generated and analyzed the first genetic models of osteoporosis by overexpression of human RANKL in transgenic mice.

These unique mouse models represent an important advance for understanding the pathogenesis of high-turnover bone diseases such as osteoporosis while also permitting the preclinical evaluation of novel inhibitors that target either human RANKL or osteoclast activity. For more information please contact This email address is being protected from spambots. You need JavaScript enabled to view it.