Naoko Kanatani

TL;DR: Data indicate that immature organization of cortical bone, which was caused by the maturational blockage of osteoblasts, led to osteopenia and fragility in transgenic mice, demonstrating that Cbfa1 inhibits osteoblast differentiation at a late stage.

TL;DR: Data show that temporally and spatially regulated expression of Cbfa1 in chondrocytes is required for skeletogenesis, including formation of joints, permanent cartilages, and endochondral bones.

TL;DR: Wnt/β-catenin signaling regulates chondrocyte phenotype, maturation, and function in a developmentally regulated manner, and regulated action by this pathway is critical for growth plate organization, cartilage boundary definition, and endochondral ossification.

TL;DR: Electrophoretic mobility shift assays and reporter assays showed that Cbfβ was necessary for the efficient DNA binding of Runx2 and for Runx 2-dependent transcriptional activation, which indicates that CBFβ is required for the function of RunX2 in skeletal development.

TL;DR: These findings indicate that the maturity and turnover rate of bone are determined by the level of functional Runx2 and Run x2 is responsible for bone loss in estrogen deficiency, but that Runx 2 is not essential for maintenance of the expression of major bone matrix protein genes in postnatal bone development and maintenance.