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细胞因子基编辑器介导的SOCS2淘汰通过PI3K/AKT/mTOR信号通路促进C2C12细胞分化

Y Wang^1,2,3, C J Zhang^2,3, Y X Li^2,3

¹College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095 , China.

Functional & integrative genomics

|November 6, 2025

概括

使用细胞因子基编辑器 (CBE) 抑制细胞因子信号传递2 (SOCS2) 淘汰会促进骨肌肉发育. 这增强了肌细胞分化,并激活了关键的生长信号通路.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
发展生物学发展生物学

背景情况:

骨肌肉的发育涉及肌细胞分化和融合.
细胞因子信号传递2 (SOCS2) 抑制剂在肌肉发育中的作用尚未完全理解.

研究的目的:

通过使用细胞酶基编辑器 (CBE) 系统,研究SOCS2在骨肌肉发育中的特定功能.
阐明SOCS2调节肌细胞分化的分子机制.

主要方法:

设计的sgRNA针对小鼠SOCS2基因,用于C2C12细胞核细胞中CBE介导的基因编辑.
已建立的单克隆细胞系具有SOCS2过早停止密码子突变.
利用西方斑点,免疫光,分化试验和蛋白质组测序来分析基因和蛋白质表达和信号通路.

主要成果:

在SOCS2中,CBE有效地引入了一个过早停止子,显著降低了蛋白质表达.
SOCS2淘汰赛增强了C2C12肌细胞分化,上调了肌源性标记物 (MyoD1,MyoG,MYH1).
SOCS2 缺乏导致生长激素受体 (GHR) 水平增加和PI3K/AKT/mTOR信号通路的激活.

结论:

氨基基基编辑器介导的SOCS2淘汰会促进C2C12细胞的分化.
SOCS2通过抑制PI3K/AKT/mTOR通路来负面调节骨肌肉的发育.
这项研究为骨肌形成的分子调节提供了新的见解.

关键词:

细胞C2C12的细胞C2C12的细胞细胞因子基编辑器细胞因子基编辑器不同化的差异化在PI3K/AKT/mTOR路径中.这就是SOCS2的SOCS2.

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