Reduction of Caenorhabditis elegans frataxin increases sensitivity to oxidative stress, reduces lifespan, and causes lethality in a mitochondrial complex II mutant Rafael P. Vázquez-Manrique * ,† , Pilar González-Cabo * , Sheila Ros * , Homera Aziz † , Howard A. Baylis † and Francesc Palau * ,1 * Laboratory of Genetics and Molecular Medicine, Department of Genomics and Proteomics, Instituto de Biomedicina, CSIC, Valencia, Spain; and † Department of Zoology, University of Cambridge, Cambridge, UK 1 Correspondence: Department of Genomics and Proteomics, Instituto de Biomedicina, CSIC, C/ Jaume Roig, 11, Valencia 46010, Spain. E-mail: fpalau@ibv.csic.es <h3>SPECIFIC AIMS</h3> Work on model systems has proven to be essential to understanding frataxin function and therefore the pathogenic basis of Friedreich ataxia (FRDA). The aim of this work was to determine the results of reproducing the diminution of frataxin function observed in FRDA patients in the nematode Caenorhabditis elegans . This is the first step in establishing a new animal model for the study of frataxin function, which also has great potential for testing drugs to treat Friedreich ataxia. <h3>PRINCIPAL FINDINGS</h3> 1. Identification and characterization of frh-1<h3>, the C. elegans FRDA ortholog</h3> We identified the C. elegans homologue of the human
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Reduction of Caenorhabditis elegans frataxin increases sensitivity to oxidative stress, reduces lifespan, and causes lethality in a mitochondrial complex II mutant
Vázquez-Manrique, Rafael P.; González-Cabo, Pilar; Ros, Sheila; Aziz, Homera; Baylis, Howard A.; Palau, Francesc
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, Volume 20 (1): 172
Fed of American Socs for Experimental Biology – Jan 1, 2006
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