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Updated: Jun 11, 2025

Analysis of Cell Cycle Position in Mammalian Cells
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P16INK4A驱动RB1通过UTP14A催化K810无处不在化驱动RB1降解

Wenjie Weng1, Baozhen Zhang1, Dajun Deng1

  • 1Key Laboratory of Carcinogenesis and Translational Research (MOE/Beijing) Division of Etiology, Peking University Cancer Hospital and Institute, Beijing 100142, China.

iScience
|October 1, 2024
PubMed
概括

该研究显示,P16INK4A通过UTP14A促进RB1降解,形成负反循环. 这个P16INK4A-UTP14A-RB1轴影响细胞循环调节和蛋白质组无化,提供潜在的抗癌药物标.

关键词:
细胞生理学 细胞生理学细胞生物学的功能方面.分子相互作用分子相互作用.分子生理学分子生理学

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