Founded in 2002 as an interdisciplinary partnership between researchers at the University of Nebraska-Lincoln (UNL) and the University of Nebraska Medical Center (UNMC), the Redox Biology Center (RBC) has grown into a nationally visible and internationally recognized program of excellence addressing fundamental questions crucial to fighting disease and improving human health. During Phases I and II, the RBC achieved its primary objective of enhancing Nebraska's biomedical research capacity through the creation of 1) a strategically linked infrastructure of strong research programs, 2) a program for mentoring talented junior faculty to independent success, 3) support for core research facilities in metabolomics/proteomics and spectroscopy/bioimaging, and 4) innovative educational activities. As a result, the RBC has developed a cadre of well-funded and productive faculty members conducting research leading to new insights in redox biology that have important implications in neurodegenerative diseases, cardiovascular health, cataracts, and cancer. Reaching the end of Phase II funding positions the RBC to move decisively toward its long-term vision of becoming a self-sustaining center of research excellence charged with providing international leadership and outstanding research resources benefiting other IDeA programs and the scientific community at large. Phase III funding will allow the RBC to attain this overarching goal by providing funds necessary to support meritorious multi-institutional research pilot projects that build the interdisciplinary collaborations necessary to maintain a strong center and compete for program project type funding while maintaining and expanding the RBC's research core facilities and promoting education and outreach. These three components - research pilot project program, core facilities (including a strong administrative core), and strong education/outreach programs, will allow the RBC to accomplish the specific aims set forth in this Phase III application: 1) Increase research capabilities, innovation, and extramural funding;2) Strengthen research training and education in redox biology;and 3) Graduate from IDeA program funding as a self-sustainable center of research excellence in redox biology.
The Redox Biology Center is driving research discoveries that are improving human health and leading to a better understanding of disease mechanisms. Continuing to strengthen the Center's research programs and infrastructure will enable investigators to elucidate complex redox mechanisms relevant to numerous diseases ranging from neurodegeneration to cancer with the aim of finding new therapeutic strategies.
|Luo, Min; Gamage, Thameesha T; Arentson, Benjamin W et al. (2016) Structures of Proline Utilization A (PutA) Reveal the Fold and Functions of the Aldehyde Dehydrogenase Superfamily Domain of Unknown Function. J Biol Chem 291:24065-24075|
|Ahmad, Iman M; Temme, James B; Abdalla, Maher Y et al. (2016) Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study. Redox Rep 21:139-45|
|Smith, Nathan; Wei, Wenzhong; Zhao, Miaoyun et al. (2016) Cadmium and Secondary Structure-dependent Function of a Degron in the Pca1p Cadmium Exporter. J Biol Chem 291:12420-31|
|Levytskyy, Roman M; Germany, Edward M; Khalimonchuk, Oleh (2016) Mitochondrial Quality Control Proteases in Neuronal Welfare. J Neuroimmune Pharmacol 11:629-644|
|Swenson, Samantha; Cannon, Andrew; Harris, Nicholas J et al. (2016) Analysis of Oligomerization Properties of Heme a Synthase Provides Insights into Its Function in Eukaryotes. J Biol Chem 291:10411-25|
|Bohovych, Iryna; Kastora, Stavroula; Christianson, Sara et al. (2016) Oma1 Links Mitochondrial Protein Quality Control and TOR Signaling To Modulate Physiological Plasticity and Cellular Stress Responses. Mol Cell Biol 36:2300-12|
|Navarro-Yepes, Juliana; Anandhan, Annadurai; Bradley, Erin et al. (2016) Inhibition of Protein Ubiquitination by Paraquat and 1-Methyl-4-Phenylpyridinium Impairs Ubiquitin-Dependent Protein Degradation Pathways. Mol Neurobiol 53:5229-51|
|Smith, Nathan; Adle, David J; Zhao, Miaoyun et al. (2016) Endoplasmic Reticulum-associated Degradation of Pca1p, a Polytopic Protein, via Interaction with the Proteasome at the Membrane. J Biol Chem 291:15082-92|
|Worley, Bradley; Powers, Robert (2016) PCA as a practical indicator of OPLS-DA model reliability. Curr Metabolomics 4:97-103|
|Jouett, Noah P; Moralez, Gilbert; White, Daniel W et al. (2016) N-Acetylcysteine reduces hyperacute intermittent hypoxia-induced sympathoexcitation in human subjects. Exp Physiol 101:387-96|
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