Correlation Engine 2.0
Clear Search sequence regions


  • Atf6b protein (1)
  • biosynthesis (1)
  • cellular (1)
  • Crebl2 (6)
  • cyclic amp (2)
  • drosophila (1)
  • element (2)
  • female (1)
  • glycolysis (1)
  • hepatoma (1)
  • humans (1)
  • liver (2)
  • mice (1)
  • mice knockout (1)
  • muscle (1)
  • myoblasts (2)
  • nutrient (1)
  • rapamycin (2)
  • regulates (1)
  • signal (1)
  • Sizes of these terms reflect their relevance to your search.

    We previously identified Drosophila REPTOR and REPTOR-BP as transcription factors downstream of mTORC1 that play an important role in regulating organismal metabolism. We study here the mammalian ortholog of REPTOR-BP, Crebl2. We find that Crebl2 mediates part of the transcriptional induction caused by mTORC1 inhibition. In C2C12 myoblasts, Crebl2 knockdown leads to elevated glucose uptake, elevated glycolysis as observed by lactate secretion, and elevated triglyceride biosynthesis. In Hepa1-6 hepatoma cells, Crebl2 knockdown also leads to elevated triglyceride levels. In sum, this works identifies Crebl2 as a regulator of cellular metabolism that can link nutrient sensing via mTORC1 to the metabolic response of cells.

    Citation

    Marcel Tiebe, Marilena Lutz, Deniz Senyilmaz Tiebe, Aurelio A Teleman. Crebl2 regulates cell metabolism in muscle and liver cells. Scientific reports. 2019 Dec 27;9(1):19869

    Expand section icon Mesh Tags

    Expand section icon Substances


    PMID: 31882710

    View Full Text