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Edward E. McKee

Researcher at Indiana University

Publications -  39
Citations -  1265

Edward E. McKee is an academic researcher from Indiana University. The author has contributed to research in topics: Mitochondrion & Thymidine. The author has an hindex of 17, co-authored 38 publications receiving 1198 citations. Previous affiliations of Edward E. McKee include Pennsylvania State University & Rosalind Franklin University of Medicine and Science.

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Inhibition of Mammalian Mitochondrial Protein Synthesis by Oxazolidinones

TL;DR: It is demonstrated that a general feature of the oxazolidinone class of antibiotics is the inhibition of mammalian mitochondrial protein synthesis, which was similar in mitochondria from all tissues studied.
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Measurement of the rate of protein synthesis and compartmentation of heart phenylalanine.

TL;DR: Neither the extracellular nor total intracellular pool of phenylalanine served as the sole precursor for protein synthesis, and two models of amino acid compartmentation involving aminoacylation of tRNA from both the extacellular and intrace cellular compartments were consistent with the steady state and transient data.
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Nonclinical and Pharmacokinetic Assessments To Evaluate the Potential of Tedizolid and Linezolid To Affect Mitochondrial Function

TL;DR: The overall results suggest that tedizolid has less potential to cause myelosuppression and neuropathy than that of linezolid during prolonged treatment courses and may therefore allow for mitochondrial recovery during antibacterial therapy.
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Mitochondrial gene expression in saccharomyces cerevisiae. I. Optimal conditions for protein synthesis in isolated mitochondria.

TL;DR: An in vitro mitochondrial protein-synthesizing system, which makes use of intact yeast mitochondria, has been developed in order to study mitochondrial gene expression and its control by nuclear-coded proteins and revealed that added adenine and guanine nucleotides increase the overall level of protein synthesis and that the added guanines facilitate polypeptide chain elongation.
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Phosphorylation of thymidine and AZT in heart mitochondria: elucidation of a novel mechanism of AZT cardiotoxicity.

TL;DR: AZT is a potent inhibitor of thymidine phosphorylation in heart mitochondria, having an inhibitory concentration (IC)50 of 7.0±0.9 μM, indicating that the toxicity of AZT in some tissues may be mediated by disrupting the substrate supply of TTP for mt-DNA replication.