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    Wnt/β-catenin signaling is differentially regulated by Gα proteins and contributes to fibrous dysplasia.

    The authors examined interactions of the four major Gα protein families (Gαs, Gαi/o, Gαq/11, and Gα12/13) with the Wnt/β-catenin signaling pathway and identify a causative role of Wnt/β-catenin signaling in fibrous dysplasia (FD) of bone.  They further demonstrate that activating Gαs mutations, which cause FD, potentiated Wnt/β-catenin signaling, and removal of Gαs led to reduced Wnt/β-catenin signaling and decreased bone formation.  These data argue that activated Gα proteins are playing physiologically significant roles during both skeletal development and disease by modulating Wnt/β-catenin signaling.


    Regard JB, Cherman N, Palmer D, Kuznetsov SA, Celi FS, Guettier JM, et al

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