{"title":"p85β驱动的致癌途径:上游信号激活p110。","authors":"Ling Rao, Lydia W T Cheung","doi":"10.1080/23723556.2020.1780900","DOIUrl":null,"url":null,"abstract":"<p><p>The phosphatidylinositol 3-kinase (PI3K), which is composed of the p85 regulatory and p110 catalytic subunits, is known to be downstream of the receptor tyrosine kinase (RTK). Our recent findings revealed that p85β increases the protein level of AXL (an RTK) to activate p110, suggesting bidirectional regulation between PI3K and RTK.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1780900"},"PeriodicalIF":0.0000,"publicationDate":"2020-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1780900","citationCount":"2","resultStr":"{\"title\":\"Oncogenic pathway driven by p85β: upstream signals to activate p110.\",\"authors\":\"Ling Rao, Lydia W T Cheung\",\"doi\":\"10.1080/23723556.2020.1780900\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The phosphatidylinositol 3-kinase (PI3K), which is composed of the p85 regulatory and p110 catalytic subunits, is known to be downstream of the receptor tyrosine kinase (RTK). Our recent findings revealed that p85β increases the protein level of AXL (an RTK) to activate p110, suggesting bidirectional regulation between PI3K and RTK.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1780900\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-07-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2020.1780900\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2020.1780900\",\"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/10.1080/23723556.2020.1780900","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}
Oncogenic pathway driven by p85β: upstream signals to activate p110.
The phosphatidylinositol 3-kinase (PI3K), which is composed of the p85 regulatory and p110 catalytic subunits, is known to be downstream of the receptor tyrosine kinase (RTK). Our recent findings revealed that p85β increases the protein level of AXL (an RTK) to activate p110, suggesting bidirectional regulation between PI3K and RTK.
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