Monica M. Montano, Nirmala Krishnamurthy, Smitha Sripathy
{"title":"针对雌激素的基因毒性效应","authors":"Monica M. Montano, Nirmala Krishnamurthy, Smitha Sripathy","doi":"10.1016/j.ddmec.2012.11.005","DOIUrl":null,"url":null,"abstract":"<div><p><span><span>Our studies indicate that expression of antioxidative stress enzymes is upregulated by Selective </span>Estrogen Receptor<span><span> Modulators (SERMs) in breast epithelial cell lines, providing protection against the genotoxic effects of estrogens and against estrogen-induced mammary tumorigenesis. This upregulation of antioxidative stress enzymes requires Estrogen Receptor beta (ERβ) and human homolog of </span>Xenopus gene which Prevents </span></span>Mitotic Catastrophe<span> (hPMC2). Further studies indicate that hPMC2 has a functional exonuclease domain that is required for upregulation of antioxidative stress enzymes by SERMs and repair of estrogen-induced abasic sites.</span></p></div>","PeriodicalId":72843,"journal":{"name":"Drug discovery today. Disease mechanisms","volume":"9 1","pages":"Pages e29-e33"},"PeriodicalIF":0.0000,"publicationDate":"2012-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ddmec.2012.11.005","citationCount":"0","resultStr":"{\"title\":\"Targeting the genotoxic effects of estrogens\",\"authors\":\"Monica M. Montano, Nirmala Krishnamurthy, Smitha Sripathy\",\"doi\":\"10.1016/j.ddmec.2012.11.005\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span><span>Our studies indicate that expression of antioxidative stress enzymes is upregulated by Selective </span>Estrogen Receptor<span><span> Modulators (SERMs) in breast epithelial cell lines, providing protection against the genotoxic effects of estrogens and against estrogen-induced mammary tumorigenesis. This upregulation of antioxidative stress enzymes requires Estrogen Receptor beta (ERβ) and human homolog of </span>Xenopus gene which Prevents </span></span>Mitotic Catastrophe<span> (hPMC2). Further studies indicate that hPMC2 has a functional exonuclease domain that is required for upregulation of antioxidative stress enzymes by SERMs and repair of estrogen-induced abasic sites.</span></p></div>\",\"PeriodicalId\":72843,\"journal\":{\"name\":\"Drug discovery today. Disease mechanisms\",\"volume\":\"9 1\",\"pages\":\"Pages e29-e33\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.ddmec.2012.11.005\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Drug discovery today. Disease mechanisms\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1740676512000235\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Drug discovery today. Disease mechanisms","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1740676512000235","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Our studies indicate that expression of antioxidative stress enzymes is upregulated by Selective Estrogen Receptor Modulators (SERMs) in breast epithelial cell lines, providing protection against the genotoxic effects of estrogens and against estrogen-induced mammary tumorigenesis. This upregulation of antioxidative stress enzymes requires Estrogen Receptor beta (ERβ) and human homolog of Xenopus gene which Prevents Mitotic Catastrophe (hPMC2). Further studies indicate that hPMC2 has a functional exonuclease domain that is required for upregulation of antioxidative stress enzymes by SERMs and repair of estrogen-induced abasic sites.
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