Abstract:
: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.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Tiebe M,Lutz M,Senyilmaz Tiebe D,Teleman AAdoi
10.1038/s41598-019-56407-wsubject
Has Abstractpub_date
2019-12-27 00:00:00pages
19869issue
1issn
2045-2322pii
10.1038/s41598-019-56407-wjournal_volume
9pub_type
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