Human/Mouse Cadherin-13 Alexa Fluor® 350-conjugated Antibody Summary
Accession # P55290
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
Cadherin-13, also known as T-cadherin and H-cadherin, is a 105 kDa member of the cadherin family of transmembrane glycoproteins that mediate calcium-dependent intercellular adhesion (1). However, Cadherin-13 is an atypical member, lacking transmembrane and cytosolic domains and containing a GPI moiety that anchors Cadherin-13 to the plasma membrane (1‑2). Human Cadherin-13 is synthesized as a 713 amino acid (aa) precursor that contains a 22 aa signal sequence, a 116 aa propeptide, a 555 aa mature chain, and a second propeptide of 20 aa that is removed in the mature form to reveal the GPI anchor. The mature form contains five cadherin domains and eight potential sites for N-linked glycosylation. Mature human Cadherin-13 shares 96% aa identity with mature mouse Cadherin-13. Cadherin-13 is expressed in various tissues. It is highly expressed in the heart, and in the CNS, Cadherin-13 is expressed in the cerebral cortex, medulla, hippocampus, amygdala, thalamus, and substantia nigra (2). There are higher levels of Cadherin-13 in the adult brain than in developing brain (2). Cadherin-13 is also expressed in skin in the basal layer of the epidermis, lung, liver, kidney, and blood vessels (2). The structural characteristics of Cadherin-13 predict that it is unlikely to function as a true adhesion molecule in vivo (2). It is suggested that it may act rather as a signaling receptor participating in recognition of the environment and regulation of cell motility, proliferation, and phenotype (2). Cellular expression levels of Cadherin-13 in various tissues often correlate, negatively or positively, with the proliferative potential of the cells (2). Cadherin-13 may also act as a suppressor of tumor cell growth (2). This potential role for Cadherin-13 was emphasized by localization of Cadherin-13 gene to chromosome 16q24, a region exhibiting loss of heterozygosity in many solid tumors (2). Allelic loss of chromosome bands 16q24.1-q24.2 and reduced expression of Cadherin-13, as well as hypermethylation of the remaining allele have been detected in a considerable number of human cancers (2).
- Tanihara, H. et al. (1994) Cell Adhes. Commun. 2:15.
- Philippova, M. et al. (2009) Cell. Signal. 21:1035.
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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