Abstract
The oxidative stress response is an important pathway involved in maintaining redox homeostasis in cells, preventing damage induced by free radicals and reactive oxygen species. The central regulator of this response is the transcription factor Nrf2. Nrf2 modulates expression of the oxidative stress genes via the antioxidant response element (ARE). Oxidative stress in cells may be both a cause of toxicity and a result of adaptation or cell death. To investigate whether the oxidative stress genes function as a group in response to toxic insult, we have designed and validated a rapid semiquantitative PCR assay for each selected gene. We demonstrate that the oxidative stress genes are not coordinately regulated in the mouse liver upon toxic insult. Instead their combined liver expression profiles present a gene expression signature that differs depending on the toxic stress.
Original language | English |
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Pages (from-to) | 512-517 |
Number of pages | 6 |
Journal | ASSAY and Drug Development Technologies |
Volume | 8 |
Issue number | 4 |
DOIs | |
Publication status | Published - Aug 2010 |
Keywords
- GAMMA-GLUTAMYLCYSTEINE SYNTHETASE
- PROSTATE CARCINOMA-CELLS
- OXIDATIVE STRESS
- RESPONSE ELEMENT
- CONSENSUS SEQUENCE
- HEME OXYGENASE-1
- UP-REGULATION
- GLUTATHIONE
- PATHWAY
- INDUCTION