{"title":"自噬和TP53之间的双向串扰决定了衰老的速度。","authors":"Valentina Sica, Guido Kroemer","doi":"10.1080/23723556.2020.1769434","DOIUrl":null,"url":null,"abstract":"<p><p>When the orthologue of tumor suppressor protein p53 (<i>TP53), cep-1</i>, is inactivated in <i>Caenorhabditis elegans</i>, the nematodes manifest an autophagy-dependent increase in lifespan. A recent paper by Yang <i>et al</i>. demonstrates that accelerated aging phenotype of autophagy-deficient mice can be reduced by the knockout (KO) of <i>Trp53</i>. These findings point to a complex bidirectional crosstalk between autophagy and TP53 that has vast implications for the aging process.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1769434"},"PeriodicalIF":0.0000,"publicationDate":"2020-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1769434","citationCount":"5","resultStr":"{\"title\":\"A bidirectional crosstalk between autophagy and TP53 determines the pace of aging.\",\"authors\":\"Valentina Sica, Guido Kroemer\",\"doi\":\"10.1080/23723556.2020.1769434\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>When the orthologue of tumor suppressor protein p53 (<i>TP53), cep-1</i>, is inactivated in <i>Caenorhabditis elegans</i>, the nematodes manifest an autophagy-dependent increase in lifespan. A recent paper by Yang <i>et al</i>. demonstrates that accelerated aging phenotype of autophagy-deficient mice can be reduced by the knockout (KO) of <i>Trp53</i>. These findings point to a complex bidirectional crosstalk between autophagy and TP53 that has vast implications for the aging process.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1769434\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-06-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2020.1769434\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2020.1769434\",\"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/10.1080/23723556.2020.1769434","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}
A bidirectional crosstalk between autophagy and TP53 determines the pace of aging.
When the orthologue of tumor suppressor protein p53 (TP53), cep-1, is inactivated in Caenorhabditis elegans, the nematodes manifest an autophagy-dependent increase in lifespan. A recent paper by Yang et al. demonstrates that accelerated aging phenotype of autophagy-deficient mice can be reduced by the knockout (KO) of Trp53. These findings point to a complex bidirectional crosstalk between autophagy and TP53 that has vast implications for the aging process.
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