|Balsa E, Marco R, Perales-Clemente E, Szklarczyk R, Calvo E, Landázuri MO, Enríquez JA. NDUFA4 Is a Subunit of Complex IV of the Mammalian Electron Transport Chain. Cell Metab (2012) 16:378-86|
|Diaz F, Enriquez JA, Moraes CT. Cells lacking Rieske Iron Sulfur Protein have a ROS-associated decrease in respiratory complexes I and IV. Mol Cell Biol (2012) 32:415-29|
|Moreno-Loshuertos R, Ferrín G, Acín-Pérez R, Gallardo ME, Viscomi C, Pérez-Martos A, Zeviani M, Fernández-Silva P, Enríquez JA. Evolution Meets Disease: Penetrance and Functional Epistasis of Mitochondrial tRNA Mutations. Plos Genet (2011) 7:e1001379|
|Bayona-Bafaluy MP, Sánchez-Cabo F, Fernández-Silva P, Pérez-Martos A, Enríquez JA. A genome-wide shRNA screen for new OxPhos related genes. Mitochondrion (2011) 11:467-75|
|Perales-Clemente E, Fernández-Silva P, Acín-Pérez R, Pérez-Martos A, Enríquez JA. Allotopic expression of mitochondrial-encoded genes in mammals: achieved goal, undemonstrated mechanism or impossible task?. Nucleic Acids Res (2011) 39:225-34|
|Fernandez-Vizarra E, Bayona-Bafaluy MP, Enriquez JA. Cardiopathies of mitochondrial origin. Nat Rev Cardiol (cnic Edition) (2010) 7:47-53|
|Leigh-Brown S, Enriquez JA, Odom DT. Nuclear transcription factors in mammalian mitochondria. Genome Biol (2010) 11:215|
|Perales-Clemente E, Fernández-Vizarra E, Acín-Pérez R, Movilla N, Bayona-Bafaluy MP, Moreno-Loshuertos R, Pérez-Martos A, Fernández-Silva P, Enríquez JA. Five Entry Points of the Mitochondrially Encoded Subunits in Mammalian Complex I Assembly. Mol Cell Biol (2010) 30:3038-47|
|Fernandez-Vizarra E, Ferrin G, Perez-Martos A, Fernandez-Silva P, Zeviani M, Enriquez JA. Isolation of mitochondria for biogenetical studies: An update. Mitochondrion (2010) 10:253-62|
|Perales-Clemente E, Bayona-Bafaluy MP, Pérez-Martos A, Barrientos A, Fernández-Silva P, Enriquez JA. Restoration of electron transport without proton pumping in mammalian mitochondria. Proc Natl Acad Sci U S A (2008) 105:18735-9|
José Antonio Enríquez graduated in Biochemistry and Molecular Biology at the Universidad Autónoma de Madrid and obtained his PhD from the Universidad de Zaragoza in 1992. His thesis examined various aspects of mitochondrial DNA biogenesis.
From 1993 to 1997 he worked with G. Attardi at the California Institute of Technology, where he studied the pathogenic action of mutant mitochondrial tRNAs. His work in this period contributed to define the molecular mechanism underlying this phenomenon, and helped to establish the general methodologies for studying mitochondrial tRNAs. These methodologies have found application in studies of mitochondrial biogenesis and in the analysis of mtDNA-linked diseases. José Antonio established his own laboratory on his return to the Universidad de Zaragoza, where he became a Full Professor in 2007. His group has made important contributions to the understanding of mitochondrial biogenesis and bioenergetics, the role of mitochondria in apoptosis, the structure, formation and regulation of the respiratory chain, and the pathological consequences of altered mitochondrial function in human disease. He recently established a possible explanation for the phenotypes associated with common mouse mtDNA variants affecting ROS production. He joined the CNIC in 2009, where his work focuses on the molecular processes underlying the involvement of mitochondrial dysfunction in cardiovascular disease and ischemic processes.