Constitutive lipid scramblase activity underpins mechanosensitive TMEM63 channelopathies.

IF 15 1区医学 Q1 NEUROSCIENCES

Neuron Pub Date : 2025-08-06 DOI:10.1016/j.neuron.2025.07.004

Remi Brynn, Kate Poole

引用次数: 0

Abstract

In this issue of Neuron, Zheng et al.¹ show that disease-causing mutations identified in human TMEM63B alter its lipid scrambling but not ion channel function. These mutations disrupt a putative hydrophobic latch that may regulate scramblase activity in response to membrane thinning.

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组成性脂质合成酶活性支持机械敏感性TMEM63通道病变。

在本期《神经元》杂志上，Zheng等人1表明，在人类TMEM63B中发现的致病突变改变了其脂质混乱，但没有改变离子通道功能。这些突变破坏了假定的疏水锁存器，该锁存器可能在响应膜变薄时调节超燃酶活性。

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

Neuron 医学-神经科学

CiteScore

24.50

自引率

3.10%

发文量

382

审稿时长

1 months

期刊介绍： Established as a highly influential journal in neuroscience, Neuron is widely relied upon in the field. The editors adopt interdisciplinary strategies, integrating biophysical, cellular, developmental, and molecular approaches alongside a systems approach to sensory, motor, and higher-order cognitive functions. Serving as a premier intellectual forum, Neuron holds a prominent position in the entire neuroscience community.