Show simple item record

dc.contributor.supervisor Kirshenbaum, Lorrie (Physiology) en_US
dc.contributor.author Mughal, Wajihah
dc.date.accessioned 2012-08-10T19:54:14Z
dc.date.available 2012-08-10T19:54:14Z
dc.date.issued 2012-08-10
dc.identifier.uri http://hdl.handle.net/1993/8158
dc.description.abstract E2F-1 is a transcription factor that is involved in cellular growth and regulates the transition between G1 and S phase during the cell cycle. However, the mechanisms by which E2F-1 regulates endoplasmic reticulum (ER) stress in ventricular myocytes remain poorly defined. ER stress was triggered by tunicamycin or thapsigargin; gene transcription was assessed by polymerase chain reaction and protein expression was detected by western blot. Cell viability and mitochondrial defects were assessed by fluorescent microscopy imaging. During ER stress, E2F-1 repressed signaling molecules of the unfolded protein response (UPR) and sensitized myocytes to cell death triggered by thapsigargin that was inhibited in Bnip3 null fibroblasts. Bnip3Δex3 rescued thapsigargin-induced cardiac apoptosis, blocked mitochondrial defects and rescued hypoxia/ER stress induced cardiac cell death. This study provides evidence that E2F-1 sensitizes ventricular myocytes to ER stress induced apoptosis 1) by repressing the UPR; 2) that is Bnip3 dependent; and 3) mediated by mitochondrial dysfunction. en_US
dc.rights info:eu-repo/semantics/openAccess
dc.subject Myocytes en_US
dc.subject Endoplasmic reticulum en_US
dc.title Regulation of endoplasmic reticulum stress by transcription factor E2F-1 in ventricular myocytes en_US
dc.type info:eu-repo/semantics/masterThesis
dc.degree.discipline Physiology en_US
dc.contributor.examiningcommittee Singal, Pawan (Physiology) Dhalla, NS (Physiology) Czubryt, Michael (Physiology) Duhamel, Todd (Kinesiology and Recreation Management) en_US
dc.degree.level Master of Science (M.Sc.) en_US
dc.description.note October 2012 en_US


Files in this item

This item appears in the following Collection(s)

Show simple item record

View Statistics