{"title":"IGF2 产生的微小核糖核酸通过抑制 IGF1 限制生长","authors":"Olivia Tysoe","doi":"10.1038/s41574-024-01050-3","DOIUrl":null,"url":null,"abstract":"<p>Insulin-like growth factor 1 (IGF1) is a key protein that contributes to control of an organism’s size after birth and during development, whereas IGF2 is the main regulator of growth and body size during fetal development. A study in <i>Cell Reports</i> describes a mechanism by which a microRNA produced from <i>Igf2</i> regulates IGF1 to suppress growth in mice.</p><p>The researchers then assessed the effect of miR-483 on fetal and postnatal development and growth. “We made a knockout mouse and two types of mouse lines that make more copies of miR-483 than the normal levels; one coming from the ‘endogenous’ location at the <i>Igf2</i> gene and one from another genomic location,” says corresponding author Miguel Constância. Knockout of <i>miR483</i> (<i>Mir483</i><sup>Pat-KO</sup> mice) did not result in a noticeable phenotypic change. Overexpression of <i>Mir-483</i> during fetal development, however, universally led to fetal death.</p>","PeriodicalId":18916,"journal":{"name":"Nature Reviews Endocrinology","volume":null,"pages":null},"PeriodicalIF":31.0000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IGF2-produced microRNA restricts growth via suppression of IGF1\",\"authors\":\"Olivia Tysoe\",\"doi\":\"10.1038/s41574-024-01050-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Insulin-like growth factor 1 (IGF1) is a key protein that contributes to control of an organism’s size after birth and during development, whereas IGF2 is the main regulator of growth and body size during fetal development. A study in <i>Cell Reports</i> describes a mechanism by which a microRNA produced from <i>Igf2</i> regulates IGF1 to suppress growth in mice.</p><p>The researchers then assessed the effect of miR-483 on fetal and postnatal development and growth. “We made a knockout mouse and two types of mouse lines that make more copies of miR-483 than the normal levels; one coming from the ‘endogenous’ location at the <i>Igf2</i> gene and one from another genomic location,” says corresponding author Miguel Constância. Knockout of <i>miR483</i> (<i>Mir483</i><sup>Pat-KO</sup> mice) did not result in a noticeable phenotypic change. Overexpression of <i>Mir-483</i> during fetal development, however, universally led to fetal death.</p>\",\"PeriodicalId\":18916,\"journal\":{\"name\":\"Nature Reviews Endocrinology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":31.0000,\"publicationDate\":\"2024-10-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Reviews Endocrinology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41574-024-01050-3\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Reviews Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41574-024-01050-3","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
IGF2-produced microRNA restricts growth via suppression of IGF1
Insulin-like growth factor 1 (IGF1) is a key protein that contributes to control of an organism’s size after birth and during development, whereas IGF2 is the main regulator of growth and body size during fetal development. A study in Cell Reports describes a mechanism by which a microRNA produced from Igf2 regulates IGF1 to suppress growth in mice.
The researchers then assessed the effect of miR-483 on fetal and postnatal development and growth. “We made a knockout mouse and two types of mouse lines that make more copies of miR-483 than the normal levels; one coming from the ‘endogenous’ location at the Igf2 gene and one from another genomic location,” says corresponding author Miguel Constância. Knockout of miR483 (Mir483Pat-KO mice) did not result in a noticeable phenotypic change. Overexpression of Mir-483 during fetal development, however, universally led to fetal death.
期刊介绍:
Nature Reviews Endocrinology aspires to be the foremost platform for reviews and commentaries catering to the scientific communities it serves. The journal aims to publish articles characterized by authority, accessibility, and clarity, enhanced with easily understandable figures, tables, and other visual aids. The goal is to offer an unparalleled service to authors, referees, and readers, striving to maximize the usefulness and impact of each article. Nature Reviews Endocrinology publishes Research Highlights, Comments, News & Views, Reviews, Consensus Statements, and Perspectives relevant to researchers and clinicians in the fields of endocrinology and metabolism. Its broad scope ensures that the work it publishes reaches the widest possible audience.