Abstract
The osteoclast (OC) is the resorptive cell of the skeleton responsible for both normal homeostasis and pathological bone loss. NF-κB is a critical signal for OC differentiation downstream of RANKL, and its global disruption protects mice from pathological bone loss. Differently from other TNF family members, RANKL activates both the classical NF-κB pathway, activating both p65 and cRel, and the alternative pathway, inducing expression and activation of RelB. In order to determine whether the classical and alternative NF-κB pathways have distinct roles in OC differentiation, we examined mice lacking p65, RelB, or cRel.
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