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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:31:37Z</responseDate> <request identifier=oai:HAL:hal-01118028v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01118028v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-TREC</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UNIV-TLSE3</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:IRSET-6</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>The uterine and vascular actions of estetrol delineate a distinctive profile of estrogen receptor α modulation, uncoupling nuclear and membrane activation.</title> <creator>Abot, Anne</creator> <creator>Fontaine, Coralie</creator> <creator>Buscato, Mélissa</creator> <creator>Solinhac, Romain</creator> <creator>Flouriot, Gilles</creator> <creator>Fabre, A. J.</creator> <creator>Drougard, Anne</creator> <creator>Rajan, Shyamala</creator> <creator>Laine, Muriel</creator> <creator>Milon, Alain</creator> <creator>Muller, Isabelle</creator> <creator>Henrion, Daniel</creator> <creator>Adlanmerini, Marine</creator> <creator>Valéra, Marie-Cécile</creator> <creator>Gompel, Anne</creator> <creator>Gerard, Céline</creator> <creator>Péqueux, Christel</creator> <creator>Mestdagt, Mélanie</creator> <creator>Raymond-Letron, Isabelle</creator> <creator>Knauf, Claude</creator> <creator>Ferriere, François</creator> <creator>Valet, Philippe</creator> <creator>Gourdy, Pierre</creator> <creator>Katzenellenbogen, Benita S</creator> <creator>Katzenellenbogen, John A</creator> <creator>Lenfant, Françoise</creator> <creator>Greene, Geoffrey L</creator> <creator>Foidart, Jean-Michel</creator> <creator>Arnal, Jean-François</creator> <contributor>Institut des Maladies Métaboliques et Cardiovasculaires (I2MC) ; Université Paul Sabatier - Toulouse 3 (UPS) - Hôpital de Rangueil - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Centre national de référence des angioedemes ; Centre national de référence des angioedemes</contributor> <contributor>Laboratory of Tumor and Developmental Biology ; Université de Liège - CHU Sart-Tilman</contributor> <contributor>Department of Molecular and Integrative Physiology ; University of Illinois and College of Medicine</contributor> <contributor>Institut de médecine moléculaire de Rangueil (I2MR) ; Université Paul Sabatier - Toulouse 3 (UPS) - IFR31 - IFR150 - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor> <contributor>Laboratoire de Biologie des Tumeurs et du Développement) ; Université de Liège</contributor> <contributor>The work at the INSERM unit U1048 was supported by INSERM, Université de Toulouse III and Faculté de Médecine Toulouse-Rangueil, Fondation de France, Conseil Régional Midi-Pyrénées and Fondation pour la Recherche Médicale (FRM). A. Abot was supported by a grant from the Groupe de Réflexion sur la Recherche Cardiovasculaire. The NMR facility is part of the genotoul-Ibisa PICT platform and was funded by CNRS, région Midi-Pyrénées, and European structural funds. The work at INSERM U1083-CNRS-UMR 6214 is supported by INSERM, CNRS, CHU and Université d'Angers, Fondation de France, Fondation de l'Avenir, and Conseil Régional Pays de la Loire. The work at ULg, GIGA-cancer was supported by grants from the F.R.S.-FNRS (Belgium), the DGO6 from SPW (Belgium), the IUAP (Belspo, Belgium). This work was supported by National Institutes of Health Grants PHS5R01 DK015556 to J.A.K.</contributor> <description>International audience</description> <source>ISSN: 1757-4676</source> <source>EISSN: 1757-4684</source> <source>EMBO Molecular Medicine</source> <publisher>Wiley Open Access</publisher> <identifier>hal-01118028</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01118028</identifier> <source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01118028</source> <source>EMBO Molecular Medicine, Wiley Open Access, 2014, 6 (10), pp.1328-46. 〈10.15252/emmm.201404112〉</source> <identifier>PUBMED : 25214462</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/25214462</relation> <identifier>PUBMEDCENTRAL : PMC4287935</identifier> <identifier>DOI : 10.15252/emmm.201404112</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.15252/emmm.201404112</relation> <language>en</language> <subject>[SDV] Life Sciences [q-bio]</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Estetrol (E4) is a natural estrogen with a long half-life produced only by the human fetal liver during pregnancy. The crystal structures of the estrogen receptor α (ERα) ligand-binding domain bound to 17β-estradiol (E2) and E4 are very similar, as well as their capacity to activate the two activation functions AF-1 and AF-2 and to recruit the coactivator SRC3. In vivo administration of high doses of E4 stimulated uterine gene expression, epithelial proliferation, and prevented atheroma, three recognized nuclear ERα actions. However, E4 failed to promote endothelial NO synthase activation and acceleration of endothelial healing, two processes clearly dependent on membrane-initiated steroid signaling (MISS). Furthermore, E4 antagonized E2 MISS-dependent effects in endothelium but also in MCF-7 breast cancer cell line. This profile of ERα activation by E4, uncoupling nuclear and membrane activation, characterizes E4 as a selective ER modulator which could have medical applications that should now be considered further.</description> <date>2014-09-30</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>