Regulation of osteoclastogenesis by protein phosphatase 2C

骨不断经历重塑，其中破骨细胞的骨吸收随后是成骨细胞的骨形成，并保持其结构和功能。骨重建调节的失衡导致许多代谢性骨病，如骨质疏松症。在这里，我们表明，低分子量的化合物，特异性激活蛋白磷酸酶2C（PP2C）抑制破骨细胞生成，以及它如何作用于RANKL诱导的破骨细胞分化。

Bone continuously undergoes remodeling, in which bone resorption by osteoclasts is followed by bone formation by osteoblasts, and maintains its structure and function. An imbalance in the regulation of bone remodeling results in many metabolic bone diseases, such as osteoporosis. Here we show that a low molecular weight compound which specifically activates protein phosphatase 2C(PP2C)suppressed osteoclastogenesis, and how it acts on the RANKL induced osteoclast differentiation.