Human Dkk-2 Alexa Fluor® 700-conjugated Antibody

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.

Preparation and Storage

Background: Dkk-2

Dickkopf related protein 2 (Dkk-2) is a member of the Dickkopf family of secreted Wnt modulators (1-3). Dkk proteins contain a signal peptide and two conserved cysteine-rich domains that are separated by a linker region. The second cysteine-rich domain mediates Dkk-2 binding activities, and its interaction with  beta -propeller domains of LRP‑5/6 has been mapped (2-4, 7). The 226 amino acid (aa), ~35 kDa mature human Dkk-2 shares 96%, 97%, 97%, 97%, 97% and 98% aa identity with mouse, rat, canine, equine, bovine and porcine Dkk-2, respectively. Mouse Dkk-2 can activate the canonical Wnt signaling pathway in Xenopus embryos, showing evolutionary conservation of function (5). Dkk proteins modify Wnt engagement of a receptor complex composed of a Frizzled protein and a low-density lipoprotein receptor-related protein, either LRP‑5 or LRP‑6 (3). Also, Kremen-1 and Kremen-2 are high affinity receptors for Dkk-1 and Dkk-2 (9). When LRP‑6 is over-expressed, direct high‑affinity binding of Dkk-2 to LRP can enhance canonical Wnt signaling (6-8). However, when Dkk‑2 and LRP‑6 form a ternary complex with Kremen‑2, Wnt signaling is inhibited due to internalization of Dkk‑2/LRP6/Krm2 complexes (9, 10). Thus, depending on the cellular context, Dkk‑2 can either activate or inhibit canonical Wnt signaling (3). In contrast, binding of Dkk-1 or Dkk-4 to LRP is consistently antagonistic (3). Dkk proteins are expressed in mesenchymal tissues and control epithelial transformations. Dkk-2 expression has been studied most in bone and eye, although it is expressed as early as periimplantation in mice (11). Mouse Dkk-1 or Dkk-2 deficiencies have opposite effects on bone homeostasis, despite down‑regulating Wnt antagonism in both cases (12, 13). Dkk-2 expression is induced by Wnts in bone, and is thought to enhance bone density by promoting terminal differentiation of osteoblasts and mineral deposition (12). In contrast, Dkk-1 negatively regulates late osteoblast proliferation, which limits bone density (13). Dkk-2-deficient mice are blind, exhibiting faulty differentiation of corneal epithelium and ectopic blood vessels in the periocular mesenchyme (14, 15).

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.

Related Research Areas

• Negative Regulators of EMT
• New Tools: for Developmental Research
• Wnt Family
• Wnt Inhibitors