R
Roy Bauerlein
Researcher at Regeneron
Publications - 3
Citations - 2560
Roy Bauerlein is an academic researcher from Regeneron. The author has contributed to research in topics: Muscle hypertrophy & Muscle atrophy. The author has an hindex of 3, co-authored 3 publications receiving 2345 citations.
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Journal ArticleDOI
Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.
Sue C. Bodine,Trevor Stitt,Michael Gonzalez,William O. Kline,Gretchen L. Stover,Roy Bauerlein,Elizabeth Zlotchenko,Angus Scrimgeour,John C. Lawrence,David J. Glass,George D. Yancopoulos +10 more
TL;DR: It is concluded that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of this pathway can oppose muscle atrophy induced by disuse.
Journal ArticleDOI
Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice
Esther Latres,Jeffrey Pangilinan,Lawrence Miloscio,Roy Bauerlein,Erqian Na,Terra Potocky,Ying Huang,Mark Eckersdorff,Ashique Rafique,Jason Mastaitis,Calvin Lin,Andrew J. Murphy,George D. Yancopoulos,Jesper Gromada,Trevor Stitt +14 more
TL;DR: It is shown that specific myostatin antagonism with the human antibody REGN1033 enhanced muscle mass and function in young and aged mice and had beneficial effects in models of skeletal muscle atrophy.
Journal ArticleDOI
Myostatin deficiency but not anti-myostatin blockade induces marked proteomic changes in mouse skeletal muscle.
Robert R. Salzler,Darshit Shah,Dore Anthony T,Roy Bauerlein,Lawrence Miloscio,Esther Latres,Nicholas J. Papadopoulos,William C. Olson,Douglas MacDonald,Xunbao Duan +9 more
TL;DR: The proteome‐wide protein expression differs between Mstn−/− mice and mice subjected to specific MstN blockade post‐developmentally, providing molecular‐level insights to inform mechanistic hypotheses to explain the observed functional differences.