Experts and Doctors on electron transport complex iv in Dallas, Texas, United States

Summary

Locale: Dallas, Texas, United States
Topic: electron transport complex iv

Top Publications

  1. Anziano P, Butow R. Splicing-defective mutants of the yeast mitochondrial COXI gene can be corrected by transformation with a hybrid maturase gene. Proc Natl Acad Sci U S A. 1991;88:5592-6 pubmed
    ..These studies show the utility of the pMIT transformation system for the expression and reverse genetic analysis of yeast mitochondrial genes. ..
  2. Wan B, Moreadith R. Structural characterization and regulatory element analysis of the heart isoform of cytochrome c oxidase VIa. J Biol Chem. 1995;270:26433-40 pubmed
  3. Hansen J, Thomas G, Harris S, Parsons W, Victor R. Differential sympathetic neural control of oxygenation in resting and exercising human skeletal muscle. J Clin Invest. 1996;98:584-96 pubmed
    ..These events are different from those involved in either metaboreceptor muscle afferent activation or reactive hyperemia...
  4. Iacovino M, Granycome C, Sembongi H, Bokori Brown M, Butow R, Holt I, et al. The conserved translocase Tim17 prevents mitochondrial DNA loss. Hum Mol Genet. 2009;18:65-74 pubmed publisher
    ..Tim17 is a conserved suppressor of mtDNA instability and is the first factor to be identified that can prevent mtDNA loss in a human cellular model of mitochondrial disease. ..
  5. Rahman M, Kylsten P. Rhomboid-7 over-expression results in Opa1-like processing and malfunctioning mitochondria. Biochem Biophys Res Commun. 2011;414:315-20 pubmed publisher
    ..Our results suggest that rho-7 and Opa1-like function in a common molecular pathway affecting mitochondrial function and apoptosis in Drosophila melanogaster. ..
  6. Williams J, Trias E, Beilby P, Lopez N, Labut E, Bradford C, et al. Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SOD(G93A) mice co-expressing the Copper-Chaperone-for-SOD. Neurobiol Dis. 2016;89:1-9 pubmed publisher
    ..All ALS patients also express human CCS, raising the hope that familial SOD ALS patients could respond to CuATSM treatment similarly to the CCSxSOD mice. ..
  7. Henke R, Butow R, Perlman P. Maturase and endonuclease functions depend on separate conserved domains of the bifunctional protein encoded by the group I intron aI4 alpha of yeast mitochondrial DNA. EMBO J. 1995;14:5094-9 pubmed
    ..This study indicates that the two functions depend on separate domains of the intron-encoded protein. ..
  8. Radford N, Wan B, Richman A, Szczepaniak L, Li J, Li K, et al. Cardiac dysfunction in mice lacking cytochrome-c oxidase subunit VIaH. Am J Physiol Heart Circ Physiol. 2002;282:H726-33 pubmed
    ..These findings suggest that a genetic deficiency of COXVIaH has a measurable impact on myocardial diastolic performance despite the presence of normal cellular ATP levels. ..
  9. Scortegagna M, Ding K, Oktay Y, Gaur A, Thurmond F, Yan L, et al. Multiple organ pathology, metabolic abnormalities and impaired homeostasis of reactive oxygen species in Epas1-/- mice. Nat Genet. 2003;35:331-40 pubmed
    ..We propose a rheostat role for HIF-2alpha that allows for the maintenance of ROS as well as mitochondrial homeostasis. ..

More Information

Publications11

  1. Son M, Fu Q, Puttaparthi K, Matthews C, Elliott J. Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo. Neurobiol Dis. 2009;34:155-62 pubmed
    ..The effects of CCS on disease are SOD1 mutation dependent and correlate with SOD1 redox susceptibility. ..
  2. Klichko V, Sohal B, Radyuk S, Orr W, Sohal R. Decrease in cytochrome c oxidase reserve capacity diminishes robustness of Drosophila melanogaster and shortens lifespan. Biochem J. 2014;459:127-35 pubmed publisher
    ..Our results demonstrate that: (i) the suppression of CcO function exerts deleterious rather than benign effects on fitness and survival, and (ii) the structure/function of CcO, an ETC oxidoreductase, can be 're-engineered' in vivo. ..