Clarification of molecular mechanisms of RANK/TRAF6 signaling pathways in osteoclastogenesis

阐明破骨细胞生成中RANK/TRAF6信号通路的分子机制

• 批准号: 20770153
• 负责人: GOHDA Jin
• 金额: $ 2.75万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20770153/
• 关键词: 発生・分化; 細胞内シグナル伝達; 骨代謝; 破骨細胞; アダブター分子; シグナル伝達; 発生・分化; 細胞内シグナル伝達; 骨代謝; 破骨細胞; アダブター分子; シグナル伝達

Osteoclasts, which are bone-resorbing cells, play a pivotal role in maintenance of bone homeostasis. The formation of osteoclasts requires the signaling pathways mediated by the receptor protein, RANK. In the present study, I demonstrated that RANK has a novel functional domain that sustains its interaction with the downstream signaling factors. Furthermore, Treatment with the peptides containing the amino aid sequence of its domain significantly suppressed osteoclast formation. These findings might contribute to development of new treatments for bone diseases, such as osteoporosis.

骨化细胞的破骨细胞在维持骨体内平衡中起关键作用。破骨细胞的形成需要由受体蛋白等级介导的信号通路。在本研究中，我证明等级具有一个新型的功能域，该域与下游信号传导因子保持了相互作用。此外，用含有其结构域的氨基辅助序列的肽处理显着抑制了破骨细胞的形成。这些发现可能有助于发展骨疾病的新疗法，例如骨质疏松症。