A University of North Florida biology professor has been awarded a prestigious four-year National Institutes of Health (NIH) grant totaling over $720K to study the functional role of an enzyme called dual-specificity phosphatase 4 (Dusp4) in skeletal muscle atrophy.
Dr. David Waddell's NIH-funded research project will help contribute to knowledge about skeletal muscle atrophy associated with neuromuscular disorders, neurodegenerative diseases and aging. Skeletal muscle atrophy is a decrease in muscle mass that occurs when protein degradation exceeds protein synthesis. This study will aim to characterize the role of Dusp4 in modulating the molecular mechanisms that regulate muscle size and strength and determine how Dusp4 may contribute to changes in muscle mass.
The project's successful completion will demonstrate for the first time that Dusp4 acts as a regulator of skeletal muscle mass through modulation of the mitogen activated protein (MAP) kinase signaling pathway. If the findings of this investigation demonstrate that Dusp4 participates in the neurogenic atrophy cascade by acting as a direct or indirect modulator of muscle wasting, then inhibition of this dual-specificity phosphatase could prove beneficial in the treatment of certain types of skeletal muscle atrophy.
Waddell is an expert in the molecular, cellular and genetic mechanisms of skeletal muscle atrophy. He has authored numerous peer-reviewed papers, presented at international research conferences and contributed to a number of grant-funded research studies about skeletal muscle wasting.
Waddell received his Ph.D. in molecular cancer biology from Duke University and then changed research focus during his post-doctoral training to study the molecular underpinnings of skeletal muscle atrophy at the University of California, Davis. His interest in skeletal muscle and the mechanisms by which muscle responds to physiological stimuli has continued at UNF where he has identified and characterized over a dozen novel genes that are differentially expressed in response to neurogenic atrophy, including Dusp4.
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