{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Drosatos K"],"funding":["NHLBI NIH HHS"],"pagination":["19556-64"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2745720"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["282(27)"],"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"],"journal":["The Journal of biological chemistry"],"pubmed_title":["A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice."],"pmcid":["PMC2745720"],"funding_grant_id":["HL33952","R01 HL033952","R01 HL048739","R01 HL068216","HL48739"],"pubmed_authors":["Kypreos KE","Drosatos K","Kardassis D","Sanoudou D","Zannis VI"],"additional_accession":[]},"is_claimable":false,"name":"A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice.","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","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Jul","modification":"2026-05-02T05:40:50.93Z","creation":"2026-04-07T17:42:06.129Z"},"accession":"S-EPMC2745720","cross_references":{"pubmed":["17456467"],"doi":["10.1074/jbc.M700986200","10.1074/jbc.m700986200"]}}