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• W2097601801 abstract "Previous studies have demonstrated that copper up-regulates hypoxia-inducible factor 1 (HIF-1). The present study was undertaken to test the hypothesis that copper is required for HIF-1 activation. Treatment of HepG2 cells with a copper chelator tetraethylenepentamine (TEPA) or short interfering RNA targeting copper chaperone for superoxide dismutase 1 (CCS) suppressed hypoxia-induced activation of HIF-1. Addition of excess copper relieved the suppression by TEPA, but not that by CCS gene silencing, indicating the requirement of copper for activation of HIF-1, which is CCS-dependent. Copper deprivation did not affect production or stability of HIF-1α but reduced HIF-1α binding to the hypoxia-responsive element (HRE) of target genes and to p300, a component of HIF-1 transcriptional complex. Copper probably inhibits the factor inhibiting HIF-1 to ensure the formation of HIF-1 transcriptional complex. This study thus defines that copper is required for HIF-1 activation through the regulation of HIF-1α binding to the HRE and the formation of the HIF-1 transcriptional complex." @default.
• W2097601801 created "2016-06-24" @default.
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• W2097601801 date "2008-10-08" @default.
• W2097601801 modified "2023-10-03" @default.
• W2097601801 title "Copper Regulation of Hypoxia-Inducible Factor-1 Activity" @default.
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• W2097601801 doi "https://doi.org/10.1124/mol.108.051516" @default.
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