Journal article
TMEPAI/PMEPA1 Is a Positive Regulator of Skeletal Muscle Mass
Adam Hagg, Swati Kharoud, Georgia Goodchild, Craig A Goodman, Justin L Chen, Rachel E Thomson, Hongwei Qian, Paul Gregorevic, Craig A Harrison, Kelly L Walton
Frontiers in Physiology | FRONTIERS MEDIA SA | Published : 2020
Abstract
Inhibition of myostatin- and activin-mediated SMAD2/3 signaling using ligand traps, such as soluble receptors, ligand-targeting propeptides and antibodies, or follistatin can increase skeletal muscle mass in healthy mice and ameliorate wasting in models of cancer cachexia and muscular dystrophy. However, clinical translation of these extracellular approaches targeting myostatin and activin has been hindered by the challenges of achieving efficacy without potential effects in other tissues. Toward the goal of developing tissue-specific myostatin/activin interventions, we explored the ability of transmembrane prostate androgen-induced (TMEPAI), an inhibitor of transforming growth factor-β (TGF..
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Awarded by National Health and Medical Research Council (NHMRC) Australia
Awarded by Cancer Council of Victoria
Funding Acknowledgements
Project Grant and Fellowship funding from the National Health and Medical Research Council (NHMRC) Australia (1078907, 1117835 and 1121500) and the Cancer Council of Victoria (1145001) awarded to PG and CH supported this work. An Early Career Seed Grant from the Victorian Cancer Agency supported KW. AH was supported by an Australian Post Graduate Award (Department of Education and Training, Australian Government) and a PhD stipend top-up award from the Baker Heart and Diabetes Institute Bright Sparks program. The Hudson Institute of Medical Research and The Baker Heart and Diabetes Institute are supported in part by the Operational Infrastructure Support Program of the Victorian Government.