title: Focal adhesion kinase and its role in skeletal muscle.
abstract: Skeletal muscle has a remarkable ability to respond to different physical stresses. Loading muscle through exercise, either anaerobic or aerobic, can lead to increases in muscle size and function while, conversely, the absence of muscle loading stimulates rapid decreases in size and function. A principal mediator of this load-induced change is focal adhesion kinase (FAK), a downstream non-receptor tyrosine kinase that translates the cytoskeletal stress and strain signals transmitted across the cytoplasmic membrane by integrins to activate multiple anti-apoptotic and cell growth pathways. Changes in FAK expression and phosphorylation have been found to correlate to specific developmental states in myoblast differentiation, muscle fiber formation and muscle size in response to loading and unloading. With the capability to regulate costamere formation, hypertrophy and glucose metabolism, FAK is a molecule with diverse functions that are important in regulating muscle cell health.
authors.affiliation: Center of Excellence for the Medical Consequences of Spinal Cord Injury, James J. Peters Veterans Affairs Medical Center, 130 W. Kingsbridge Rd., Bronx, NY, 10468, USA.|Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
authors.forename: Zachary A
authors.initials: ZA
authors.lastname: Graham
authors.affiliation: Applied Physiology Laboratory, University of Kansas, Lawrence, KS, USA.
authors.forename: Philip M
authors.initials: PM
authors.lastname: Gallagher
authors.affiliation: Center of Excellence for the Medical Consequences of Spinal Cord Injury, James J. Peters Veterans Affairs Medical Center, 130 W. Kingsbridge Rd., Bronx, NY, 10468, USA. christopher.cardozo@mssm.edu.|Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. christopher.cardozo@mssm.edu.|Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. christopher.cardozo@mssm.edu.|Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY, USA. christopher.cardozo@mssm.edu.
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cardozo
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology*; D051417:Focal Adhesion Kinase 1 / Q000096:biosynthesis*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006801:Humans; D018482:Muscle, Skeletal / Q000166:cytology / Q000201:enzymology*; D032448:Myoblasts, Skeletal / Q000166:cytology / Q000201:enzymology; D015398:Signal Transduction / Q000502:physiology*; D013312:Stress, Physiological / Q000502:physiology*
chemical_list: D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human
keywords: Exercise; Focal adhesion kinase; Hypertrophy; Muscle development