通过抑制Rag GTPases,MORG1限制了mTORC1的信号传递
Yakubu Princely Abudu1, Athanasios Kournoutis2, Hanne Britt Brenne2
1Autophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway; Nanoscopy Group, Department of Physics and Technology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.
Molecular cell
|December 16, 2023
概括
WD域重复蛋白MORG1抑制了mTORC1的信号传递,促进了基底自. 减少MORG1增强了细胞增殖和迁移,与癌症存活率差的相关性.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 自是恒温的关键细胞过程,由mTORC1信号调节.
- 在基础自的营养可用性期间mTORC1的精确调节仍然不清楚.
研究的目的:
- 为了研究MORG1在调节基底自中的作用.
- 阐明MORG1控制mTORC1信号的机制.
主要方法:
- 研究了MORG1与Rag GTPases和mTORC1.1.的相互作用.
- 利用HeLa细胞来评估MORG1枯竭对mTORC1活动和自的影响.
- 研究了p62/SQSTM1在MORG1介导调节中的作用.
主要成果:
- MORG1通过与活跃的Rag GTPases结合来抑制mTORC1的信号传递,防止mTORC1的溶酶招募.
- MORG1 枯竭导致mTORC1 活性增加和自减少.
- 在重新养时p62/SQSTM1与MORG1结合,可以防止MORG1介导的mTORC1抑制.
- 由于MORG1的枯竭,细胞增殖和迁移会得到加强.
结论:
- 通过抑制mTORC1信号传递,MORG1是基础构成性自的关键调节者.
- 根据营养的可用性,MORG1的功能是由p62/SQSTM1调节的.
- 在抑制细胞增殖和迁移方面,MORG1的作用表明它具有抑制瘤的潜力.
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