Functional Redundancy of Type I and Type II Receptors in the Regulation Of
Functional redundancy of type I and type II receptors in INAUGURAL ARTICLE the regulation of skeletal muscle growth by myostatin and activin A Se-Jin Leea,b,1, Adam Lehara, Yewei Liua, Chi Hai Lyc,d, Quynh-Mai Phama, Michael Michauda, Renata Rydzike, Daniel W. Youngstrome, Michael M. Shenf, Vesa Kaartineng, Emily L. Germain-Leeh,i, and Thomas A. Randoc,d,j aThe Jackson Laboratory for Genomic Medicine, Farmington, CT 06032; bDepartment of Genetics and Genome Sciences, University of Connecticut School of Medicine, Farmington, CT 06030; cPaul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine, Stanford, CA 94305; dDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305; eDepartment of Orthopaedic Surgery, University of Connecticut School of Medicine, Farmington, CT 06030; fDepartment of Genetics and Development, Columbia University, New York, NY 10032; gDepartment of Biologic and Materials Sciences and Prosthodontics, University of Michigan School of Dentistry, Ann Arbor, MI 48109; hDepartment of Pediatrics, University of Connecticut School of Medicine, Farmington, CT 06030; iConnecticut Children’s Center for Rare Bone Disorders, Farmington, CT 06032; and jNeurology Service, VA Palo Alto Health Care System, Palo Alto, CA 94304 This contribution is part of the special series of Inaugural Articles by members of the National Academy of Sciences elected in 2012. Contributed by Se-Jin Lee, October 13, 2020 (sent for review September 14, 2020; reviewed by Chen-Ming Fan and S. Paul Oh) Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family atrophy following falls and hip fracture surgery, age-related member that normally acts to limit muscle growth.
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