Peter Pediaditakis
University of North Carolina at Chapel Hill
20 Papers
47 Citations
Peter Pediaditakis is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Mitochondrion & Mitochondrial permeability transition pore. The author has an hindex of 9, co-authored 20 publications. Previous affiliations of Peter Pediaditakis include Medical University of South Carolina.
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Papers
Minocycline and N-methyl-4-isoleucine cyclosporin (NIM811) mitigate storage/reperfusion injury after rat liver transplantation through suppression of the mitochondrial permeability transition.
Tom P. Theruvath,Zhi Zhong,Peter Pediaditakis,Venkat K. Ramshesh,Robert T. Currin,Andrey P. Tikunov,Ekhson Holmuhamedov,John J. Lemasters +7 more
TL;DR: Minocycline and NIM811 attenuated graft injury after rat liver transplantation and improved graft survival and might be useful clinically in hepatic surgery and transplantation.
113
Inhibition of Mitochondrial Respiration as a Source of Adaphostin-Induced Reactive Oxygen Species and Cytotoxicity*
Son B. Le,M. Katie Hailer,Sarah A. Buhrow,Qi Wang,Karen S. Flatten,Peter Pediaditakis,Keith C. Bible,Lionel D. Lewis,Edward A. Sausville,Yuan Ping Pang,Matthew M. Ames,John J. Lemasters,Ekhson Holmuhamedov,Scott H. Kaufmann +13 more
TL;DR: In this paper, the authors investigated the source of reactive oxygen species (ROS) generated by adaphostin under aqueous conditions, and found that the highest concentration of adhostin was found in mitochondria.
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Inhibition of Mitochondrial Respiration as a Source of Adaphostin-induced Reactive Oxygen Species
M. Katie Hailer,Sarah A. Buhrow,Karen S. Flatten,Peter Pediaditakis,Keith C. Bible,Lionel D. Lewis,Edward A. Sausville,Yuan Ping Pang,Matthew M. Ames,John J. Lemasters,Ekhson Holmuhamedov,Scott H. Kaufmann +11 more
- 01 Jan 2007
TL;DR: Observations demonstrate that mitochondrial respiration rather than direct redox cycling of the hydroquinone moiety is a source of adaphostin-induced ROS and identify complex III as a potential target for antineoplastic agents.
38
Deleterious mutations in ALDH1L2 suggest a novel cause for neuro-ichthyotic syndrome.
Catherine Sarret,Zahra Ashkavand,Evan M Paules,Imen Dorboz,Peter Pediaditakis,Susan Sumner,Eleonore Eymard-Pierre,Christine Francannet,Natalia I. Krupenko,Odile Boespflug-Tanguy,Sergey A. Krupenko +10 more
TL;DR: Re-expression of functional ALDH1L2 enzyme in deficient cells restored the mitochondrial morphology and the metabolic profile of fibroblasts from healthy individuals and suggests the loss of the enzyme as the cause of neuro-cutaneous disease.
Cytosolic 10-formyltetrahydrofolate dehydrogenase regulates glycine metabolism in mouse liver.
Natalia I. Krupenko,Jaspreet Sharma,Peter Pediaditakis,Baharan Fekry,Baharan Fekry,Kristi L. Helke,Xiuxia Du,Susan Sumner,Sergey A. Krupenko +8 more
TL;DR: It is indicated that in the absence of ALDH1L1 enzyme, 10-formyl-THF cannot be efficiently metabolized in the liver, which leads to the decrease in THF causing reduced generation of glycine from serine and impaired histidine degradation, two pathways strictly dependent on THF.