The Wnt/β-Catenin signaling pathway is a key regulator in bone development and bone homeostasis. Inactivating mutations in the Wnt co-receptor Low density lipoprotein Receptor related Protein 5 (LRP5) results in osteoporosis while “activating” mutations in LRP5 results in high bone mass. Dickkopf-1 (Dkk1) is a secreted Wnt inhibitor that binds to LRP5 and LRP6 reducing their availability to form a complex with Wnt and Frizzled and resulting in unrestrained Wnt signaling. It is expected that a decrease in Dkk1 will result in an increase in Wnt activity and ultimately a high bone mass phenotype. An allelic series of Dkk1 mutant mice were generated to examine the affects of reduced Dkk1 levels on bone density, morphology, and mechanical properties.

This content is only available via PDF.
You do not currently have access to this content.