GPR56：GPCR 是防止铁变态反应的卫士

IF 27.7 1区生物学 Q1 CELL BIOLOGY

Cell metabolism Pub Date : 2024-11-05 DOI:10.1016/j.cmet.2024.08.011

Yuelong Yan, Li Zhuang, Boyi Gan

引用次数: 0

摘要

跨膜受体蛋白善于感知外部信号并启动下游通路来控制细胞存活。Lin等人证实，GPR56是一种G蛋白偶联受体，可被其激动剂激活，抑制铁蛋白沉积（一种细胞死亡形式），并有效减轻铁蛋白沉积相关的肝损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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GPR56: GPCR as a guardian against ferroptosis

Transmembrane receptor proteins are proficient in sensing external signals and initiating downstream pathways to control cell survival. Lin et al. demonstrated that GPR56, a G-protein-coupled receptor, can be activated by its agonist to suppress ferroptosis—a form of cell death—and effectively mitigate ferroptosis-associated liver damage.

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来源期刊

Cell metabolism 生物-内分泌学与代谢

CiteScore

48.60

自引率

1.40%

发文量

173

审稿时长

2.5 months

期刊介绍： Cell Metabolism is a top research journal established in 2005 that focuses on publishing original and impactful papers in the field of metabolic research.It covers a wide range of topics including diabetes, obesity, cardiovascular biology, aging and stress responses, circadian biology, and many others. Cell Metabolism aims to contribute to the advancement of metabolic research by providing a platform for the publication and dissemination of high-quality research and thought-provoking articles.