Please use this identifier to cite or link to this item: http://dspace.mediu.edu.my:8181/xmlui/handle/1957/6291
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dc.contributorHagen, Tory M.-
dc.contributorAhern, Kevin-
dc.date2007-08-06T23:25:35Z-
dc.date2007-08-06T23:25:35Z-
dc.date2007-08-06T23:25:35Z-
dc.date.accessioned2013-10-16T08:06:26Z-
dc.date.available2013-10-16T08:06:26Z-
dc.date.issued2013-10-16-
dc.identifierhttp://hdl.handle.net/1957/6291-
dc.identifier.urihttp://koha.mediu.edu.my:8181/xmlui/handle/1957/6291-
dc.descriptionThe endoplasmic reticulum (ER) is a crucial organelle in the cell where protein folding and processing occurs, and conditions that negatively affect ER functions are highly detrimental to the cell. The accumulation of unfolded/misfolded proteins in the ER leads to a condition known as ER Stress. The ER has developed various pro-survival and pro-apoptosis signaling pathways that attempt to cope with this stress. ER stress is relevant to many clinical studies and has been linked to a variety of age-related diseases, including Huntington’s, Alzheimer’s, Parkinson’s and heart disease. Despite these findings, the manner in which ER stress response is altered with age hasn’t been thoroughly studied and constitutes a gap in knowledge. In this study, we investigated the age-related loss of ER stress response in young and old rats. Our results suggest that, in both young and old cells, the pro-apoptosis pathway which utilizes the transcription factor, CHOP, remains intact with age. However, the pro-survival pathway acting through PERK/Nrf2 and the phase II detoxification enzyme NQO1 show elevated activity in the young cells, but a loss of function in the old. These results suggest that stresses which would not cause cell death in young individuals may induce cell death in the elderly.-
dc.languageen_US-
dc.subjectER stress-
dc.subjectAge-
dc.titleInvestigating the age-related loss of endoplasmic reticulum stress response-
dc.typeThesis-
Appears in Collections:ScholarsArchive@OSU

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