David J Glass

Summary

Affiliation: Novartis Institutes for BioMedical Research

Publications

  1. pmc Two tales concerning skeletal muscle
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA
    J Clin Invest 117:2388-91. 2007
  2. ncbi request reprint Skeletal muscle hypertrophy and atrophy signaling pathways
    David J Glass
    Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591 6707, USA
    Int J Biochem Cell Biol 37:1974-84. 2005
  3. doi request reprint A brief history of the hypothesis
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Cell 134:378-81. 2008
  4. ncbi request reprint The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors
    Trevor N Stitt
    Regeneron Pharmaceuticals, Inc, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA
    Mol Cell 14:395-403. 2004
  5. ncbi request reprint A signaling role for dystrophin: inhibiting skeletal muscle atrophy pathways
    David J Glass
    Novartis Institutes for BioMedical Research, 400 Technology Square, Cambridge, Massachusetts 02139, USA
    Cancer Cell 8:351-2. 2005
  6. pmc Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science
    David J Glass
    Novartis Institutes for BioMedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA
    Skelet Muscle 2:11. 2012
  7. pmc TAK-1/p38/nNFκB signaling inhibits myoblast differentiation by increasing levels of Activin A
    Anne Ulrike Trendelenburg
    Novartis Institutes for BioMedical Research, Forum 1, Novartis Campus, 4056 Basel, Switzerland
    Skelet Muscle 2:3. 2012
  8. pmc Treating cancer cachexia to treat cancer
    Se Jin Lee
    Johns Hopkins University School of Medicine, Department of Molecular Biology and Genetics, 725 N, Wolfe St, PCTB 803, Baltimore, Maryland 21205, USA
    Skelet Muscle 1:2. 2011
  9. ncbi request reprint Signaling pathways perturbing muscle mass
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Curr Opin Clin Nutr Metab Care 13:225-9. 2010
  10. doi request reprint A critique of the hypothesis, and a defense of the question, as a framework for experimentation
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA, USA
    Clin Chem 56:1080-5. 2010

Collaborators

  • Jun Shi
  • Monte S Willis
  • Zhizhong Li
  • Christine Li
  • Tea Shavlakadze
  • Zhidan Wu
  • John Eash
  • Yama A Abassi
  • C Patterson
  • Rhonda Bassel-Duby
  • Per Olof J Hasselgren
  • Sergey Rakhilin
  • Chikwendu Ibebunjo
  • Brian A Clarke
  • Trevor N Stitt
  • Joseph Cruz
  • Qicheng Ma
  • Shou Ih Hu
  • Anne Ulrike Trendelenburg
  • Se Jin Lee
  • Jens Fielitz
  • Tiziana Crepaldi
  • Doreen Drujan
  • William O Kline
  • Michael Gonzalez
  • George D Yancopoulos
  • Dongsheng Cai
  • Ka Man V Lai
  • Robert W Burgess
  • Sophie Brachat
  • Joel M Chick
  • Michelle Broome
  • Michelle Steinkrauss
  • Yunyu Zhang
  • Chad Vickers
  • Jean Rene Galarneau
  • Tracee Kendall
  • Elizabeth Skuba
  • Brigitte Fournier
  • Judit Markovits
  • Sabine Gutzwiller
  • Steven P Gygi
  • Xiaoqing Qi
  • Shanchuan Zhao
  • Amy Chen
  • Sherry Chin
  • Mark Katz
  • Angelika Meyer
  • Carsten Jacobi
  • Jerome N Feige
  • Christian Leo
  • Claudio Scuoppo
  • Chiara Prunotto
  • Eric N Olson
  • Jeffrey A Spencer
  • Jennifer Griffiths
  • Riccardo Taulli
  • John M Shelton
  • Leon O Murphy
  • Shuaib Latif
  • Elena Burova
  • Roberto Chiarle
  • James A Richardson
  • Francesca Bersani
  • Richard A Corpina
  • Paolo E Forni
  • Carola Ponzetto
  • Mi Sung Kim
  • Paolo Accornero
  • Esther Latres
  • Elizabeth Zlotchenko
  • Frank Panaro
  • Yekatarina Timofeyva
  • Hart G W Lidov
  • Byung Chul Oh
  • Steven E Shoelson
  • Aris N Economides
  • Peter A Melendez
  • Walter R Frontera
  • J Daniel Frantz
  • Jongsoon Lee
  • Nicholas E Tawa
  • William T Poueymirou
  • Erqian Na
  • Dion K Dickman
  • Joshua R Sanes
  • Lorna Nunez

Detail Information

Publications26

  1. pmc Two tales concerning skeletal muscle
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA
    J Clin Invest 117:2388-91. 2007
    ..Here it is shown that nNOS is similarly perturbed in a setting of skeletal muscle atrophy. Both of these studies suggest new avenues for the treatment of skeletal muscle disease...
  2. ncbi request reprint Skeletal muscle hypertrophy and atrophy signaling pathways
    David J Glass
    Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591 6707, USA
    Int J Biochem Cell Biol 37:1974-84. 2005
    ..This review will focus on the recent progress in the understanding of molecular signalling, which governs skeletal muscle atrophy and hypertrophy, and the known instances of cross-regulation between the two systems...
  3. doi request reprint A brief history of the hypothesis
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Cell 134:378-81. 2008
    ..Two terms used as frameworks for scientific experimentation--the "hypothesis" and the "model"--carry distinct philosophical assumptions, with important consequences for the practicing scientist...
  4. ncbi request reprint The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors
    Trevor N Stitt
    Regeneron Pharmaceuticals, Inc, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA
    Mol Cell 14:395-403. 2004
    ....
  5. ncbi request reprint A signaling role for dystrophin: inhibiting skeletal muscle atrophy pathways
    David J Glass
    Novartis Institutes for BioMedical Research, 400 Technology Square, Cambridge, Massachusetts 02139, USA
    Cancer Cell 8:351-2. 2005
    ..These data reposition dystrophin as a signaling protein and connect an important cellular complex required for the structural integrity of muscle to the pathways that modulate muscle size...
  6. pmc Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science
    David J Glass
    Novartis Institutes for BioMedical Research, 100 Technology Square, RM4210, Cambridge, MA 02139, USA
    Skelet Muscle 2:11. 2012
    ..He also determined the primary binding receptor for myostatin, and has characterized additional transforming growth factor-β family members acting in this pathway...
  7. pmc TAK-1/p38/nNFκB signaling inhibits myoblast differentiation by increasing levels of Activin A
    Anne Ulrike Trendelenburg
    Novartis Institutes for BioMedical Research, Forum 1, Novartis Campus, 4056 Basel, Switzerland
    Skelet Muscle 2:3. 2012
    ..abstract:..
  8. pmc Treating cancer cachexia to treat cancer
    Se Jin Lee
    Johns Hopkins University School of Medicine, Department of Molecular Biology and Genetics, 725 N, Wolfe St, PCTB 803, Baltimore, Maryland 21205, USA
    Skelet Muscle 1:2. 2011
    ....
  9. ncbi request reprint Signaling pathways perturbing muscle mass
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Curr Opin Clin Nutr Metab Care 13:225-9. 2010
    ..To discuss the mechanisms of muscle loss during cachexia...
  10. doi request reprint A critique of the hypothesis, and a defense of the question, as a framework for experimentation
    David J Glass
    Novartis Institutes for BioMedical Research, Cambridge, MA, USA
    Clin Chem 56:1080-5. 2010
    ..Presented is an alternative framework-the query/model approach-which many scientists may discover is the framework they are actually using, despite being required to give lip service to the hypothesis...
  11. doi request reprint PI3 kinase regulation of skeletal muscle hypertrophy and atrophy
    David J Glass
    Novartis Institute for Biomedical Research, Cambridge, MA 02139, USA
    Curr Top Microbiol Immunol 346:267-78. 2010
    ..These findings show that myostatin signaling acts by blocking genes induced during differentiation, even in a myotube, as opposed to activating the distinct "atrophy program."..
  12. pmc Genomic and proteomic profiling reveals reduced mitochondrial function and disruption of the neuromuscular junction driving rat sarcopenia
    Chikwendu Ibebunjo
    Muscle Diseases Group, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA
    Mol Cell Biol 33:194-212. 2013
    ..Together, these findings suggest that therapeutic approaches that simultaneously stimulate mitochondrogenesis and reduce muscle proteolysis and inflammation have potential for treating sarcopenia...
  13. doi request reprint MNK2 inhibits eIF4G activation through a pathway involving serine-arginine-rich protein kinase in skeletal muscle
    Shou Ih Hu
    Novartis Institutes for BioMedical Research, 100 Technology Square, Cambridge, MA 02139, USA
    Sci Signal 5:ra14. 2012
    ..These data indicate that MNK2 plays a unique role, not shared by its closest paralog MNK1, in limiting protein translation through its negative effect on eIF4G Ser¹¹⁰⁸ phosphorylation and p70S6K activation...
  14. pmc Oncogenic NRAS, required for pathogenesis of embryonic rhabdomyosarcoma, relies upon the HMGA2-IGF2BP2 pathway
    Zhizhong Li
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Cancer Res 73:3041-50. 2013
    ..Taken together, these findings implicate the HMGA2-IGFBP2-NRAS signaling pathway as a critical oncogenic driver in ERMS...
  15. ncbi request reprint The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle
    Brian A Clarke
    Novartis Institutes for BioMedical Research, 100 Technology Square, Cambridge, MA 02139, USA
    Cell Metab 6:376-85. 2007
    ..These data identify the mechanism by which MYH is depleted under atrophy conditions and demonstrate that inhibition of a single E3 ligase, MuRF1, is sufficient to maintain this important sarcomeric protein...
  16. pmc An HMGA2-IGF2BP2 axis regulates myoblast proliferation and myogenesis
    Zhizhong Li
    Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Dev Cell 23:1176-88. 2012
    ..These data demonstrate that the HMGA2-IGF2BP2 axis functions as a key regulator of satellite cell activation and therefore skeletal muscle development...
  17. doi request reprint Electrical impedance as a novel biomarker of myotube atrophy and hypertrophy
    Sergey Rakhilin
    Novartis Institute for Biomedical Research, Cambridge, MA, USA
    J Biomol Screen 16:565-74. 2011
    ..Application of this technique to drug screening might be beneficial in finding novel treatments preventing muscle atrophy and other diseases associated with any morphological change in cell shape...
  18. doi request reprint The SCF-Fbxo40 complex induces IRS1 ubiquitination in skeletal muscle, limiting IGF1 signaling
    Jun Shi
    Novartis Institutes for BioMedical Research, 100 Technology Square, Cambridge, MA 02139, USA
    Dev Cell 21:835-47. 2011
    ..These findings establish an important means of restraining IGF1's effects on skeletal muscle...
  19. doi request reprint Voluntary running, skeletal muscle gene expression, and signaling inversely regulated by orchidectomy and testosterone replacement
    Chikwendu Ibebunjo
    Department of Musculoskeletal Diseases, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA
    Am J Physiol Endocrinol Metab 300:E327-40. 2011
    ..These data demonstrate the necessity of testosterone for both speed and endurance of voluntary wheel running in mice and suggest a potential mechanism for declined activity in humans where androgens are deficient...
  20. ncbi request reprint IKKbeta/NF-kappaB activation causes severe muscle wasting in mice
    Dongsheng Cai
    Research Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    Cell 119:285-98. 2004
    ....
  21. pmc Conditional activation of akt in adult skeletal muscle induces rapid hypertrophy
    Ka Man V Lai
    Regeneron Pharmaceuticals, Inc, 777 Old Saw Mill River Rd, Tarrytown, NY 10591 6707, USA
    Mol Cell Biol 24:9295-304. 2004
    ..These findings suggest that pharmacologic approaches directed toward activating Akt will be useful in inducing skeletal muscle hypertrophy and that an increase in lean muscle mass is sufficient to decrease fat storage...
  22. ncbi request reprint Conditional activation of MET in differentiated skeletal muscle induces atrophy
    Tiziana Crepaldi
    Center for Experimental Research and Medical Studies, University of Turin, 10126 Turin, Italy
    J Biol Chem 282:6812-22. 2007
    ....
  23. ncbi request reprint Molecular mechanisms modulating muscle mass
    David J Glass
    Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591 6707, USA
    Trends Mol Med 9:344-50. 2003
    ..The pathways modulating hypertrophy and atrophy will be further discussed, to highlight potential targets for clinical intervention...
  24. ncbi request reprint Signalling pathways that mediate skeletal muscle hypertrophy and atrophy
    David J Glass
    Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591 6707, USA
    Nat Cell Biol 5:87-90. 2003
    ....
  25. pmc Myosin accumulation and striated muscle myopathy result from the loss of muscle RING finger 1 and 3
    Jens Fielitz
    Department of Molecular Biology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390 9148, USA
    J Clin Invest 117:2486-95. 2007
    ..These findings identify MuRF1 and MuRF3 as key E3 ubiquitin ligases for the UPS-dependent turnover of sarcomeric proteins and reveal a potential basis for myosin storage myopathies...
  26. ncbi request reprint Mapping sites responsible for interactions of agrin with neurons
    Robert W Burgess
    Department of Anatomy and Neurobiology, Washington University Medical School, St Louis, Missouri 63110, USA
    J Neurochem 83:271-84. 2002
    ..Together, these studies define sites that contribute to the subcellular localization of and signaling by neuronal agrin...