ProfessorOffice: G651Lab: G655Office: (601) 815-6831Email
The overall goal of our research proposal is to elucidate the molecular mechanism by which the pro-malignant transcription factor Twist1 contributes to muscle cachexia. We intend to apply both genetic and pharmacological approaches to obtain compelling evidence that Twist1 mediates cancer-driven muscle cachexia through its ability to integrate Activin/Myostatin signaling. Activin and Myostatin are two members of the transforming growth factor beta (TGF-) superfamily that exert their biological functions in skeletal muscle through activation of Smad transcription factors.
Since my research efforts were entirely devoted to investigating the roles of TGF-/Smad signaling in normal cell function and diseases over the past 20 years, I believe I hold the necessary skills to lead this research project. From 2008-11, I received extensive training at Harvard Medical School on genetic-modified mouse models of cancer and muscle cachexia.
Since I joined the University of Mississippi Medical Center in 2011, I serve as the director of the Tumor Cell Biology Program that comprises 12 independent investigators working on many aspects of cancer, which provides me with a unique opportunity to broaden my knowledge on the molecular etiology and fundamentals of cancer pathogenesis and muscle cachexia. As such, my expertise will be instrumental to the successful completion of our proposed experimental approaches, including muscle histology, imaging cancer growth in live mice, analyzing muscle cell proliferation and differentiation in vitro and in vivo, assessing protein-protein and protein-DNA interactions, and evaluating transcriptional processes by a multitude of molecular biology and biochemistry approaches.
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