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Publication : The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling.

First Author  Hunt LC Year  2015
Journal  Genes Dev Volume  29
Issue  23 Pages  2475-89
PubMed ID  26584623 Mgi Jnum  J:227117
Mgi Id  MGI:5699766 Doi  10.1101/gad.267419.115
Citation  Hunt LC, et al. (2015) The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling. Genes Dev 29(23):2475-89
abstractText  Metabolic stress and changes in nutrient levels modulate many aspects of skeletal muscle function during aging and disease. Growth factors and cytokines secreted by skeletal muscle, known as myokines, are important signaling factors, but it is largely unknown whether they modulate muscle growth and differentiation in response to nutrients. Here, we found that changes in glucose levels increase the activity of the glucose-responsive transcription factor MLX (Max-like protein X), which promotes and is necessary for myoblast fusion. MLX promotes myogenesis not via an adjustment of glucose metabolism but rather by inducing the expression of several myokines, including insulin-like growth factor 2 (IGF2), whereas RNAi and dominant-negative MLX reduce IGF2 expression and block myogenesis. This phenotype is rescued by conditioned medium from control muscle cells and by recombinant IGF2, which activates the myogenic kinase Akt. Importantly, MLX-null mice display decreased IGF2 induction and diminished muscle regeneration in response to injury, indicating that the myogenic function of MLX is manifested in vivo. Thus, glucose is a signaling molecule that regulates myogenesis and muscle regeneration via MLX/IGF2/Akt signaling.
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