Hyperoxia-induced Apoptosis Does Not Require Mitochondrial Reactive Oxygen Species and Is Regulated by Bcl-2 Proteins

This publication has 39 references indexed in Scilit:

• Inhibition of early apoptotic events by Akt/PKB is dependent on the first committed step of glycolysis and mitochondrial hexokinase
  Genes & Development, 2001
• Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
  Science, 2001
• Endoplasmic reticulum localized Bcl-2 prevents apoptosis when redistribution of cytochrome c is a late event
  Oncogene, 2001
• Activated Akt Protects the Lung from Oxidant-Induced Injury and Delays Death of Mice
  Journal of Experimental Medicine, 2001
• Cells depleted of mitochondrial DNA (p⁰) yield insight into physiological mechanisms
  FEBS Letters, 1999
• Extracellular superoxide dismutase in the airways of transgenic mice reduces inflammation and attenuates lung toxicity following hyperoxia
  Journal of Clinical Investigation, 1999
• Mitochondria and Apoptosis
  Science, 1998
• Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt
  Science, 1997
• Hyperoxic sheep pulmonary microvascular endothelial cells generate free radicals via mitochondrial electron transport.
  Journal of Clinical Investigation, 1993
• Transgenic mice with expression of elevated levels of copper-zinc superoxide dismutase in the lungs are resistant to pulmonary oxygen toxicity.
  Journal of Clinical Investigation, 1991