Peroxiredoxin Gene Expression Signatures in Liver Reflect Toxic Insult

Rachel Young, John D. Hayes, Ken Brown, C. Roland Wolf, C. Bruce A. Whitelaw

    Research output: Contribution to journalArticle

    5 Citations (Scopus)

    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 languageEnglish
    Pages (from-to)512-517
    Number of pages6
    JournalASSAY and Drug Development Technologies
    Volume8
    Issue number4
    DOIs
    Publication statusPublished - Aug 2010

    Keywords

    • GAMMA-GLUTAMYLCYSTEINE SYNTHETASE
    • PROSTATE CARCINOMA-CELLS
    • OXIDATIVE STRESS
    • RESPONSE ELEMENT
    • CONSENSUS SEQUENCE
    • HEME OXYGENASE-1
    • UP-REGULATION
    • GLUTATHIONE
    • PATHWAY
    • INDUCTION

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