{"title":"JAK-STAT in heterochromatin and genome stability.","authors":"Louise Silver-Morse, Willis X Li","doi":"10.4161/jkst.26090","DOIUrl":null,"url":null,"abstract":"<p><p>The canonical JAK-STAT signaling pathway transmits signals from the cell membrane to the nucleus, to regulate transcription of particular genes involved in development and many other physiological processes. It has been shown in Drosophila that JAK and STAT also function in a non-canonical mode, to regulate heterochromatin. This review discusses the non-canonical functioning of JAK and STAT, and its effects on biological processes. Decreased levels of activated JAK and increased levels of unphosphorylated STAT generate higher levels of heterochromatin. These higher heterochromatin levels result in suppression of hematopoietic tumor-like masses, increased resistance to DNA damage, and longer lifespan. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e26090"},"PeriodicalIF":0.0000,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.26090","citationCount":"26","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JAK-STAT","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4161/jkst.26090","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/8/8 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 26
Abstract
The canonical JAK-STAT signaling pathway transmits signals from the cell membrane to the nucleus, to regulate transcription of particular genes involved in development and many other physiological processes. It has been shown in Drosophila that JAK and STAT also function in a non-canonical mode, to regulate heterochromatin. This review discusses the non-canonical functioning of JAK and STAT, and its effects on biological processes. Decreased levels of activated JAK and increased levels of unphosphorylated STAT generate higher levels of heterochromatin. These higher heterochromatin levels result in suppression of hematopoietic tumor-like masses, increased resistance to DNA damage, and longer lifespan.
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