Loss of 4E-BPs prevents the hindlimb immobilization-induced decrease in protein synthesis in skeletal muscle
Gregory N. Kincheloe, Paul A. Roberson, Allyson L. Toro, Bruce A. Stanley, Anne Stanley, Leonard S. Jefferson, Michael D. Dennis, Scot R. Kimball
Abstract
Basal rates of protein synthesis are elevated in skeletal muscle in the immobilized leg of mice lacking the translational repressors, 4E-BP1 and 4E-BP2 (knockout mice), compared with wild-type mice. However, disuse-induced muscle atrophy occurs to the same extent in both wild-type and knockout mice suggesting that compensatory mechanisms are induced that overcome the upregulation of muscle protein synthesis. Proteomic analysis revealed that mRNAs encoding several glycolytic enzymes are differentially translated in wild-type and knockout mice.
Topics & Concepts
Skeletal muscleHindlimbDownregulation and upregulationKnockout mouseMuscle atrophyEndocrinologyInternal medicineBiologyProtein biosynthesisWild typeAtrophyGlycolysisBasal (medicine)Cell biologyChemistryMutantMolecular biologyBiochemistryMetabolismGeneMedicineInsulinMuscle Physiology and DisordersMuscle metabolism and nutritionGenetic Neurodegenerative Diseases