Recombinant Human Dkk-2 Protein


Recombinant Human Wnt‑3a (Catalog # 5036-WN) induces a dose responsive increase in Wnt reporter activity in HEK293 cells (green circles). Recombinant Human Dkk‑2 (Catalog # 6628‑DK) inhibits a constant dose more

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Recombinant Human Dkk-2 Protein Summary

Details of Functionality
Measured by its ability to inhibit Wnt induced TCF reporter activity in HEK293 human embryonic kidney cells. Recombinant Human Dkk-2 (Catalog # 6628-DK) inhibits a constant dose of 500 ng/mL of Recombinant Human Wnt-3a (Catalog # 5036‑WN). The ED50 for this effect is 50-300 ng/mL.
Chinese Hamster Ovary cell line, CHO-derived human Dkk-2 protein
Accession #
N-terminal Sequence
Protein/Peptide Type
Recombinant Proteins
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.


Theoretical MW
25.8 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
32-36 kDa, reducing conditions
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6628-DK in the following applications:

Packaging, Storage & Formulations

Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
Lyophilized from a 0.2 μm filtered solution in PBS and EDTA with BSA as a carrier protein.
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 100 μg/mL in PBS.


This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Human Dkk-2 Protein

  • dickkopf (Xenopus laevis) homolog 2
  • dickkopf 2
  • dickkopf homolog 2 (Xenopus laevis)
  • dickkopf related protein-2
  • dickkopf-2
  • dickkopf-related protein 2
  • Dkk2
  • Dkk-2
  • hDkk-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).

  1. Monaghan, A.P. et al. (1999) Mech. Dev. 87:45.
  2. Krupnik, V.E. et al. (1999) Gene 238:301.
  3. Niehrs, C. (2006) Oncogene 25:7469.
  4. Chen, L. et al. (2008) J. Biol. Chem. 283:23364.
  5. Wu, W. et al. (2000) Current Biol. 10:1611.
  6. Mao, B. et al. (2001) Nature 411:321.
  7. Li, L. et al. (2002) J. Biol. Chem. 277:5977.
  8. Brott, B. and S.Y. Sokol (2002) Mol. Cell. Biol. 22:6100.
  9. Mao, B. et al. (2002) Nature 417:664.
  10. Mao, B. and C. Niehrs (2003) Gene 302:179.
  11. Zhang, Y. et al. (2009) J. Reprod. Dev. 55:17.
  12. Li, X. et al. (2005) Nat. Genet. 37:945.
  13. van der Horst, G. et al. (2005) J. Bone Miner. Res. 20:1867.
  14. Mukhopadhyay, M. et al. (2006) Development 133:2149.
  15. Gage, P.J. et al. (2008) Dev. Biol. 317:310.

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Gene Symbol DKK2