also called GPIa, cooperates with another adhesion protein, GPVI, to coordinate platelet collagen binding and activation (3, 6, 7). Other alpha 2 beta 1 ligands include laminin, decorin, E-cadherin, and collagen-like regions of collectin molecules such as C1q (4). Adhesion is synergized by crosstalk with syndecan-1 or HGF R/c-Met, and antagonized by crosstalk with Integrin alpha 1 beta 1 (8‑10). In addition to expression on selected hematopoietic cells, alpha 2 beta 1 is present on a wide variety of non-hematopoietic cells (4). Mice deficient in the alpha 2 subunit have defects in innate immune responses, wound mast cell infiltration and angiogenesis, and platelet responses to collagen (6, 11, 12). In innate immunity, alpha 2 beta 1 binding to C1q initiates the complement cascade and costimulates mast cell activation, triggering neutrophil influx (4, 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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