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    Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation.

    The authors generated osteoclast- and osteoblast-targeted cathepsin K (Ctsk) knockout mice. Deletion of Ctsk in cells of the monocyte-osteoclast lineage, resulted in increased bone volume and bone formation as well as osteoclast and osteoblast number, while deletion of Ctsk in osteoblasts had no effect on bone. Deletion of Ctsk in hematopoietic cells increased their sphingosine kinase 1 (Sphk1) expression and production of sphingosine-1-phosphate (S1P). This, in turn, increased alkaline phosphatase and mineralized nodules in osteoblast cultures. 

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