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

IF 14.6 1区医学 Q1 NEUROSCIENCES

Trends in Neurosciences Pub Date : 2024-05-01 Epub Date: 2024-03-28 DOI:10.1016/j.tins.2024.03.006

Eun-Jin Bae, Seung-Jae Lee

引用次数: 0

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.

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基于 CRISPR 的突触核蛋白病 N 端乙酰化鉴定。

库马尔等人最近的一项研究确定了调节内源性α-突触核蛋白（α-synuclein）水平的几种生物途径。他们特别强调，N-末端乙酰化（NTA）途径是维持内源性α-突触核蛋白稳定性的重要因素，并建议将 NTA 途径作为一种潜在的治疗方法。

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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来源期刊

Trends in Neurosciences 医学-神经科学

CiteScore

26.50

自引率

1.30%

发文量

123

审稿时长

6-12 weeks

期刊介绍： For over four decades, Trends in Neurosciences (TINS) has been a prominent source of inspiring reviews and commentaries across all disciplines of neuroscience. TINS is a monthly, peer-reviewed journal, and its articles are curated by the Editor and authored by leading researchers in their respective fields. The journal communicates exciting advances in brain research, serves as a voice for the global neuroscience community, and highlights the contribution of neuroscientific research to medicine and society.