<HashMap><database>biostudies-other</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Dr. Irem Bayindir-Buchhalter</submitter><funding>Deutsche Forschungsgemeinschaft (DFG)</funding><funding>Novo Nordisk</funding><funding>Helmholtz International Graduate School for Cancer Research</funding><funding>Brain Tumor Network</funding><funding>Human Frontier Science Program (HFSP)</funding><funding>German Ministry of Education and Research</funding><journal>EMBO Molecular Medicine</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-SCDT-EMM-2017-08613</full_dataset_link><abstract>Most antidiabetic drugs treat disease symptoms rather than adipose tissue dysfunction as a key pathogenic cause in the metabolic syndrome and type 2 diabetes. Pharmacological targeting of adipose tissue through the nuclear receptor PPARg, as exemplified by glitazone treatments, mediates efficacious insulin sensitization. However, a better understanding of the context-specific PPARg responses is required for the development of novel approaches with reduced side effects. Here we identified the transcriptional cofactor Cited4 as a target and mediator of rosiglitazone in human and murine adipocyte progenitor cells, where it promoted specific sets of the rosiglitazone-dependent transcriptional program. In mice, Cited4 was required for the proper induction of thermogenic expression by Rosi speci</abstract><repository>biostudies-other</repository><funding_grant_id>Infrafrontier grant 01KX1012</funding_grant_id><funding_grant_id>RGY0082/2014</funding_grant_id><funding_grant_id>NGFNplus #01GS0883</funding_grant_id><funding_grant_id>HE 3260/8-1</funding_grant_id><pubmed_authors>Dr. Lars Ketscher</pubmed_authors><pubmed_authors>Dr. Damir Krunic</pubmed_authors><pubmed_authors>Dr. Alexandros Vegiopoulos</pubmed_authors><pubmed_authors>Prof. Mathias Heikenwälder</pubmed_authors><pubmed_authors>Dr. Jorge, Lira Ruas</pubmed_authors><pubmed_authors>Dr. Adrian, T Billeter</pubmed_authors><pubmed_authors>Prof. Peter Lichter</pubmed_authors><pubmed_authors>Dr. Irem Bayindir-Buchhalter</pubmed_authors><pubmed_authors>Dr. Rohollah Babaei</pubmed_authors><pubmed_authors>Tjeerd Sijmonsma</pubmed_authors><pubmed_authors>Dr. Gretchen Wolff</pubmed_authors><pubmed_authors>Dr. Jan Gronych</pubmed_authors><pubmed_authors>Mrs. Sarah Lerch</pubmed_authors><pubmed_authors>Dr. Nadine Spielmann</pubmed_authors><pubmed_authors>Prof. Martin Hrabě de Angelis</pubmed_authors><pubmed_authors>Mr. Maximilian Schuster</pubmed_authors><pubmed_authors>Prof. Beat, P Müller-Stich</pubmed_authors><pubmed_authors>Prof. Stephan Herzig</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cited4 is a sex-biased mediator of the antidiabetic glitazone response in adipocyte progenitors</name><description>Most antidiabetic drugs treat disease symptoms rather than adipose tissue dysfunction as a key pathogenic cause in the metabolic syndrome and type 2 diabetes. Pharmacological targeting of adipose tissue through the nuclear receptor PPARg, as exemplified by glitazone treatments, mediates efficacious insulin sensitization. However, a better understanding of the context-specific PPARg responses is required for the development of novel approaches with reduced side effects. Here we identified the transcriptional cofactor Cited4 as a target and mediator of rosiglitazone in human and murine adipocyte progenitor cells, where it promoted specific sets of the rosiglitazone-dependent transcriptional program. In mice, Cited4 was required for the proper induction of thermogenic expression by Rosi speci</description><dates><release>2018-12-05T16:19:33Z</release><modification>2018-12-05T16:19:33Z</modification><creation>2018-12-04T11:03:02Z</creation></dates><accession>S-SCDT-EMM-2017-08613</accession><cross_references><doi>10.15252/emmm.201708613</doi></cross_references></HashMap>