Rictor is required for optimal bone accrual in response to anti-sclerostin therapy in the mouse
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文摘

Rictor-deficient mice contain normal trabecular but low cortical bone mass.

Rictor-deficient mice exhibit less bone resorption than normal.

Rictor deletion reduces Rankl expression by bone marrow stromal cells.

Rictor deficiency blunts bone anabolic effect of anti-sclerotin treatment.

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