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Here, we show that mice genetically engineered to lack GASP-1 and\/or GASP-2 exhibit muscle and skeletal phenotypes consistent with overactivity of myostatin and\/or GDF-11. These studies also reveal the enormous complexity of this regulatory system in vivo and the delicate balance that must be maintained between signaling molecules and their inhibitory proteins for proper levels of signaling to be achieved.<\/jats:p>","DOI":"10.1073\/pnas.1309907110","type":"journal-article","created":{"date-parts":[[2013,9,9]],"date-time":"2013-09-09T22:31:16Z","timestamp":1378765876000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":91,"title":["Regulation of GDF-11 and myostatin activity by GASP-1 and GASP-2"],"prefix":"10.1073","volume":"110","author":[{"given":"Yun-Sil","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Se-Jin","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and 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