Reactive Oxygen Species Are Required for Hyperoxia-induced Bax Activation and Cell Death in Alveolar Epithelial Cells
Open Access
- 1 February 2004
- journal article
- Published by Elsevier BV
- Vol. 279 (8), 6753-6760
- https://doi.org/10.1074/jbc.m310145200
Abstract
No abstract availableThis publication has 38 references indexed in Scilit:
- JNK-Mediated BIM Phosphorylation Potentiates BAX-Dependent ApoptosisNeuron, 2003
- Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosisThe Journal of cell biology, 2002
- Hyperoxia-induced Apoptosis Does Not Require Mitochondrial Reactive Oxygen Species and Is Regulated by Bcl-2 ProteinsPublished by Elsevier BV ,2002
- Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteinsCell Death & Differentiation, 2002
- Doxorubicin-induced Apoptosis Is Associated with Increased Transcription of Endothelial Nitric-oxide SynthasePublished by Elsevier BV ,2001
- Extracellular superoxide dismutase in the airways of transgenic mice reduces inflammation and attenuates lung toxicity following hyperoxiaJCI Insight, 1999
- Superoxide in ApoptosisPublished by Elsevier BV ,1998
- Hyperoxic sheep pulmonary microvascular endothelial cells generate free radicals via mitochondrial electron transport.JCI Insight, 1993
- Transgenic mice with expression of elevated levels of copper-zinc superoxide dismutase in the lungs are resistant to pulmonary oxygen toxicity.JCI Insight, 1991
- A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye bindingAnalytical Biochemistry, 1976