{"title":"SF3B1突变的代谢重编程和易感性。","authors":"W Brian Dalton","doi":"10.1080/23723556.2019.1697619","DOIUrl":null,"url":null,"abstract":"<p><p>Mutations in the splicing factor 3b subunit 1 (<i>SF3B1</i>) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that <i>SF3B1</i> <sup>MUT</sup> induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1697619"},"PeriodicalIF":0.0000,"publicationDate":"2020-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2019.1697619","citationCount":"4","resultStr":"{\"title\":\"The metabolic reprogramming and vulnerability of <i>SF3B1</i> mutations.\",\"authors\":\"W Brian Dalton\",\"doi\":\"10.1080/23723556.2019.1697619\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Mutations in the splicing factor 3b subunit 1 (<i>SF3B1</i>) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that <i>SF3B1</i> <sup>MUT</sup> induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1697619\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-02-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2019.1697619\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2019.1697619\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & cellular oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2019.1697619","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
The metabolic reprogramming and vulnerability of SF3B1 mutations.
Mutations in the splicing factor 3b subunit 1 (SF3B1) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that SF3B1MUT induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.