靶向敲除Smad3对睫状神经营养因子抑制成肌细胞分化作用的影响
基本信息
结项摘要
成肌细胞分化调控在临床肌病的形成和治疗中起着重要作用，但其分子信号机制尚未明了。我们以往的研究揭示了CNTF可通过激活ERK信号通路抑制成肌细胞的体外分化。而近来研究发现靶向敲除Smad3可增强成肌细胞的体外分化，且这种作用依赖于ERK信号通路的抑制。据此，我们提出CNTF与Smad3可能通过ERK信号途径耦联，共同参与成肌细胞分化调控的设想。在本课题中,利用Smad3基因敲除小鼠建立成肌细胞单克
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数据更新时间：2023-05-31
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