Sodium arsenite induces aggresome formation by promoting PICK1 BAR domain homodimer formation.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-10-01 Epub Date: 2024-07-31 DOI:10.1091/mbc.E24-05-0201
John Ho Chun Lai, Marianthi Tsogka, Jun Xia
{"title":"Sodium arsenite induces aggresome formation by promoting PICK1 BAR domain homodimer formation.","authors":"John Ho Chun Lai, Marianthi Tsogka, Jun Xia","doi":"10.1091/mbc.E24-05-0201","DOIUrl":null,"url":null,"abstract":"<p><p>The aggresome is a perinuclear structure that sequesters misfolded proteins. It is implicated in various neurodegenerative diseases. The perinuclear structure enriched with protein interacting with C kinase 1 (PICK1) was found to be inducible by cellular stressors, colocalizing with microtubule-organizing center markers and ubiquitin, hence classifying it as an aggresome. Sodium arsenite but not arsenate was found to potently induce aggresome formation through an integrated stress response-independent pathway. In HEK293T cells, under arsenite stress, PICK1 localization to the aggresome was prioritized, and formation of PICK1 homodimers was favored. Additionally, PICK1 could enhance protein entry into aggresomes. This study shows that arsenite can induce the formation of both RNA stress granules and aggresomes at the same time, and that PICK1 shows conditional localization to aggresomes, suggesting a possible involvement of PICK1 in neurodegenerative diseases.</p>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11481693/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1091/mbc.E24-05-0201","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/31 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}
引用次数: 0

Abstract

The aggresome is a perinuclear structure that sequesters misfolded proteins. It is implicated in various neurodegenerative diseases. The perinuclear structure enriched with protein interacting with C kinase 1 (PICK1) was found to be inducible by cellular stressors, colocalizing with microtubule-organizing center markers and ubiquitin, hence classifying it as an aggresome. Sodium arsenite but not arsenate was found to potently induce aggresome formation through an integrated stress response-independent pathway. In HEK293T cells, under arsenite stress, PICK1 localization to the aggresome was prioritized, and formation of PICK1 homodimers was favored. Additionally, PICK1 could enhance protein entry into aggresomes. This study shows that arsenite can induce the formation of both RNA stress granules and aggresomes at the same time, and that PICK1 shows conditional localization to aggresomes, suggesting a possible involvement of PICK1 in neurodegenerative diseases.

亚砷酸钠通过促进 PICK1 BAR 结构域同源二聚体的形成来诱导凝集体的形成。
凝集体(aggresome)是一种核周结构,能封存折叠错误的蛋白质。它与多种神经退行性疾病有关。研究发现,富含 PICK1 的核周结构可被细胞应激物诱导,并与微管组织中心(MTOC)标记物和泛素共定位,因此被归类为侵袭体。研究发现,亚砷酸钠(而非砷酸盐)能通过综合应激反应(ISR)独立途径有效诱导侵染体的形成。在HEK293T细胞中,在亚砷酸盐胁迫下,PICK1优先定位到侵染体,并有利于PICK1同源二聚体的形成。此外,PICK1 还能促进蛋白质进入侵染体。这项研究表明,亚砷酸盐可同时诱导 RNA 应激颗粒和侵染体的形成,而 PICK1 则显示出有条件地定位到侵染体,这表明 PICK1 可能参与了神经退行性疾病的研究。[媒体:见正文] [媒体:见正文]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信