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在哺乳动物细胞的压力刺激下,由β-catenin/RSK1轴介导的替代葡萄糖吸收
Caizhu Wang1, Ruqin Lin1, Xueying Qi1
1Guangdong Provincial Key Laboratory of Protein Function and Regulation in Agricultural Organisms, College of Life Sciences, South China Agricultural University, Guangzhou, Guangdong 510642, PR China; Guangdong Laboratory for Lingnan Modern Agriculture, Guangzhou, Guangdong 510642, PR China; Key Laboratory of Zoonosis of Ministry of Agriculture and Rural Affairs, South China Agricultural University, Guangzhou, Guangdong 510642, PR China.
细胞通过β-catenin/RSK1通路在压力下增加葡萄糖的吸收. 这种机制增强了葡萄糖载体 (GLUT) 转位,帮助细胞适应LPS和DON等刺激.
科学领域:
- 细胞生物学 细胞生物学
- 分子机制的分子机制
- 压力反应应激反应
背景情况:
- 细胞增加葡萄糖的吸收作为压力下的细胞保护策略.
- 葡萄糖载体 (GLUT) 转移到细胞膜是葡萄糖吸收效率的关键.
- 化和激活TBC1D4密切控制GLUT转位.
研究的目的:
- 阐明在压力条件下葡萄糖吸收的机制.
- 调查β-catenin和RSK1在压力诱导的葡萄糖吸收中的作用.
- 了解细胞如何适应它们的能量利用,以应对刺激.
主要方法:
- 研究了对葡萄糖饥饿,LPS和脱氧尼瓦伦醇 (DON) 的细胞反应.
- 分析了β-catenin,RSK1和TBC1D4在葡萄糖吸收中的作用.
- 检查了蛋白质-蛋白质相互作用和酸化事件.
主要成果:
- 作为对葡萄糖饥饿,LPS和DON的反应,葡萄糖吸收增加.
- 压力诱导的葡萄糖吸收是由升高的β-catenin介导的,并激活了RSK1.
- 确定了一种β-catenin/RSK1/TBC1D4复合体,促进TBC1D4酸化和GLUT4转位.
结论:
- 在细胞应激期间,β-catenin/RSK1轴对葡萄糖吸收增加至关重要.
- 这一途径促进GLUT4转位,增强细胞适应.
- 揭示了在压力下细胞能量代谢的新见解.
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