G
Gretchen A. Meyer
Researcher at Washington University in St. Louis
Publications - 54
Citations - 1509
Gretchen A. Meyer is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Skeletal muscle & Medicine. The author has an hindex of 15, co-authored 42 publications receiving 1085 citations. Previous affiliations of Gretchen A. Meyer include University of California, San Diego & University of Washington.
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Journal ArticleDOI
Sirtuin 1 (SIRT1) Deacetylase Activity Is Not Required for Mitochondrial Biogenesis or Peroxisome Proliferator-activated Receptor-γ Coactivator-1α (PGC-1α) Deacetylation following Endurance Exercise
Andrew Philp,Ai Chen,Debin Lan,Gretchen A. Meyer,Anne N. Murphy,Amy E. Knapp,I. Mark Olfert,Carrie E. McCurdy,George R. Marcotte,Michael C. Hogan,Keith Baar,Simon Schenk +11 more
TL;DR: It is demonstrated that SIRT1 deacetylase activity is not required for exercise-induced de acetylation of PGC-1α or mitochondrial biogenesis in skeletal muscle and suggested that changes in GCN5 acetyltransferase activity may be an important regulator of P GC-1 α activity after exercise.
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Elucidation of extracellular matrix mechanics from muscle fibers and fiber bundles.
TL;DR: A new method to quantify viscoelastic ECM modulus is presented by combining tests of single muscle fibers and fiber bundles, which demonstrate that ECM is a highly nonlinearly elastic material, while muscle fibers are linearly elastic.
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Extracellular matrix regulation in the muscle satellite cell niche
TL;DR: A review of the ECM components that comprise the muscle satellite cell niche, how they are modulated in health and disease and how these changes are thought to affect SC function is focused on.
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Obscurin determines the architecture of the longitudinal sarcoplasmic reticulum
Stephan Lange,Kunfu Ouyang,Gretchen A. Meyer,Gretchen A. Meyer,Li Cui,Hongqiang Cheng,Richard L. Lieber,Richard L. Lieber,Ju Chen +8 more
TL;DR: Obscurin knockout mice display centralized nuclei in skeletal muscles as a sign of mild myopathy, but have normal sarcomeric structure and preserved muscle function.
Journal ArticleDOI
Infiltration of intramuscular adipose tissue impairs skeletal muscle contraction
Nicole K. Biltz,Kelsey H. Collins,Kelsey H. Collins,Karen C. Shen,Kendall Schwartz,Charles A. Harris,Gretchen A. Meyer +6 more
TL;DR: It is demonstrated that IMAT deposition causes decreased muscle strength using mouse models, which indicates IMAT is a novel therapeutic target for muscle dysfunction.