Masahito Matsumoto

TL;DR: Results indicate that activation of the p38 MAP kinase pathway plays an important role in RANKL-induced osteoclast differentiation of precursor bone marrow cells.

TL;DR: The results suggest that the RANKL-induced cathepsin K gene expression is cooperatively regulated by the combination of the transcription factors and p38 MAP kinase in a gradual manner.

TL;DR: The results indicate that p38α insufficiency may cause an inflammatory disorder, resulting in a delay of histological and functional nerve recovery following crush injury, and conclude that p 38 MAPK has an important physiological role in nerve regeneration and may be important for controlling both initiation of inflammation and recovery from nerve injury.

TL;DR: The results indicate that the p38 MAP kinase pathway plays a crucial role in TNF‐mediated osteoclast differentiation and the number of multinucleated osteoclasts induced by TNF in bone marrow cell cultures derived from p38MAP kinase gene deficient mice was significantly less than that from control mice.

TL;DR: It is proposed that vascular endothelial cells interact with bone in suppressing bone through netrin‐4, and this work shows that netrin-4 inhibits osteoclast differentiation in vitro and in vivo.