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 B-propeller domains of LRP-5/6 has been mapped (2-4, 7). The 226aa, 35kD 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 overexpressed, 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).
Source:Recombinant corresponding to aa1-259 from human Dkk-2 expressed in CHO cells.
Molecular Weight:~25.8kD
Endotoxin Level:≤1EU/1ug (LAL)
Biological Activity:Measured in a competitive binding assay. When recombinant mouse Kremen-1 is immobilized at 4ug/ml (100ul/well), recombinant human Dkk-2 inhibits 50% binding of biotinylated recombinant human Dkk-1 (200ng/mL) at the concentration range of 1.5-6ug/ml.
Storage and Stability:Lyophilized powder may be stored at -20°C. Stable for 12 months at -20°C. Reconstitute with PBS. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Reconstituted product is stable for 6 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.
仕様
Size：10ug
Source Antigen：Recombinant, CHO
Grade：Highly Purified
Purity：~95% (SDS-PAGE)
Form：Supplied as a lyophilized powder in PBS, EDTA. Reconstitute with PBS to 100ug/ml.
