短的内部开放的读取框架抑制了N端截断的蛋白形体的翻译
Raphael Fettig1, Zita Gonda1, Niklas Walter1
1Karlsruhe Institute of Technology (KIT), Institute for Biological and Chemical Systems-Biological Information Processing (IBCS-BIP), Karlsruhe, Germany.
EMBO reports
|February 17, 2025
概括
内部短开放的读取框架 (sORFs) 调节N-终端截断蛋白质的翻译. 这项研究表明,sORFs通过mTORC1信号抑制TRIP6的核蛋白形式nTRIP6的翻译.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 遗传学 遗传学 是一个
背景情况:
- 内部翻译启动站点可以产生N-终端截断的蛋白质形式.
- 短核蛋白形 nTRIP6 调节了骨肌肉原始体的分化.
研究的目的:
- 研究内部短开放阅读框架 (sORFs) 在调节蛋白质翻译中的作用.
- 确定控制nTRIP6蛋白形生成及其调节的机制.
主要方法:
- 核糖体造型,以确定翻译启动地点.
- 肌原分化的体外模型.
- 机械性目标的拉帕米辛复合物1 (mTORC1) 途径分析.
主要成果:
- 编码序列内的内部sORF抑制了N端截断蛋白质形式的翻译.
- nTRIP6是由内部翻译启动产生的,被上游sORF抑制.
- 在肌体分化过程中,mTORC1的激活会导致nTRIP6的暂时上调.
结论:
- 内部sORF是调节截断的蛋白形转化的一个一般机制.
- 截断的蛋白形翻译可以独立于正规的开放阅读框架来控制.
- nTRIP6法规突出了肌肉发育中转录后控制的新层.
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