Dahyeon Koh , Hyeong Bin Jeon , Chaehwan Oh , Ji Heon Noh , Kyoung Mi Kim
{"title":"RNA-binding proteins in cellular senescence","authors":"Dahyeon Koh , Hyeong Bin Jeon , Chaehwan Oh , Ji Heon Noh , Kyoung Mi Kim","doi":"10.1016/j.mad.2023.111853","DOIUrl":null,"url":null,"abstract":"<div><p><span>Cellular senescence<span> is a state of irreversible cell cycle arrest that is triggered and controlled by various external and/or internal factors. Among them, the regulation of senescence-associated genes is an important molecular event that plays a role in senescence. The regulation of gene expression can be achieved by various types of modulating mechanisms, and RNA-binding proteins (RBPs) are commonly known as critical regulators targeting a global range of transcripts. RBPs bind to RNA-binding motifs of the target transcripts and are involved in post-transcriptional processes such as </span></span>RNA transport<span>, stabilization, splicing, and decay. These RBPs may also play critical roles in cellular senescence by regulating the expression of senescence-associated genes. The biological functions of RBPs in controlling cellular senescence are being actively studied. Herein, we summarized the RBPs that influence cellular senescence, particularly by regulating processes such as the senescence-associated secretory phenotype, cell cycle, and mitochondrial function.</span></p></div>","PeriodicalId":18340,"journal":{"name":"Mechanisms of Ageing and Development","volume":"214 ","pages":"Article 111853"},"PeriodicalIF":5.3000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mechanisms of Ageing and Development","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0047637423000799","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Cellular senescence is a state of irreversible cell cycle arrest that is triggered and controlled by various external and/or internal factors. Among them, the regulation of senescence-associated genes is an important molecular event that plays a role in senescence. The regulation of gene expression can be achieved by various types of modulating mechanisms, and RNA-binding proteins (RBPs) are commonly known as critical regulators targeting a global range of transcripts. RBPs bind to RNA-binding motifs of the target transcripts and are involved in post-transcriptional processes such as RNA transport, stabilization, splicing, and decay. These RBPs may also play critical roles in cellular senescence by regulating the expression of senescence-associated genes. The biological functions of RBPs in controlling cellular senescence are being actively studied. Herein, we summarized the RBPs that influence cellular senescence, particularly by regulating processes such as the senescence-associated secretory phenotype, cell cycle, and mitochondrial function.
期刊介绍:
Mechanisms of Ageing and Development is a multidisciplinary journal aimed at revealing the molecular, biochemical and biological mechanisms that underlie the processes of aging and development in various species as well as of age-associated diseases. Emphasis is placed on investigations that delineate the contribution of macromolecular damage and cytotoxicity, genetic programs, epigenetics and genetic instability, mitochondrial function, alterations of metabolism and innovative anti-aging approaches. For all of the mentioned studies it is necessary to address the underlying mechanisms.
Mechanisms of Ageing and Development publishes original research, review and mini-review articles. The journal also publishes Special Issues that focus on emerging research areas. Special issues may include all types of articles following peered review. Proposals should be sent directly to the Editor-in-Chief.