Calcium signaling and transcription: elongation, DoGs, and eRNAs.

Receptors & clinical investigation Pub Date : 2016-01-01 Epub Date: 2016-02-01 DOI:10.14800/rci.1169
Anna Vilborg, Maria C Passarelli, Joan A Steitz
{"title":"Calcium signaling and transcription: elongation, DoGs, and eRNAs.","authors":"Anna Vilborg,&nbsp;Maria C Passarelli,&nbsp;Joan A Steitz","doi":"10.14800/rci.1169","DOIUrl":null,"url":null,"abstract":"<p><p>The calcium ion (Ca<sup>2+</sup>) is a key intracellular signaling molecule with far-reaching effects on many cellular processes. One of the most important such Ca<sup>2+</sup> regulated processes is transcription. A body of literature describes the effect of Ca<sup>2+</sup> signaling on transcription initiation as occurring mainly through activation of gene-specific transcription factors by Ca<sup>2+</sup>-induced signaling cascades. However, the reach of Ca<sup>2+</sup> extends far beyond the first step of transcription. In fact, Ca<sup>2+</sup> can regulate all phases of transcription, with additional effects on transcription-associated events such as alternative splicing. Importantly, Ca<sup>2+</sup> signaling mediates reduced transcription termination in response to certain stress conditions. This reduction allows readthrough transcription, generating a highly inducible and diverse class of downstream of gene containing transcripts (DoGs) that we have recently described.</p>","PeriodicalId":74650,"journal":{"name":"Receptors & clinical investigation","volume":"3 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685190/pdf/nihms885336.pdf","citationCount":"13","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Receptors & clinical investigation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/rci.1169","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2016/2/1 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 13

Abstract

The calcium ion (Ca2+) is a key intracellular signaling molecule with far-reaching effects on many cellular processes. One of the most important such Ca2+ regulated processes is transcription. A body of literature describes the effect of Ca2+ signaling on transcription initiation as occurring mainly through activation of gene-specific transcription factors by Ca2+-induced signaling cascades. However, the reach of Ca2+ extends far beyond the first step of transcription. In fact, Ca2+ can regulate all phases of transcription, with additional effects on transcription-associated events such as alternative splicing. Importantly, Ca2+ signaling mediates reduced transcription termination in response to certain stress conditions. This reduction allows readthrough transcription, generating a highly inducible and diverse class of downstream of gene containing transcripts (DoGs) that we have recently described.

Abstract Image

Abstract Image

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
钙信号和转录:延伸,狗和erna。
钙离子(Ca2+)是一种重要的细胞内信号分子,对许多细胞过程具有深远的影响。最重要的Ca2+调控过程之一是转录。大量文献描述了Ca2+信号对转录起始的影响,主要是通过Ca2+诱导的信号级联反应激活基因特异性转录因子来发生的。然而,Ca2+的作用范围远远超出了转录的第一步。事实上,Ca2+可以调节转录的所有阶段,并对转录相关事件(如选择性剪接)产生额外影响。重要的是,Ca2+信号在某些应激条件下介导转录终止减少。这种还原允许读通转录,产生我们最近描述的高度诱导和多样化的下游基因转录本(狗)。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
CD28 family of receptors inter-connect in the regulation of T-cells Urokinase-type plasminogen activator (uPA) and its receptor (uPAR) promote neurorepair in the ischemic brain Bacterial superantigen toxins induce a lethal cytokine storm by enhancing B7-2/CD28 costimulatory receptor engagement, a critical immune checkpoint. Bacterial superantigen toxins induce a lethal cytokine storm by enhancing B7-2/CD28 costimulatory receptor engagement, a critical immune checkpoint. An entry-competent intermediate state of the HIV-1 envelope glycoproteins.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1