| http://purl.uniprot.org/citations/23842279 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23842279 | http://www.w3.org/2000/01/rdf-schema#comment | "HIV infection and its therapy are associated with disorders of lipid metabolism and bioenergetics. Previous work has suggested that viral protein R (Vpr) may contribute to the development of lipodystrophy and insulin resistance observed in HIV-1-infected patients. In adipocytes, Vpr suppresses mRNA expression of peroxisomal proliferator-activating receptor-γ (PPARγ)-responsive genes and inhibits differentiation. We investigated whether Vpr might interact with PPARβ/δ and influence its transcriptional activity. In the presence of PPARβ/δ, Vpr induced a 3.3-fold increase in PPAR response element-driven transcriptional activity, a 1.9-fold increase in pyruvate dehydrogenase kinase 4 (PDK4) protein expression, and a 1.6-fold increase in the phosphorylated pyruvate dehydrogenase subunit E1α leading to a 47% decrease in the activity of the pyruvate dehydrogenase complex in HepG2 cells. PPARβ/δ knockdown attenuated Vpr-induced enhancement of endogenous PPARβ/δ-responsive PDK4 mRNA expression. Vpr induced a 1.3-fold increase in mRNA expression of both carnitine palmitoyltransferase I (CPT1) and acetyl-coenzyme A acyltransferase 2 (ACAA2) and doubled the activity of β-hydroxylacyl coenzyme A dehydrogenase (HADH). Vpr physically interacted with the ligand-binding domain of PPARβ/δ in vitro and in vivo. Consistent with a role in energy expenditure, Vpr increased state-3 respiration in isolated mitochondria (1.16-fold) and basal oxygen consumption rate in intact HepG2 cells (1.2-fold) in an etomoxir-sensitive manner, indicating that the oxygen consumption rate increase is β-oxidation-dependent. The effects of Vpr on PPAR response element activation, pyruvate dehydrogenase complex activity, and β-oxidation were reversed by specific PPARβ/δ antagonists. These results support the hypothesis that Vpr contributes to impaired energy metabolism and increased energy expenditure in HIV patients."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.org/dc/terms/identifier | "doi:10.1210/me.2012-1370"xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Abe Y."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Lee H."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Okamoto K."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Kopp J.B."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Kino T."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Lopaschuk G.D."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Balasubramanyam A."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Shrivastav S."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/author | "Lagranha C."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/name | "Mol Endocrinol"xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/pages | "1564-1576"xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/title | "HIV-1 Vpr enhances PPARbeta/delta-mediated transcription, increases PDK4 expression, and reduces PDC activity."xsd:string |
| http://purl.uniprot.org/citations/23842279 | http://purl.uniprot.org/core/volume | "27"xsd:string |
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