Antioxid Redox Signal. 2010 Feb 16.
Santos R, Lefevre S, Sliwa D, Seguin A, Camadro JM, Lesuisse E.
Institut Jacques Monod, Mitochondria, Metals and Oxidative Stress Laboratory, Bât.Buffon, 15 rue Hélène Brion, Paris, France, 75013, +331 57 27 80 28, +331 57 27 81 01; santos.renata@ijm.univ-paris-diderot.fr.
Keywords: Mitochondrial dysfunction, oxidative damage, neurodegenerative diseases, Alzheimer's, Parkinson's, Friedreich's ataxia (FRDA), GAA trinucleotide repeat expansion, FXN, frataxin, respiration, iron-sulfur cluster assembly, iron homeostasis, maintenance of the redox status, therapeutic approaches.
Wednesday, February 17, 2010
Posttranslational stability of the heme biosynthetic enzyme ferrochelatase is dependent on iron availability and intact iron-sulfur cluster assembly machinery
Blood, 28 January 2010, Vol. 115, No. 4, pp. 860-869.
Daniel R. Crooks1,2, Manik C. Ghosh2, Ronald G. Haller3, Wing-Hang Tong2, and Tracey A. Rouault2
1 Department of Biochemistry, Molecular and Cellular Biology, Georgetown University Medical Center, Washington, DC; 2 Molecular Medicine Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD; and 3 Department of Neurology, University of Texas Southwestern Medical Center and Veterans Administration North Texas Medical Center, and Neuromuscular Center, Institute for Exercise and Environmental Medicine, Dallas
Keywords: ferrochelatase, iron-sulfur [2Fe-2S] cluster, posttranscriptional regulation of ferrochelatase, in vivo. We propose that decreased heme biosynthesis resulting from impaired Fe-S cluster assembly can contribute to the pathogenesis of diseases caused by defective Fe-S cluster biogenesis.
Daniel R. Crooks1,2, Manik C. Ghosh2, Ronald G. Haller3, Wing-Hang Tong2, and Tracey A. Rouault2
1 Department of Biochemistry, Molecular and Cellular Biology, Georgetown University Medical Center, Washington, DC; 2 Molecular Medicine Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD; and 3 Department of Neurology, University of Texas Southwestern Medical Center and Veterans Administration North Texas Medical Center, and Neuromuscular Center, Institute for Exercise and Environmental Medicine, Dallas
Keywords: ferrochelatase, iron-sulfur [2Fe-2S] cluster, posttranscriptional regulation of ferrochelatase, in vivo. We propose that decreased heme biosynthesis resulting from impaired Fe-S cluster assembly can contribute to the pathogenesis of diseases caused by defective Fe-S cluster biogenesis.
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