Mitochondrial genes as sites of primary action of steroid hormones
Identifieur interne : 001651 ( Istex/Corpus ); précédent : 001650; suivant : 001652Mitochondrial genes as sites of primary action of steroid hormones
Auteurs : Constantine V. Demonacos ; Niki Karayanni ; Evi Hatzoglou ; Christos Tsiriyiotis ; Demetrios A. Spandidos ; Constantine E. SekerisSource :
- Steroids [ 0039-128X ] ; 1996.
English descriptors
- Teeft :
- Dexamethasone, Genome, Glucocorticoid, Glucocorticoid receptor, Grea, Greb, Gres, Hres, Liver mitochondria, Mitochondrial, Mitochondrial gene transcription, Mitochondrial genes, Mitochondrial genome, Mitochondrial proteins, Mitochondrion, Molecular weight markers, Monoclonal antibody, Nonspecific competitor, Nuclear genes, Nucleotide sequences, Oxid, Partial similarity, Plasmid, Polyacrylamide, Putative, Putative gres, Putative mitochondrial hres, Receptor, Regulatory region, Reticulocyte lysate, Specific competitor, Steroid, Strong similarity, Tgttct, Thyroid hormone, Thyroid hormones, Transcription, Transfection experiments, Translocation.
Abstract
Abstract: Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TRα) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.
Url:
DOI: 10.1016/0039-128X(96)00019-0
Links to Exploration step
ISTEX:1B7E1A9B23088F887B2E8112E4AA023D1AF62588Le document en format XML
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Demonacos</name><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation></author><author><name sortKey="Karayanni, Niki" sort="Karayanni, Niki" uniqKey="Karayanni N" first="Niki" last="Karayanni">Niki Karayanni</name><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation></author><author><name sortKey="Hatzoglou, Evi" sort="Hatzoglou, Evi" uniqKey="Hatzoglou E" first="Evi" last="Hatzoglou">Evi Hatzoglou</name><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation></author><author><name sortKey="Tsiriyiotis, Christos" sort="Tsiriyiotis, Christos" uniqKey="Tsiriyiotis C" first="Christos" last="Tsiriyiotis">Christos Tsiriyiotis</name><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation></author><author><name sortKey="Spandidos, Demetrios A" sort="Spandidos, Demetrios A" uniqKey="Spandidos D" first="Demetrios A." last="Spandidos">Demetrios A. Spandidos</name><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Molecular Virology, Medical School, University of Crete, Crete, Greece</mods:affiliation></affiliation></author><author><name sortKey="Sekeris, Constantine E" sort="Sekeris, Constantine E" uniqKey="Sekeris C" first="Constantine E." last="Sekeris">Constantine E. Sekeris</name><affiliation><mods:affiliation>Address reprint requests to Dr. Constantine E. Sekeris, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Vassileos Constantinou Ave. 48, Athens, 116-35, Greece.</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Steroids</title><title level="j" type="abbrev">STE</title><idno type="ISSN">0039-128X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">61</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="226">226</biblScope><biblScope unit="page" to="232">232</biblScope></imprint><idno type="ISSN">0039-128X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0039-128X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Dexamethasone</term><term>Genome</term><term>Glucocorticoid</term><term>Glucocorticoid receptor</term><term>Grea</term><term>Greb</term><term>Gres</term><term>Hres</term><term>Liver mitochondria</term><term>Mitochondrial</term><term>Mitochondrial gene transcription</term><term>Mitochondrial genes</term><term>Mitochondrial genome</term><term>Mitochondrial proteins</term><term>Mitochondrion</term><term>Molecular weight markers</term><term>Monoclonal antibody</term><term>Nonspecific competitor</term><term>Nuclear genes</term><term>Nucleotide sequences</term><term>Oxid</term><term>Partial similarity</term><term>Plasmid</term><term>Polyacrylamide</term><term>Putative</term><term>Putative gres</term><term>Putative mitochondrial hres</term><term>Receptor</term><term>Regulatory region</term><term>Reticulocyte lysate</term><term>Specific competitor</term><term>Steroid</term><term>Strong similarity</term><term>Tgttct</term><term>Thyroid hormone</term><term>Thyroid hormones</term><term>Transcription</term><term>Transfection experiments</term><term>Translocation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TRα) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>mitochondrial</json:string><json:string>mitochondrion</json:string><json:string>receptor</json:string><json:string>genome</json:string><json:string>hres</json:string><json:string>gres</json:string><json:string>glucocorticoid</json:string><json:string>putative</json:string><json:string>translocation</json:string><json:string>mitochondrial genome</json:string><json:string>plasmid</json:string><json:string>oxid</json:string><json:string>tgttct</json:string><json:string>polyacrylamide</json:string><json:string>steroid</json:string><json:string>grea</json:string><json:string>greb</json:string><json:string>mitochondrial genes</json:string><json:string>glucocorticoid receptor</json:string><json:string>liver mitochondria</json:string><json:string>nucleotide sequences</json:string><json:string>mitochondrial proteins</json:string><json:string>partial similarity</json:string><json:string>specific competitor</json:string><json:string>putative gres</json:string><json:string>reticulocyte lysate</json:string><json:string>nuclear genes</json:string><json:string>strong similarity</json:string><json:string>thyroid hormones</json:string><json:string>transcription</json:string><json:string>regulatory region</json:string><json:string>putative mitochondrial hres</json:string><json:string>monoclonal antibody</json:string><json:string>molecular weight markers</json:string><json:string>transfection experiments</json:string><json:string>mitochondrial gene transcription</json:string><json:string>nonspecific competitor</json:string><json:string>thyroid hormone</json:string><json:string>dexamethasone</json:string></teeft></keywords><author><json:item><name>Constantine V. Demonacos</name><affiliations><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string></affiliations></json:item><json:item><name>Niki Karayanni</name><affiliations><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string></affiliations></json:item><json:item><name>Evi Hatzoglou</name><affiliations><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string></affiliations></json:item><json:item><name>Christos Tsiriyiotis</name><affiliations><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string></affiliations></json:item><json:item><name>Demetrios A. Spandidos</name><affiliations><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string><json:string>Department of Molecular Virology, Medical School, University of Crete, Crete, Greece</json:string></affiliations></json:item><json:item><name>Constantine E. Sekeris</name><affiliations><json:string>Address reprint requests to Dr. Constantine E. Sekeris, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Vassileos Constantinou Ave. 48, Athens, 116-35, Greece.</json:string><json:string>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</json:string><json:string>Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>hormone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>thyroid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mitochondria</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>regulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>transcription</value></json:item></subject><arkIstex>ark:/67375/6H6-3L71DGTM-8</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TRα) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.</abstract><qualityIndicators><score>8.663</score><pdfWordCount>3891</pdfWordCount><pdfCharCount>25463</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>620 x 850 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>231</abstractWordCount><abstractCharCount>1667</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Mitochondrial genes as sites of primary action of steroid hormones</title><pmid><json:string>8733006</json:string></pmid><pii><json:string>0039-128X(96)00019-0</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc Natl Acad Sci USA</title><language><json:string>unknown</json:string></language><volume>83</volume><pages><first>6277</first><last>6281</last></pages></serie><host><title>Steroids</title><language><json:string>unknown</json:string></language><publicationDate>1996</publicationDate><issn><json:string>0039-128X</json:string></issn><pii><json:string>S0039-128X(00)X0016-5</json:string></pii><volume>61</volume><issue>4</issue><pages><first>226</first><last>232</last></pages><genre><json:string>journal</json:string></genre><conference><json:item><name>XVII Meeting of the International Study Group for Steroid Hormones, Berlin, Germany 19951125 19951128</name></json:item></conference><editor><json:item><name>J.W. 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Demonacos</json:string><json:string>Niki Karayanni</json:string><json:string>Sequences</json:string><json:string>Nikos Tsawdaroglou</json:string><json:string>Evi Hatzoglou</json:string><json:string>Constantine E. 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Sekeris, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Vassileos Constantinou Ave. 48, Athens, 116-35, Greece.</affiliation><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><affiliation>Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece</affiliation></author><idno type="istex">1B7E1A9B23088F887B2E8112E4AA023D1AF62588</idno><idno type="ark">ark:/67375/6H6-3L71DGTM-8</idno><idno type="DOI">10.1016/0039-128X(96)00019-0</idno><idno type="PII">0039-128X(96)00019-0</idno></analytic><monogr><title level="j">Steroids</title><title level="j" type="abbrev">STE</title><idno type="pISSN">0039-128X</idno><idno type="PII">S0039-128X(00)X0016-5</idno><meeting><addName>XVII Meeting of the International Study Group for Steroid Hormones, Berlin, Germany</addName><date>19951125</date><date>19951128</date></meeting><editor xml:id="book-author-0000"><persName>J.W. Funder</persName></editor><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996"></date><biblScope unit="volume">61</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="226">226</biblScope><biblScope unit="page" to="232">232</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TRα) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>hormone</term></item><item><term>thyroid</term></item><item><term>receptor</term></item><item><term>mitochondria</term></item><item><term>regulation</term></item><item><term>transcription</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-3L71DGTM-8/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>STE</jid><aid>96000190</aid><ce:pii>0039-128X(96)00019-0</ce:pii><ce:doi>10.1016/0039-128X(96)00019-0</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Paper</ce:textfn></ce:dochead><ce:title>Mitochondrial genes as sites of primary action of steroid hormones</ce:title><ce:author-group><ce:author><ce:given-name>Constantine V.</ce:given-name><ce:surname>Demonacos</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Niki</ce:given-name><ce:surname>Karayanni</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Evi</ce:given-name><ce:surname>Hatzoglou</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Christos</ce:given-name><ce:surname>Tsiriyiotis</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Demetrios A.</ce:given-name><ce:surname>Spandidos</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Constantine E.</ce:given-name><ce:surname>Sekeris</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF3"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>∗</ce:label><ce:textfn>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>†</ce:label><ce:textfn>Department of Molecular Virology, Medical School, University of Crete, Crete, Greece</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>‡</ce:label><ce:textfn>Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Address reprint requests to Dr. Constantine E. Sekeris, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Vassileos Constantinou Ave. 48, Athens, 116-35, Greece.</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TR<ce:inf>α</ce:inf>) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>hormone</ce:text></ce:keyword><ce:keyword><ce:text>thyroid</ce:text></ce:keyword><ce:keyword><ce:text>receptor</ce:text></ce:keyword><ce:keyword><ce:text>mitochondria</ce:text></ce:keyword><ce:keyword><ce:text>regulation</ce:text></ce:keyword><ce:keyword><ce:text>transcription</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Mitochondrial genes as sites of primary action of steroid hormones</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Mitochondrial genes as sites of primary action of steroid hormones</title></titleInfo><name type="personal"><namePart type="given">Constantine V.</namePart><namePart type="family">Demonacos</namePart><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Niki</namePart><namePart type="family">Karayanni</namePart><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Evi</namePart><namePart type="family">Hatzoglou</namePart><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christos</namePart><namePart type="family">Tsiriyiotis</namePart><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Demetrios A.</namePart><namePart type="family">Spandidos</namePart><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><affiliation>Department of Molecular Virology, Medical School, University of Crete, Crete, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Constantine E.</namePart><namePart type="family">Sekeris</namePart><affiliation>Address reprint requests to Dr. Constantine E. Sekeris, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Vassileos Constantinou Ave. 48, Athens, 116-35, Greece.</affiliation><affiliation>Institute for Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece</affiliation><affiliation>Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Steroid and thyroid hormones act on nuclear gene transcription by activating protein receptors, which in turn bind to hormone response elements (HREs). Among the cell-specific processes regulated by steroid receptors is energy metabolism through increased synthesis of respiratory enzymes. As some of these enzymes are encoded by both nuclear and mitochondrial genes, coordination of their synthesis is probable, inter alia at the transcriptional level. We have postulated a direct effect of steroid hormones on mitochondrial gene transcription and here present the following evidence in support of this hypothesis. 1) The human and rodent mitochondrial genomes contain nucleotide sequences similar both to type I and type II HREs. 2) Glucocorticoid receptors (GR) rapidly translocate from the cytoplasm into mitochondria after administration of glucocorticoids. This process has been reproduced in vitro and deletion of the N-terminal part of the glucocorticoid receptor stops translocation into mitochondria. 3) Gel shift analysis has demonstrated binding of GR to putative mitochondrial GR elements. 4) In transfection experiments, mitochondrial HREs confer dexamethasone inducibility on hybrid reporter constructs, abolished in the presence of excess RU38486. 5) Similar results were obtained for thyroid hormone receptor (TRα) localization, import, and binding to TR elements. These findings, taken with the demonstrated effects of steroid (and thyroid) hormones on mitochondrial transcription and respiratory enzyme biosynthesis, strongly support the hypothesis of a direct effect of steroid (and thyroid) hormones on mitochondrial gene transcription.</abstract><note type="content">Section title: Paper</note><subject><genre>Keywords</genre><topic>hormone</topic><topic>thyroid</topic><topic>receptor</topic><topic>mitochondria</topic><topic>regulation</topic><topic>transcription</topic></subject><relatedItem type="host"><titleInfo><title>Steroids</title></titleInfo><titleInfo type="abbreviated"><title>STE</title></titleInfo><name type="conference"><namePart>XVII Meeting of the International Study Group for Steroid Hormones, Berlin, Germany</namePart><namePart type="date">19951125</namePart><namePart type="date">19951128</namePart></name><name type="personal"><namePart>J.W. Funder</namePart><role><roleTerm type="text">editor</roleTerm></role></name><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued></originInfo><identifier type="ISSN">0039-128X</identifier><identifier type="PII">S0039-128X(00)X0016-5</identifier><part><date>1996</date><detail type="issue"><title>XVII Meeting of the International Study Group for Steroid Hormones, Berlin, Germany</title></detail><detail type="volume"><number>61</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue-pages"><start>153</start><end>276</end></extent><extent unit="pages"><start>226</start><end>232</end></extent></part></relatedItem><identifier type="istex">1B7E1A9B23088F887B2E8112E4AA023D1AF62588</identifier><identifier type="ark">ark:/67375/6H6-3L71DGTM-8</identifier><identifier type="DOI">10.1016/0039-128X(96)00019-0</identifier><identifier type="PII">0039-128X(96)00019-0</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-3L71DGTM-8/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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