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dc.contributor.supervisorCzubryt, Michael (Physiology)en_US
dc.contributor.authorBlant, Alexandra
dc.date.accessioned2014-01-10T19:37:59Z
dc.date.available2014-01-10T19:37:59Z
dc.date.issued2014-01-10
dc.identifier.urihttp://hdl.handle.net/1993/23146
dc.description.abstractThe normal adult heart prefers fatty acids as an energy substrate. In the case of heart failure, the heart switches its preference from fatty acids to glucose, adopting a pattern similar to fetal metabolism. PGC-1α is heavily involved in the shift towards glucose oxidation. p65, which belongs to the NF-κB transcription factor family is another crucial molecule involved in maintaining cardiac homeostasis. There is a substantial amount of evidence suggesting that PGC-1α and NF-κB directly interact, thereby connecting metabolic and inflammatory processes. Dysregulation of either PGC-1α or NF-κB signalling correlates to many diseases including heart disease. In this study, we provide further evidence that the NF-κB family has the ability to repress PGC-1α. We also show that the PGC-1α promoter contains a p65 binding site through which p65 imparts control on the PGC-1α gene. Metabolic homeostasis and inflammation pathways are closely linked and play crucial roles in heart dysfunction.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectheart diseaseen_US
dc.subjectPGC-1α promoteren_US
dc.subjectNF-κBen_US
dc.subjectinflammationen_US
dc.subjectfatty acid metabolismen_US
dc.subjectmetabolism and inflammationen_US
dc.subjectfetal metabolic profileen_US
dc.subjectcardiac homeostasisen_US
dc.titleNegative regulation of PGC-1α by NF-κBen_US
dc.typeinfo:eu-repo/semantics/masterThesis
dc.typemaster thesisen_US
dc.degree.disciplinePhysiologyen_US
dc.contributor.examiningcommitteeDuhamel, Todd (Kinesiology and Recreation Management) Singal, Pawan (Physiology) Kirshenbaum, Lorrie (Physiology)en_US
dc.degree.levelMaster of Science (M.Sc.)en_US
dc.description.noteFebruary 2014en_US


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