<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Drosatos K</submitter><funding>NHLBI NIH HHS</funding><pagination>19556-64</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2745720</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>282(27)</volume><pubmed_abstract>c-Jun is a transcription factor activated by phosphorylation by the stress-activated protein kinase/c-Jun N-terminal kinase pathway in response to extracellular signals and cytokines. We show that adenovirus-mediated gene transfer of the dominant negative form of c-Jun (dn-c-Jun) in C57BL/6 mice increased greatly apoE hepatic mRNA and plasma levels, increased plasma cholesterol, triglyceride, and very low density lipoprotein levels, and resulted in the accumulation of discoidal high density lipoprotein particles. A similar but more severe phenotype was generated by overexpression of the mouse apoE in C57BL/6 mice, suggesting that dyslipidemia induced by dn-c-Jun was the result of apoE overexpression. Unexpectedly, infection of apoE(-/-) mice with adenovirus expressing dn-c-Jun reduced plas</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice.</pubmed_title><pmcid>PMC2745720</pmcid><funding_grant_id>HL33952</funding_grant_id><funding_grant_id>R01 HL033952</funding_grant_id><funding_grant_id>R01 HL048739</funding_grant_id><funding_grant_id>R01 HL068216</funding_grant_id><funding_grant_id>HL48739</funding_grant_id><pubmed_authors>Kypreos KE</pubmed_authors><pubmed_authors>Drosatos K</pubmed_authors><pubmed_authors>Kardassis D</pubmed_authors><pubmed_authors>Sanoudou D</pubmed_authors><pubmed_authors>Zannis VI</pubmed_authors></additional><is_claimable>false</is_claimable><name>A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice.</name><description>c-Jun is a transcription factor activated by phosphorylation by the stress-activated protein kinase/c-Jun N-terminal kinase pathway in response to extracellular signals and cytokines. We show that adenovirus-mediated gene transfer of the dominant negative form of c-Jun (dn-c-Jun) in C57BL/6 mice increased greatly apoE hepatic mRNA and plasma levels, increased plasma cholesterol, triglyceride, and very low density lipoprotein levels, and resulted in the accumulation of discoidal high density lipoprotein particles. A similar but more severe phenotype was generated by overexpression of the mouse apoE in C57BL/6 mice, suggesting that dyslipidemia induced by dn-c-Jun was the result of apoE overexpression. Unexpectedly, infection of apoE(-/-) mice with adenovirus expressing dn-c-Jun reduced plas</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Jul</publication><modification>2026-05-02T05:40:50.93Z</modification><creation>2026-04-07T17:42:06.129Z</creation></dates><accession>S-EPMC2745720</accession><cross_references><pubmed>17456467</pubmed><doi>10.1074/jbc.M700986200</doi><doi>10.1074/jbc.m700986200</doi></cross_references></HashMap>