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DC Field | Value | Language |
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dc.contributor | Hagen, Tory M. | - |
dc.contributor | Ahern, Kevin | - |
dc.date | 2007-08-06T23:25:35Z | - |
dc.date | 2007-08-06T23:25:35Z | - |
dc.date | 2007-08-06T23:25:35Z | - |
dc.date.accessioned | 2013-10-16T08:06:26Z | - |
dc.date.available | 2013-10-16T08:06:26Z | - |
dc.date.issued | 2013-10-16 | - |
dc.identifier | http://hdl.handle.net/1957/6291 | - |
dc.identifier.uri | http://koha.mediu.edu.my:8181/xmlui/handle/1957/6291 | - |
dc.description | The 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.language | en_US | - |
dc.subject | ER stress | - |
dc.subject | Age | - |
dc.title | Investigating the age-related loss of endoplasmic reticulum stress response | - |
dc.type | Thesis | - |
Appears in Collections: | ScholarsArchive@OSU |
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