FOS Promoter is Overactive Outside of Genome Context and Weakly Regulated by Changes in the Na+i/K+i Ratio

IF 2.2 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Andrey M. Gorbunov, Dmitrii A. Fedorov, Olga E. Kvitko, Olga D. Lopina, Elizaveta A. Klimanova
{"title":"FOS Promoter is Overactive Outside of Genome Context and Weakly Regulated by Changes in the Na+i/K+i Ratio","authors":"Andrey M. Gorbunov,&nbsp;Dmitrii A. Fedorov,&nbsp;Olga E. Kvitko,&nbsp;Olga D. Lopina,&nbsp;Elizaveta A. Klimanova","doi":"10.1134/S0006297925600371","DOIUrl":null,"url":null,"abstract":"<p>Changes in the Na<sup>+</sup> and K<sup>+</sup> intracellular concentrations affect expression of the <i>FOS</i> gene. Here, we obtained a genetic construct coding for the TurboGFP-dest1 protein under control of the human <i>FOS</i> promoter (−549 to +155) and studied its expression in HEK293T cells exposed to monovalent metal cations. Amplification of the <i>FOS</i> promoter sequence from genomic DNA was efficient only in the presence of Li<sup>+</sup> ions. Incubation of cells with ouabain or in a medium containing Li<sup>+</sup> ions instead of Na<sup>+</sup> ions caused intracellular accumulation of Na<sup>+</sup> and Li<sup>+</sup> ions, respectively. In addition, both stimuli increased the levels of endogenous <i>FOS</i> mRNA and the average fluorescence intensity of TurboGFP-dest1 in transfected cells. The mRNA levels of TurboGFP-dest1 were significantly higher than the <i>FOS</i> mRNA levels and were little affected by the stimuli.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"90 5","pages":"582 - 589"},"PeriodicalIF":2.2000,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry (Moscow)","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1134/S0006297925600371","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Changes in the Na+ and K+ intracellular concentrations affect expression of the FOS gene. Here, we obtained a genetic construct coding for the TurboGFP-dest1 protein under control of the human FOS promoter (−549 to +155) and studied its expression in HEK293T cells exposed to monovalent metal cations. Amplification of the FOS promoter sequence from genomic DNA was efficient only in the presence of Li+ ions. Incubation of cells with ouabain or in a medium containing Li+ ions instead of Na+ ions caused intracellular accumulation of Na+ and Li+ ions, respectively. In addition, both stimuli increased the levels of endogenous FOS mRNA and the average fluorescence intensity of TurboGFP-dest1 in transfected cells. The mRNA levels of TurboGFP-dest1 were significantly higher than the FOS mRNA levels and were little affected by the stimuli.

FOS启动子在基因组外过度活跃,受Na+i/K+i比值变化的调控较弱。
细胞内Na+和K+浓度的变化影响FOS基因的表达。在这里,我们获得了在人类FOS启动子(-549至+155)控制下编码TurboGFP-dest1蛋白的遗传构建体,并研究了其在暴露于一价金属阳离子的HEK293T细胞中的表达。从基因组DNA中扩增FOS启动子序列只有在Li+离子存在的情况下才有效。用瓦巴因或在含Li+离子而非Na+离子的培养基中孵育细胞,分别引起细胞内Na+和Li+离子的积累。此外,这两种刺激都增加了转染细胞中内源性FOS mRNA的水平和TurboGFP-dest1的平均荧光强度。TurboGFP-dest1 mRNA水平显著高于FOS mRNA水平,且受刺激影响较小。
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
Biochemistry (Moscow)
Biochemistry (Moscow) 生物-生化与分子生物学
CiteScore
4.70
自引率
3.60%
发文量
139
审稿时长
2 months
期刊介绍: Biochemistry (Moscow) is the journal that includes research papers in all fields of biochemistry as well as biochemical aspects of molecular biology, bioorganic chemistry, microbiology, immunology, physiology, and biomedical sciences. Coverage also extends to new experimental methods in biochemistry, theoretical contributions of biochemical importance, reviews of contemporary biochemical topics, and mini-reviews (News in Biochemistry).
×
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:604180095
Book学术官方微信