Ruben K. Dagda Ph.D.
Contact Ruben K. Dagda Ph.D.
- Phone: (775) 784-4121
- Email: firstname.lastname@example.org
- Fax: (775) 784-1620
Manville Health Sciences
Manville Health Sciences
Reno, NV 89557
- B.S., 1998, University of Texas at El Paso, Microbiology
- Ph.D., 2006, University of Iowa, Pharmacology
Ruben Dagda, Ph.D. has published research manuscripts and review articles in the areas of toxicology, mitochondrial biology and neurobiology. As an Assistant Professor at the University of Nevada, Reno, he is currently interested in understanding how reversible phosphorylation at the mitochondria regulates mitochondrial function, mitochondrial turnover and development in neurons. The overall goal of his research is to develop future "mitoprotective" therapies that can reverse mitochondrial dysfunction and neurodegeneration associated with neurodegenerative diseases. In addition, he is interested in enhancing public awareness on the benefits of biomedical research in improving the quality of life, and understanding brain-related diseases. He has presented his research at national conferences and has received numerous awards for his contributions to Parkinson's disease research.
Regulation of mitochondrial biology and bioenergetics by serine/threonine kinases and phosphatases in neurons and in cardiac cells; new signaling pathways that promote synaptic connectivity; development of alternative therapies to reverse mitochondrial dysfunction in age-related brain diseases.
Persistent dephosphorylation mediated by mitochondrial localized protein phosphatase 2A accelerates neurodegeneration, fragments mitochondria and impairs mitochondrial function. On the other hand, mitochondrial serine/threonine kinases, PTEN induced kinase 1 (PINK1) and mitochondrial PKA confer neuroprotection and regulate overlapping mitochondrial functions including mitochondrial morphology and bioenergetics. Neurons rely on functionally efficient mitochondria to power critical neuronal functions. Given that impaired mitochondrial turnover and dysfunction underlie the etiology of many neurodegenerative diseases, understanding how reversible phosphorylation at the mitochondria regulates mitochondrial function and turnover will lay the basic groundwork for developing future "mitoprotective" therapies for reversing mitochondrial dysfunction and neurodegeneration. We have previously found that PINK1 and mitochondrial PKA converge at the outer mitochondrial membrane to regulate mitochondrial function and survival. We are examining how mitochondrial PKA and PINK1 interact at the mitochondria to modulate mitochondrial function, calcium signaling, and survival. A second area of interest employing proteomics and biochemical approaches in neurons is to determine how mitochondrial turnover (mitophagy) is regulated by mitochondrial PKA and phosphatases by reversibly phosphorylating specific components of the "mitophagosome" complex. A final goal of this project is to synthesize functionalized nanoreagents that can activate prosurvival signaling pathways at the mitochondria as an alternative therapy for reversing mitochondrial pathology induced by neurodegenerative diseases and by normal brain aging.
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