| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2048188 | FEBS Letters | 2010 | 8 Pages |
Oxidative stress induces apoptosis or necrosis of many cell types, which can cause tissue injury. Hydrogen peroxide (H2O2) induced apoptotic death of Jurkat cells. This effect was inhibited by overexpression of human Bcl-2, by silencing of cytochrome c, and by ablation of Bax/Bak, indicating that H2O2-induced apoptosis was mediated by the mitochondrial pathway in Jurkat cells. Treatment with H2O2 caused an increase of Noxa protein, via activating transcription factor 4-dependent accumulation of Noxa mRNA and inhibition of Noxa protein degradation. H2O2-induced apoptosis was strongly suppressed by silencing of Noxa, indicating that Noxa plays a crucial role in this form of apoptosis.Structured summaryMINT-7543162: Mcl-1 (uniprotkb:Q07820) physically interacts (MI:0914) with Bim EL (uniprotkb:O43521), Bim L (uniprotkb:O43521) and NOXA (uniprotkb:Q13794) by anti bait coimmunoprecipitation (MI:0006)
