My research interests are concerned with the molecular, cellular, and genetics mechanisms of skeletal muscle atrophy. Muscle loss or atrophy occurs as the result of a number of different conditions including disuse, cachexia, inflammation, exposure to corticosteroids and aging. A number of studies aimed at identifying differentially expressed genes in atrophy and aging models have found a number of interesting genes, including the E3 Ubiquitin Ligase, MuRF1, which is expressed predominantly in skeletal muscle and is up-regulated in virtually all atrophy models. In addition to MuRF1, hundreds of other genes have been found to be significantly up-regulated under neurogenic skeletal muscle atrophy. Furthermore, a targeted disruption of the MuRF1 gene in mice leads to a resistance in muscle wasting under atrophic conditions and a subset of genes are differentially regulated in MuRF1-null mice. These observations, among others, have led us to the hypothesize that these genes may play a pivotal role in regulating the atrophy cascade by modulating skeletal muscle structure, metablism and cell signaling cascades. With this hypothesis in mind, my research is focused on understanding the “atrophy signature” of skeletal muscle and how this complex process is regulated at the molecular, cellular, and genetic levels. Several projects will be undertaken in the lab, including: 1) identifying and analyzing genes that are differentially expressed in response to disparate atrophy-promoting stimuli , 2) determining how these differently expressed genes may be regulated, and 3) studying the functional role that differentially expressed genes may play in regulating and/or promoting muscle wasting.