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      G protein-coupled receptor 56 regulates mechanical overload-induced muscle hypertrophy.

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          Abstract

          Peroxisome proliferator-activated receptor gamma coactivator 1-alpha 4 (PGC-1α4) is a protein isoform derived by alternative splicing of the PGC1α mRNA and has been shown to promote muscle hypertrophy. We show here that G protein-coupled receptor 56 (GPR56) is a transcriptional target of PGC-1α4 and is induced in humans by resistance exercise. Furthermore, the anabolic effects of PGC-1α4 in cultured murine muscle cells are dependent on GPR56 signaling, because knockdown of GPR56 attenuates PGC-1α4-induced muscle hypertrophy in vitro. Forced expression of GPR56 results in myotube hypertrophy through the expression of insulin-like growth factor 1, which is dependent on Gα12/13 signaling. A murine model of overload-induced muscle hypertrophy is associated with increased expression of both GPR56 and its ligand collagen type III, whereas genetic ablation of GPR56 expression attenuates overload-induced muscle hypertrophy and associated anabolic signaling. These data illustrate a signaling pathway through GPR56 which regulates muscle hypertrophy associated with resistance/loading-type exercise.

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          Author and article information

          Journal
          Proc. Natl. Acad. Sci. U.S.A.
          Proceedings of the National Academy of Sciences of the United States of America
          Proceedings of the National Academy of Sciences
          1091-6490
          0027-8424
          Nov 04 2014
          : 111
          : 44
          Affiliations
          [1 ] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115; Department of Cell Biology, Harvard Medical School, Boston, MA 02115;
          [2 ] Endocrine Research Unit, Division of Endocrinology, The Mayo Clinic, Rochester, MN 55905;
          [3 ] Department of Cell Biology, Harvard Medical School, Boston, MA 02115;
          [4 ] Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706;
          [5 ] Department of Physiology and Pharmacology, Karolinska Institute, S-171 77, Stockholm, Sweden;
          [6 ] Novartis Institutes for Biomedical Research, Cambridge, MA 02139; and.
          [7 ] Division of Newborn Medicine, Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115.
          [8 ] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115; Department of Cell Biology, Harvard Medical School, Boston, MA 02115; Bruce_Spiegelman@dfci.harvard.edu.
          Article
          1417898111
          10.1073/pnas.1417898111
          4226111
          25336758
          c2054af2-a2ea-4833-aef5-70b3654b009a
          History

          GPR56,Gα12/13,mTOR,muscle hypertrophy,overload
          GPR56, Gα12/13, mTOR, muscle hypertrophy, overload

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