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Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science

Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science Se-Jin Lee was elected member to the National Academy of Sciences on 28 April 2012. Dr Lee is responsible for the discovery of myostatin, a critical regulator of skeletal muscle mass and function. He also determined the primary binding receptor for myostatin, and has characterized additional transforming growth factor–β family members acting in this pathway. Keywords: National Academy of Sciences, Skeletal muscle development, Myostatin Commentary have naturally occurring disruptions of the myostatin Professor Se-Jin Lee was elected on 28 April to the Uni- locus [3]. ted States National Academy of Sciences for his research Dr Lee went on to extensively study myostatin, and in achievements, most notably the discovery of myostatin subsequent papers demonstrated the loss of white fat and its role in skeletal muscle maintenance. that occurs upon induction of hypermuscularity by Dr Lee is a Professor of Molecular Biology and Genet- myostatin inhibition [4], and that administration of ics at Johns Hopkins University. He holds an MD and myostatin was sufficient to cause a phenotype reminis- PhD, and he joined Hopkins after a period as an associ- cent of cachexia [5]. He next showed that myostatin was ate at the Carnegie Institution for Science. regulated by a metalloprotease that activates it from a la- His first major paper in the area that led him on his tent state [6], and identified the activin receptor type IIb most fruitful research path was published in Nature in receptor as one of the key receptors for myostatin [7]. 1994 [1]. In that study, Professor Lee reported on the This last paper highlighted an ongoing trend of first-au- discovery of several transforming growth facto (TGF)-β thor manuscripts for Dr Lee, a testament to his contin- family members: growth differentiation factor (GDF)5, 6 ued commitment to working at the bench. and 7. Next, in 1997, Professor Lee and his co-authors Finally, Dr Lee has shown that other molecules in the Alexandra McPherron and Ann Lawler described the TGF-β pathway, notably the activins and follistatin, also identification of myostatin, also known as GDF8, via RT- regulate muscle mass [8,9]. PCR, using degenerate primers from TGF-β family Dr Lee’s contributions include the demonstration of member homology domains [2]. In that same manu- potential therapeutic benefits for myostatin inhibition. script, they described the myostatin mouse knockout, The precise clinical setting in which myostatin blockade and the dramatic skeletal muscle hypertrophy caused by might be beneficial has not yet been finally determined deletion of myostatin, a phenotype that still manages to in humans, but it is at least clear that human null muta- startle. A two- to three-fold increase in muscle mass was tions for myostatin have a similar phenotype of hyper- observed in the GDF8 null muscle [2]. Later that year, muscularity [10]. One potential area for blockade of this McPherron and Lee also reported that Piedmontese and family of factors is cancer cachexia, as was demonstrated Belgian Blue cattle, notable for their hypermuscularity, with an activin receptor IIb trap [11]. Dr Lee’s election to the Academy represents great rec- ognition both for him and for the skeletal muscle field as a whole. His career is a testament to continued close * Correspondence: david.glass@novartis.com study of a mechanism, leading to the initiation of an en- Novartis Institutes for Biomedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA tirely new field of basic and biomedical research. Full list of author information is available at the end of the article © 2012 Glass and Spiegelman; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Glass and Spiegelman Skeletal Muscle 2012, 2:11 Page 2 of 2 http://www.skeletalmusclejournal.com/content/2/1/11 Author details Novartis Institutes for Biomedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA. Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Received: 8 May 2012 Accepted: 7 June 2012 Published: 7 June 2012 References 1. Storm EE, Huynh TV, Copeland NG, Jenkins NA, Kingsley DM, Lee S-J: Limb alterations in brachypodism mice due to mutations in a new member of the TGF[beta]-superfamily. Nature 1994, 368(6472):639–643. 2. McPherron AC, Lawler AM, Lee SJ: Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature 1997, 387(6628):83–90. 3. McPherron AC, Lee SJ: Double muscling in cattle due to mutations in the myostatin gene. Proc Natl Acad Sci U S A 1997, 94(23):12457–12461. 4. McPherron AC, Lee SJ: Suppression of body fat accumulation in myostatin-deficient mice. J Clin Invest 2002, 109(5):595–601. 5. Zimmers TA, Davies MV, Koniaris LG, Haynes P, Esquela AF, Tomkinson KN, McPherron AC, Wolfman NM, Lee SJ: Induction of cachexia in mice by systemically administered myostatin. Science 2002, 296(5572):1486–1488. 6. Wolfman NM, McPherrin A, Pappano W, Davies M, Song K, Tonkinson K, Wright J, Zhao L, Sebald S, Grenspan D, et al: Activation of latent myostatin by the BMP-1/tolloid family of metalloproteinases. Proc Natl Acad Sci U S A 2003, 100(26):15842–15846. 7. Lee S-J, Reed LA, Davies MV, Girgenrath S, Goad MEP, Tomkinson KN, Wright JF, Barker C, Ehrmantraut G, Holmstrom J, et al: Regulation of muscle growth by multiple ligands signaling through activin type II receptors. Proc Natl Acad Sci USA 2005, 102(50):18117–18122. 8. Lee SJ, McPherron AC: Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci USA 2001, 98(16):9306–9311. 9. Lee S-J: Quadrupling muscle mass in mice by targeting TGFbeta signaling pathways. PLoS One 2007, 2(8):e789. 10. Schuelke M, Wagner KR, Stolz LE, Hubner C, Riebel T, Komen W, Braun T, Lee S-J: Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med 2004, 350(26):2682–2688. 11. Zhou X, Wang LJ, Lu J, Song Y, Kwak KS, Jiao Q, Rosenfeld R, Chen Q, Boone T, Simonett WS, et al: Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. Cell 2010, 142:531–543. doi:10.1186/2044-5040-2-11 Cite this article as: Glass and Spiegelman: Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science. Skeletal Muscle 2012 2:11. Submit your manuscript to a journal and benefi t from: 7 Convenient online submission 7 Rigorous peer review 7 Immediate publication on acceptance 7 Open access: articles freely available online 7 High visibility within the fi eld 7 Retaining the copyright to your article Submit your next manuscript at 7 springeropen.com http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Skeletal Muscle Springer Journals

Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science

Skeletal Muscle , Volume 2 (1) – Jun 7, 2012

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Springer Journals
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Copyright © 2012 by Glass and Spiegelman; licensee Springer.
Subject
Life Sciences; Cell Biology; Developmental Biology; Biochemistry, general; Systems Biology; Biotechnology
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2044-5040
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10.1186/2044-5040-2-11
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22676848
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Abstract

Se-Jin Lee was elected member to the National Academy of Sciences on 28 April 2012. Dr Lee is responsible for the discovery of myostatin, a critical regulator of skeletal muscle mass and function. He also determined the primary binding receptor for myostatin, and has characterized additional transforming growth factor–β family members acting in this pathway. Keywords: National Academy of Sciences, Skeletal muscle development, Myostatin Commentary have naturally occurring disruptions of the myostatin Professor Se-Jin Lee was elected on 28 April to the Uni- locus [3]. ted States National Academy of Sciences for his research Dr Lee went on to extensively study myostatin, and in achievements, most notably the discovery of myostatin subsequent papers demonstrated the loss of white fat and its role in skeletal muscle maintenance. that occurs upon induction of hypermuscularity by Dr Lee is a Professor of Molecular Biology and Genet- myostatin inhibition [4], and that administration of ics at Johns Hopkins University. He holds an MD and myostatin was sufficient to cause a phenotype reminis- PhD, and he joined Hopkins after a period as an associ- cent of cachexia [5]. He next showed that myostatin was ate at the Carnegie Institution for Science. regulated by a metalloprotease that activates it from a la- His first major paper in the area that led him on his tent state [6], and identified the activin receptor type IIb most fruitful research path was published in Nature in receptor as one of the key receptors for myostatin [7]. 1994 [1]. In that study, Professor Lee reported on the This last paper highlighted an ongoing trend of first-au- discovery of several transforming growth facto (TGF)-β thor manuscripts for Dr Lee, a testament to his contin- family members: growth differentiation factor (GDF)5, 6 ued commitment to working at the bench. and 7. Next, in 1997, Professor Lee and his co-authors Finally, Dr Lee has shown that other molecules in the Alexandra McPherron and Ann Lawler described the TGF-β pathway, notably the activins and follistatin, also identification of myostatin, also known as GDF8, via RT- regulate muscle mass [8,9]. PCR, using degenerate primers from TGF-β family Dr Lee’s contributions include the demonstration of member homology domains [2]. In that same manu- potential therapeutic benefits for myostatin inhibition. script, they described the myostatin mouse knockout, The precise clinical setting in which myostatin blockade and the dramatic skeletal muscle hypertrophy caused by might be beneficial has not yet been finally determined deletion of myostatin, a phenotype that still manages to in humans, but it is at least clear that human null muta- startle. A two- to three-fold increase in muscle mass was tions for myostatin have a similar phenotype of hyper- observed in the GDF8 null muscle [2]. Later that year, muscularity [10]. One potential area for blockade of this McPherron and Lee also reported that Piedmontese and family of factors is cancer cachexia, as was demonstrated Belgian Blue cattle, notable for their hypermuscularity, with an activin receptor IIb trap [11]. Dr Lee’s election to the Academy represents great rec- ognition both for him and for the skeletal muscle field as a whole. His career is a testament to continued close * Correspondence: david.glass@novartis.com study of a mechanism, leading to the initiation of an en- Novartis Institutes for Biomedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA tirely new field of basic and biomedical research. Full list of author information is available at the end of the article © 2012 Glass and Spiegelman; licensee Springer. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Glass and Spiegelman Skeletal Muscle 2012, 2:11 Page 2 of 2 http://www.skeletalmusclejournal.com/content/2/1/11 Author details Novartis Institutes for Biomedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA. Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Received: 8 May 2012 Accepted: 7 June 2012 Published: 7 June 2012 References 1. Storm EE, Huynh TV, Copeland NG, Jenkins NA, Kingsley DM, Lee S-J: Limb alterations in brachypodism mice due to mutations in a new member of the TGF[beta]-superfamily. Nature 1994, 368(6472):639–643. 2. McPherron AC, Lawler AM, Lee SJ: Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature 1997, 387(6628):83–90. 3. McPherron AC, Lee SJ: Double muscling in cattle due to mutations in the myostatin gene. Proc Natl Acad Sci U S A 1997, 94(23):12457–12461. 4. McPherron AC, Lee SJ: Suppression of body fat accumulation in myostatin-deficient mice. J Clin Invest 2002, 109(5):595–601. 5. Zimmers TA, Davies MV, Koniaris LG, Haynes P, Esquela AF, Tomkinson KN, McPherron AC, Wolfman NM, Lee SJ: Induction of cachexia in mice by systemically administered myostatin. Science 2002, 296(5572):1486–1488. 6. Wolfman NM, McPherrin A, Pappano W, Davies M, Song K, Tonkinson K, Wright J, Zhao L, Sebald S, Grenspan D, et al: Activation of latent myostatin by the BMP-1/tolloid family of metalloproteinases. Proc Natl Acad Sci U S A 2003, 100(26):15842–15846. 7. Lee S-J, Reed LA, Davies MV, Girgenrath S, Goad MEP, Tomkinson KN, Wright JF, Barker C, Ehrmantraut G, Holmstrom J, et al: Regulation of muscle growth by multiple ligands signaling through activin type II receptors. Proc Natl Acad Sci USA 2005, 102(50):18117–18122. 8. Lee SJ, McPherron AC: Regulation of myostatin activity and muscle growth. Proc Natl Acad Sci USA 2001, 98(16):9306–9311. 9. Lee S-J: Quadrupling muscle mass in mice by targeting TGFbeta signaling pathways. PLoS One 2007, 2(8):e789. 10. Schuelke M, Wagner KR, Stolz LE, Hubner C, Riebel T, Komen W, Braun T, Lee S-J: Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med 2004, 350(26):2682–2688. 11. Zhou X, Wang LJ, Lu J, Song Y, Kwak KS, Jiao Q, Rosenfeld R, Chen Q, Boone T, Simonett WS, et al: Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. Cell 2010, 142:531–543. doi:10.1186/2044-5040-2-11 Cite this article as: Glass and Spiegelman: Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science. Skeletal Muscle 2012 2:11. Submit your manuscript to a journal and benefi t from: 7 Convenient online submission 7 Rigorous peer review 7 Immediate publication on acceptance 7 Open access: articles freely available online 7 High visibility within the fi eld 7 Retaining the copyright to your article Submit your next manuscript at 7 springeropen.com

Journal

Skeletal MuscleSpringer Journals

Published: Jun 7, 2012

References