O
Oleh Khalimonchuk
Researcher at University of Nebraska–Lincoln
Publications - 85
Citations - 4380
Oleh Khalimonchuk is an academic researcher from University of Nebraska–Lincoln. The author has contributed to research in topics: Mitochondrion & Cytochrome c oxidase. The author has an hindex of 31, co-authored 74 publications receiving 3709 citations. Previous affiliations of Oleh Khalimonchuk include Dresden University of Technology & University of Nebraska Medical Center.
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Journal ArticleDOI
SDH5, a Gene Required for Flavination of Succinate Dehydrogenase, Is Mutated in Paraganglioma
Huai Xiang Hao,Oleh Khalimonchuk,Margit Schraders,Noah Dephoure,Jean-Pierre Bayley,Henricus P. M. Kunst,Peter Devilee,Cor W. R. J. Cremers,Joshua D. Schiffman,Brandon G. Bentz,Steven P. Gygi,Dennis R. Winge,Hannie Kremer,Jared Rutter +13 more
TL;DR: A combination of bioinformatics, yeast genetics, biochemistry, and human genetics was used to show that a previously uncharacterized mitochondrial protein (Sdh5) is required for the activity of respiratory complex II, leading to the discovery of a human tumor susceptibility gene.
Journal ArticleDOI
Oxidative Stress, Redox Signaling, and Autophagy: Cell Death Versus Survival
Juliana Navarro-Yepes,Juliana Navarro-Yepes,Michaela Burns,Annadurai Anandhan,Oleh Khalimonchuk,Luz M. Del Razo,Betzabet Quintanilla-Vega,Aglaia Pappa,Mihalis I. Panayiotidis,Rodrigo Franco +9 more
TL;DR: This review will focus on the molecular mechanism by which ROS/RNS generation, redox signaling, and/or oxidative stress/damage alter autophagic flux rates, and the role of autophagy as a cell death process or survival mechanism in response to oxidative stress.
Contribution Of Impaired Myocardial InsulinSignaling To Mitochondrial Dysfunction AndOxidative Stress In The Heart
Sihem Boudina,Heiko Bugger,Sandra Sena,Brian T. O'Neill,Vlad G. Zaha,Olesya Ilkun,Jordan J. Wright,Pradip K. Mazumber,Eric Palfreyman,Timothy Tidwell,Heather A. Theobald,Oleh Khalimonchuk,Benjamin Wayment,Xiaoming Sheng,Kenneth J. Rodnick,Ryan Centini,Dong Chen,Sheldon E. Litwin,Bart E. Weimer,E. Dale Abel +19 more
TL;DR: The hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondrial function is tested and defects in fatty acid and pyruvate metabolism and tricarboxylic acid flux may explain the mitochondrial dysfunction observed.
Journal ArticleDOI
Contribution of Impaired Myocardial Insulin Signaling to Mitochondrial Dysfunction and Oxidative Stress in the Heart
Sihem Boudina,Heiko Bugger,Sandra Sena,Brian T. O’Neill,Vlad G. Zaha,Olesya Ilkun,Jordan J. Wright,Pradip K. Mazumder,Eric Palfreyman,Timothy Tidwell,Heather A. Theobald,Oleh Khalimonchuk,Benjamin Wayment,Xiaoming Sheng,Kenneth J. Rodnick,Ryan Centini,Dong Chen,Sheldon E. Litwin,Bart E. Weimer,E. Dale Abel +19 more
TL;DR: In this paper, the authors tested the hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondria function and found that the contribution of altered myocardial insulin action independent of associated changes in systemic metabolism is incompletely understood.
Journal ArticleDOI
Proteomic remodelling of mitochondrial oxidative pathways in pressure overload-induced heart failure
Heiko Bugger,Michael Schwarzer,Dong Chen,Andrea Schrepper,Paulo A. Amorim,Maria Schoepe,T. Dung Nguyen,Friedrich W. Mohr,Oleh Khalimonchuk,Bart C. Weimer,Bart C. Weimer,Torsten Doenst +11 more
TL;DR: Pressure overload-induced heart failure is characterized by a substantial defect in cardiac oxidative capacity, at least in part due to a mitochondrial defect downstream of substrate-specific pathways, as reported in Sprague-Dawley rats.