Kong et al. generated opgl gene knockout mice to test whether OPGL/RANKL — a TNF-family molecule expressed by osteoblasts and T cells — is truly essential for osteoclast formation and bone remodeling in vivo, and whether it has additional roles in the immune system beyond what cell culture suggested.
This work established the molecular foundation for understanding RANKL's central role in osteoclast function, which became critical for developing osteoporosis treatments like denosumab (anti-RANKL antibody).
The complete osteopetrotic phenotype in knockout mice demonstrated that RANKL inhibition can profoundly affect bone remodeling.
Kong et al. generated opgl gene knockout mice to test whether OPGL/RANKL — a TNF-family molecule expressed by osteoblasts and T cells — is truly essential for osteoclast formation and bone remodeling in vivo, and whether it has additional roles in the immune system beyond what cell culture suggested.
This work established the molecular foundation for understanding RANKL's central role in osteoclast function, which became critical for developing osteoporosis treatments like denosumab (anti-RANKL antibody).
The complete osteopetrotic phenotype in knockout mice demonstrated that RANKL inhibition can profoundly affect bone remodeling.