Protection from oxidative stress-induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia-inducible factor-1 and ATF-1/CREB and increased expression of glycolytic enzymes, p21(waf1/cip1), and erythropoietin.

@article{Zaman1999ProtectionFO,
  title={Protection from oxidative stress-induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia-inducible factor-1 and ATF-1/CREB and increased expression of glycolytic enzymes, p21(waf1/cip1), and erythropoietin.},
  author={Khalequz Zaman and Hoon Ryu and David. Hall and K. J. O'Donovan and Kuo I Lin and Michael A. Miller and John C. Marquis and Jay M Baraban and Gregg L Semenza and Rajiv R Ratan},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={1999},
  volume={19 22},
  pages={9821-30}
}
Iron chelators are pluripotent neuronal antiapoptotic agents that have been shown to enhance metabolic recovery in cerebral ischemia models. The precise mechanism(s) by which these agents exert their effects remains unclear. Recent studies have demonstrated that iron chelators activate a hypoxia signal transduction pathway in non-neuronal cells that culminates in the stabilization of the transcriptional activator hypoxia-inducible factor-1 (HIF-1) and increased expression of gene products that… CONTINUE READING
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cell line involves inhibition of cystine transport leading to oxidative stress

  • TH Murphy, RL Schnaar, JT Coyle
  • 1990
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