基于 CRISPR 的突触核蛋白病中 N 端乙酰化的鉴定。

CRISPR-based identification of N-terminal acetylation in synucleinopathies.

机构信息

Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Seoul, South Korea; Convergence Research Center for Dementia, Seoul National University College of Medicine, Seoul, South Korea; Neuramedy Co. Ltd, Seoul, South Korea.

出版信息

Trends Neurosci. 2024 May;47(5):324-325. doi: 10.1016/j.tins.2024.03.006. Epub 2024 Mar 28.

DOI:10.1016/j.tins.2024.03.006

PMID:38553385

Abstract

A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach.

摘要

库马尔等人最近的一项研究确定了几个调节内源性α-突触核蛋白（α-synuclein）水平的生物学途径。他们特别强调了 N 端乙酰化（NTA）途径是维持内源性α-synuclein 稳定性的重要因素，这表明靶向 NTA 途径可能是一种潜在的治疗方法。