Palmitoylation and regulation of potassium-dependent sodium/calcium exchangers (NCKX).

IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Bioscience Reports Pub Date : 2025-01-30 DOI:10.1042/BSR20241051
Ran Tao, Alan D Robertson, William Fuller, Caglar Gök
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Abstract

Cellular Ca2+ homeostasis is critical for normal cell physiology and is regulated by several mechanisms. Two major players in intracellular Ca2+ homeostasis in multiple tissues belong to the SLC8 (Na+/Ca2+ exchangers (NCXs); NCX1-3) and SLC24 (K+ dependent Na+/Ca2+ exchangers (NCKXs); NCKX1-5) families. It has been established that NCXs and NCKX4 are palmitoylated, and that palmitoylation promotes NCX1 inactivation. However, there is still little known about NCKXs' palmitoylation. We found that (1) NCKX3 and NCKX5, but not NCKX1, are palmitoylated, (2) Cys to Ala mutation at position 467 for NCXK3 and 325 for NCKX5 notably diminished palmitoylation and (3) reduced palmitoylation enhanced NCKX3 activity. Our findings bring novel insights into NCKX1, NCKX3 and NCKX5 palmitoylation and establish palmitoylation as an endogenous regulator of NCKX3 activity, paving the way for investigations evaluating the role of palmitoylation in NCKX3 function in health and disease.

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棕榈酰化和钾依赖性钠/钙交换剂(NCKX)的调控。
细胞Ca2+稳态对正常细胞生理至关重要,并受到多种机制的调节。多个组织中细胞内Ca2+稳态的两个主要参与者属于SLC8 (Na+/Ca2+交换器(nxs));NCX1-3)和SLC24 (K+依赖性Na+/Ca2+交换剂(NCKXs);NCKX1-5)的家庭。已经确定NCXs和NCKX4是棕榈酰化的,棕榈酰化促进NCX1失活。然而,对于NCKXs的棕榈酰化作用,目前所知甚少。我们发现(1)NCKX3和NCKX5存在棕榈酰化,而NCKX1不存在;(2)NCXK3和NCKX5的467和325位点的Cys to Ala突变显著降低了棕榈酰化;(3)棕榈酰化的降低增强了NCKX3的活性。我们的研究结果为NCKX1、NCKX3和NCKX5棕榈酰化提供了新的见解,并确立了棕榈酰化是NCKX3活性的内源性调节因子,为研究评估棕榈酰化在NCKX3健康和疾病功能中的作用铺平了道路。
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来源期刊
Bioscience Reports
Bioscience Reports 生物-细胞生物学
CiteScore
8.50
自引率
0.00%
发文量
380
审稿时长
6-12 weeks
期刊介绍: Bioscience Reports provides a home for sound scientific research in all areas of cell biology and molecular life sciences. Since 2012, Bioscience Reports has been fully Open Access and publishes all papers under the liberal CC BY licence, giving the life science community quality research to share and discuss.Content before 2012 is subscription-only, and is accessible via archive purchase. Articles are assessed on soundness, providing a home for valid findings and data. We welcome papers that span disciplines (e.g. chemistry, medicine), including papers describing: -new methodologies -tools and reagents to probe biological questions -mechanistic details -disease mechanisms -metabolic processes and their regulation -structure and function -bioenergetics
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