Analysis of the function of KLF5 in blood cells and elucidation of its underlying molecular mechanism which leads to clinical application

分析KLF5在血细胞中的功能并阐明其分子机制并应用于临床

• 批准号: 23791072
• 负责人: MATSUMURA Takayoshi
• 金额: $ 2.66万
• 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: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791072/
• 关键词: 血球細胞; 巨核球; 血小板; 血管新生; 転写因子; 血液内科学; KLF5

With a broad analysis of the function of KLF5 in blood cells, I found that KLF5 is critical especially to normal functions of platelets. Platelet lineage-specific Klf5-knockout mice showed impaired in vivo thrombus formation and angiogenesis activity, and I investigated the underlying molecular mechanisms. Our results can lead to future therapeutic interventions for various cardiovascular and cancer diseases

通过对KLF5在血细胞中的功能进行广泛的分析，我发现KLF5对血小板的正常功能尤其重要。血小板谱系特异性Klf5基因敲除小鼠体内血栓形成和血管生成活性受损，我研究了潜在的分子机制。我们的研究结果可能会导致未来对各种心血管和癌症疾病的治疗干预

项目成果

Platelet surface molecules regulated by KLF5 are critical to in vivo thrombus formation and angiogenesis

KLF5 调节的血小板表面分子对于体内血栓形成和血管生成至关重要

• 发表时间: 2013
• 作者: 松村 貴由;他
• 通讯作者: 他