相关实验视频

Updated: Jul 3, 2025

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

USP18 稳定FTO蛋白通过抑制m6A修改SIRT6激活缺血性中风中的线粒

Mingyu Song^1,2,3, Fang Yi^2,4, Feiyue Zeng⁵

¹Department of Neurology, Xiangya Hospital, Central South University, Hunan Province, Changsha, 410008, People's Republic of China.

Molecular neurobiology

|February 10, 2024

概括

乌比基特异性酶18 (USP18) 通过稳定FTO蛋白,激活细胞和增强SIRT6/AMPK/PGC-1α/AKT通路来预防缺血性中风. 这种新的机制为缺血性脑损伤提供了一个有希望的治疗点.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
生物化学生化学

背景情况:

缺血性中风 (IS) 是导致死亡和残疾的主要原因.
乌比基特异性酶18 (USP18) 显示神经保护作用,但其在IS中的调节机制尚未完全理解.

研究的目的:

阐明USP18减轻缺血性脑损伤的分子机制.
研究USP18和脂肪质量和与肥胖相关的蛋白质 (FTO) 在IS病原和潜在的治疗干预中的作用.

主要方法:

在体内 (MCAO) 和体内 (OGD/R) 建立的缺血性中风模型.
使用MTT,LDH,ROS,线粒体膜潜力和流细胞计评估神经细胞损伤.
通过qPCR,西式涂抹,免疫光,Co-IP,RIP和MeRIP评估分子表达;使用TEM观察到线粒菌.

主要成果:

在OGD/R模型中,USP18和FTO表达率下降.
USP18过度表达增加了FTO蛋白质的稳定性通过de-ubiquitination.
通过YTHDF2进行FTO上调,减少了SIRT6的m6A修饰,增强SIRT6的表达,并激活AMPK/PGC-1α/AKT通路.
在IS模型中,USP18/FTO过度表达激活了线粒,改善了神经细胞损伤并改善了神经功能.

结论:

USP18通过增加FTO稳定性来缓解缺血性中风,这反过来又通过AMPK/PGC-1α/AKT通路促进SIRT6介导的线粒.
USP18代表了缺血性中风治疗的新型治疗标.

关键词:

在 FTO FTO FTO.缺血性中风是因为缺血性中风.线粒细胞衰变 - - 线粒细胞衰变 (mitophagy) 是一种在SIRT6上 USP18 美元

更多相关视频

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Published on: December 15, 2023

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

相关概念视频

Translocation of Proteins into the Mitochondria

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...