Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression
Gonadal hormone 17β-estradiol (E2) and its receptors are key regulators of gene transcription by binding to estrogen responsive elements in the genome. Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Dependin...
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description | Gonadal hormone 17β-estradiol (E2) and its receptors are key regulators of gene transcription by binding to estrogen responsive elements in the genome. Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. The particular relevance of these mechanisms to physiological processes in memory formation, embryonic development, spermatogenesis and aging as well as in pathophysiological changes in carcinogenesis is also discussed. |
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Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. 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Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. The particular relevance of these mechanisms to physiological processes in memory formation, embryonic development, spermatogenesis and aging as well as in pathophysiological changes in carcinogenesis is also discussed.</description><subject>17β-Estradiol</subject><subject>Aging</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Chromatin remodeling</subject><subject>Demethylation</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA Methylation - drug effects</subject><subject>DNA Methylation - genetics</subject><subject>Embryogenesis</subject><subject>Enzymes</subject><subject>Epigenesis, Genetic - drug effects</subject><subject>Epigenesis, Genetic - genetics</subject><subject>Epigenetics</subject><subject>Estradiol - pharmacology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Histones</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proteins</subject><subject>Regulators</subject><subject>Review</subject><subject>Spermatogenesis</subject><subject>Transcription</subject><subject>Transcription factors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpVUd9LwzAQDqK4OX3zWQq-Ws2PNm1eBBl1DjYEUV9DmqRbRpfWpBX335uxOebL3XH33Xff3QFwjeA9IQw-mNXaYwQZQVl2AoYowTiGkGanR_EAXHi_ghATnLJzMCCY0JRhOASfhe-cUKap46lVvdQqKlqz0FZ3Roq63kRzrYzoQn6u5VJY49c-ElZFb3rR16IzjY2aKpqEjqj4aZ32PqQuwVklaq-v9n4EPp6L9_FLPHudTMdPs1imGHUxVkhRpBJIMpTrVKGc5DhFEklKdMmIyNIKsYwKIRJJS8wYkrkoRTBVWEuQEXjc8bZ9udZKahu2qXnrzFq4DW-E4f8r1iz5ovnmGU5ojmkguN0TuOar177jq6Z3NmjmmLCtHJSkAXW3Q0nXeO90dZiAIN9-gR9_IcBvjlUdwH9nJ7-IKoR7</recordid><startdate>20200430</startdate><enddate>20200430</enddate><creator>Kovács, Tamás</creator><creator>Szabó-Meleg, Edina</creator><creator>Ábrahám, István M</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20200430</creationdate><title>Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression</title><author>Kovács, Tamás ; Szabó-Meleg, Edina ; Ábrahám, István M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-2d1d61d403718e5d1838251c1c63eb93a75f1976aaa4c6b2991c8abac8af067a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>17β-Estradiol</topic><topic>Aging</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Chromatin remodeling</topic><topic>Demethylation</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA Methylation - drug effects</topic><topic>DNA Methylation - genetics</topic><topic>Embryogenesis</topic><topic>Enzymes</topic><topic>Epigenesis, Genetic - drug effects</topic><topic>Epigenesis, Genetic - genetics</topic><topic>Epigenetics</topic><topic>Estradiol - pharmacology</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Histones</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proteins</topic><topic>Regulators</topic><topic>Review</topic><topic>Spermatogenesis</topic><topic>Transcription</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kovács, Tamás</creatorcontrib><creatorcontrib>Szabó-Meleg, Edina</creatorcontrib><creatorcontrib>Ábrahám, István M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kovács, Tamás</au><au>Szabó-Meleg, Edina</au><au>Ábrahám, István M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2020-04-30</date><risdate>2020</risdate><volume>21</volume><issue>9</issue><spage>3177</spage><pages>3177-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Gonadal hormone 17β-estradiol (E2) and its receptors are key regulators of gene transcription by binding to estrogen responsive elements in the genome. Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. 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subjects | 17β-Estradiol Aging Animals Binding sites Carcinogenesis Carcinogens Chromatin remodeling Demethylation Deoxyribonucleic acid DNA DNA methylation DNA Methylation - drug effects DNA Methylation - genetics Embryogenesis Enzymes Epigenesis, Genetic - drug effects Epigenesis, Genetic - genetics Epigenetics Estradiol - pharmacology Estrogen receptors Estrogens Gene expression Genomes Histones Histones - metabolism Humans Kinases Ligands Promoter Regions, Genetic - genetics Proteins Regulators Review Spermatogenesis Transcription Transcription factors |
title | Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression |
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