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doi: 10.15586/ijfs.v37i4.3033 128
In this study, we elucidate the novel genomic and nongenomic AR actions on PDCs to accelerate bone callus formation in mouse femoral defect models via promoting collagen-integrin expression and interaction to activate AR/ARA55/FAK axis, therefore increasing the transduction of androgen signaling to focal adhesion complex in regulating PDCs migrated to the site of skeletal injury (Fig
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