The San Diego Skeletal Muscle Research Center (SDMRC) is composed of 21 scientists who span five research institutions and nine academic Departments. The mission of the SDMRC is twofold: (1) to provide investigators with an effective infrastructure and environment to accelerate their cutting-edge research in an efficient and cost-effective manner, and (2) to provide an organizational structure that enhances communication amongst members and provides education and training for the San Diego community. The creation of this Center will integrate, educate and synergize laboratories on a more formalized basis than currently exists. Specifically, this Center will provide a mechanism for rapidly performing common assays needed by all investigators with minimal overhead in terms of time and money by creating three Cores: Phenotyping, Imaging, and High Throughput Cell Analysis. This will automatically enhance each of the individual programs since state-of-the-art methods will instantly become available to members. Access to new methods will undoubtedly spawn new ideas that accompany the experimental data. SDMRC will increase efficiency (since a mechanism is in place to collaborate and share information) and productivity (since studies will be routinely multidisciplinary) that will enable individuals to have a larger impact in their individual research programs than would be possible in isolation.

Public Health Relevance

Skeletal muscle research is necessarily translational since muscle diseases compromise quality of life, mobility, and overall health. Numerous diseases can be primarily or secondarily attributable to muscle problems which include primary myopathies such as the muscular dystrophies and also the secondary effects of muscle disease that lead to fragility, osteoporosis, obesity, diabetes and aging. The routine direct access to human muscle tissue in the operating room and in the clinic instantly provides extremely valuable tissue to all Center investigators using animal models of disease and this will insure that the work in this Core maintains clinical relevance since the results from model systems can be calibrated against the actual disease itself.

National Institute of Health (NIH)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Center Core Grants (P30)
Project #
Application #
Study Section
Special Emphasis Panel (ZAR1)
Program Officer
Boyce, Amanda T
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of California San Diego
Schools of Medicine
La Jolla
United States
Zip Code
Gokhin, David S; Fowler, Velia M (2017) Software-based measurement of thin filament lengths: an open-source GUI for Distributed Deconvolution analysis of fluorescence images. J Microsc 265:11-20
Kinney, Matthew C; Dayanidhi, Sudarshan; Dykstra, Peter B et al. (2017) Reduced skeletal muscle satellite cell number alters muscle morphology after chronic stretch but allows limited serial sarcomere addition. Muscle Nerve 55:384-392
Jordan, Sabine D; Kriebs, Anna; Vaughan, Megan et al. (2017) CRY1/2 Selectively Repress PPAR? and Limit Exercise Capacity. Cell Metab 26:243-255.e6
Wu, Tongbin; Mu, Yongxin; Bogomolovas, Julius et al. (2017) HSPB7 is indispensable for heart development by modulating actin filament assembly. Proc Natl Acad Sci U S A 114:11956-11961
Latella, Lucia; Dall'Agnese, Alessandra; Boscolo, Francesca Sesillo et al. (2017) DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation. Genes Dev 31:648-659
Consalvi, Silvia; Brancaccio, Arianna; Dall'Agnese, Alessandra et al. (2017) Praja1 E3 ubiquitin ligase promotes skeletal myogenesis through degradation of EZH2 upon p38? activation. Nat Commun 8:13956
Zogby, Andrew M; Dayanidhi, Sudarshan; Chambers, Henry G et al. (2017) Skeletal muscle fiber-type specific succinate dehydrogenase activity in cerebral palsy. Muscle Nerve 55:122-124
McKeithan, Wesley L; Savchenko, Alex; Yu, Michael S et al. (2017) An Automated Platform for Assessment of Congenital and Drug-Induced Arrhythmia with hiPSC-Derived Cardiomyocytes. Front Physiol 8:766
Pérez-Schindler, Joaquín; Esparza, Mary C; McKendry, James et al. (2017) Overload-mediated skeletal muscle hypertrophy is not impaired by loss of myofiber STAT3. Am J Physiol Cell Physiol 313:C257-C261
Gibbons, Michael C; Singh, Anshuman; Engler, Adam J et al. (2017) The role of mechanobiology in progression of rotator cuff muscle atrophy and degeneration. J Orthop Res :

Showing the most recent 10 out of 80 publications