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      Dependence of dexamethasone-induced Akt/FOXO1 signaling, upregulation of MAFbx, and protein catabolism upon the glucocorticoid receptor

      , , , , ,
      Biochemical and Biophysical Research Communications
      Elsevier BV

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          Abstract

          The muscle ubiquitin ligases MAFbx and MuRF1 are upregulated in and promote muscle atrophy. Upregulation of MAFbx and MuRF1 by glucocorticoids has been linked to activation of FOXO1 and FOXO3A resulting from reduced Akt activity. We determined the requirements for the glucocorticoid receptor (GR) in these biological responses in C2C12 cells in which GR expression was knocked down by stable expression of an shRNA. Loss of GR prevented dexamethasone-induced increases in protein catabolism. Loss of GR, or inhibition of ligand binding to GR with RU486, prevented upregulation of MAFbx and MuRF1 by dexamethasone. Loss of GR also prevented dexamethasone-induced decreases in Akt phosphorylation, and increases in the fraction of FOXO1 that was unphosphorylated. The findings establish a requirement for the GR in activating molecular signals that promote muscle protein catabolism.

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          Author and article information

          Journal
          Biochemical and Biophysical Research Communications
          Biochemical and Biophysical Research Communications
          Elsevier BV
          0006291X
          January 2009
          January 2009
          : 378
          : 3
          : 668-672
          Article
          10.1016/j.bbrc.2008.11.123
          19059383
          1e796b75-8b73-4b88-9ffc-a62e47779192
          © 2009

          https://www.elsevier.com/tdm/userlicense/1.0/

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