{'fraction_non_alphanumeric': 0.013238289205702648, 'fraction_numerical': 0.009674134419551934, 'mean_word_length': 5.661016949152542, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Ubiquitin Specific Peptidase 3 (USP3) is Expressed in Skeletal Muscle and is Upregulated in Response to Neurogenic Atrophy

Skeletal muscle atrophy is a physiological condition that is caused by a variety of conditions, including immobilization, denervation, spinal cord injury and aging and results in decreased muscle size and strength. To better characterize the molecular genetic events of neurogenic atrophy, a previous study isolated gastrocnemius muscle from mice following 3 days and 14 days of denervation. The gene expression profile in the denervated muscle tissue was then analyzed by microarray and compared to control muscle tissue to identify novel neurogenic atrophy‐induced genes. The microarray data revealed for the first time that Ubiquitin Specific Peptidase 3 (USP3) is expressed in skeletal muscle and is significantly induced in response to denervation at 3 days post‐denervation but returns to baseline expression levels by 14 days post‐denervation. USP3 is a deubiquitinase that has been shown previously to stabilize p53 by deubiquitination. To confirm that USP3 is expressed in skeletal muscle, we cloned the USP3 cDNA from cultured muscle cells. In addition, quantitative PCR (qPCR) was performed to assess USP3 expression levels in both proliferating and differentiated muscle cells and the results demonstrate that USP3 expression levels are relatively equal in both proliferating myoblasts and in differentiated myotubes. Furthermore, Western blot analysis of protein lysates isolated from proliferating and differentiating muscle cells revealed that USP3 is expressed in proliferating myoblasts, but then decreases modestly as the cells differentiate in culture. The discovery that USP3 is induced in response to neurogenic atrophy helps further our understanding of the molecular genetic events of atrophy and may eventually lead to the identification of new therapeutic targets for the treatment and prevention of muscle wasting.