A College of North Florida biology professor has been awarded a prestigious four-year Nationwide Institutes of Well being (NIH) grant totaling over $720K to review the useful function of an enzyme referred to as dual-specificity phosphatase 4 (Dusp4) in skeletal muscle atrophy. 

Dr. David Waddell’s NIH-funded analysis undertaking will assist contribute to data about skeletal muscle atrophy related to neuromuscular issues, neurodegenerative ailments and ageing. Skeletal muscle atrophy is a lower in muscle mass that happens when protein degradation exceeds protein synthesis. This examine will purpose to characterize the function of Dusp4 in modulating the molecular mechanisms that regulate muscle dimension and power and decide how Dusp4 might contribute to adjustments in muscle mass. 

The undertaking’s profitable completion will exhibit for the primary time that Dusp4 acts as a regulator of skeletal muscle mass by way of modulation of the mitogen activated protein (MAP) kinase signaling pathway. If the findings of this investigation exhibit that Dusp4 participates within the neurogenic atrophy cascade by performing as a direct or oblique modulator of muscle losing, then inhibition of this dual-specificity phosphatase might show useful within the remedy of sure varieties of skeletal muscle atrophy. 

Waddell is an professional within the molecular, mobile and genetic mechanisms of skeletal muscle atrophy. He has authored quite a few peer-reviewed papers, offered at worldwide analysis conferences and contributed to plenty of grant-funded analysis research about skeletal muscle losing. 

Waddell obtained his Ph.D. in molecular most cancers biology from Duke College after which modified analysis focus throughout his post-doctoral coaching to review the molecular underpinnings of skeletal muscle atrophy on the College of California, Davis. His curiosity in skeletal muscle and the mechanisms by which muscle responds to physiological stimuli has continued at UNF the place he has recognized and characterised over a dozen novel genes which might be differentially expressed in response to neurogenic atrophy, together with Dusp4.