A scaffold for directing bone breakdown

Abstract

Bone Biology Too much bone breakdown by osteoclasts and not enough bone formation by osteoblasts can lead to osteoporosis. The cytokine RANKL and the kinase p38 stimulate precursor cells in the bone to become osteoclasts. Lin et al. found that the binding of RANKL to its receptor complex recruited the scaffold protein RACK1, leading to the activation of p38. RANKL was less effective at stimulating osteoclast formation and bone loss in those portions of mouse skulls treated to reduce RACK1 levels than in untreated parts. These results provide a potential therapeutic target for osteoporosis. Sci. Signal. 8 , ra54 (2015).