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Fig. 6 | Epigenetics & Chromatin

Fig. 6

From: Phosphorylation of TET2 by AMPK is indispensable in myogenic differentiation

Fig. 6

S97E mutation of TET2 partly rescues the differentiation defect of the AMPK-/- C2C12 cells. a The strategy for knocking in (KI) the p.S97E mutation of TET2 in AMPK-/- C2C12 cells. Upper panel: the target region. Lower panel: the HDR (homology-directed repair) donor. The c.289A > G;290G > A;291T > G mutation (red line) was introduced into the 3′ arm of exon 3 of the mouse TET2 gene to encode the phosphor mimic (serine-97-glutamic acid, S97E) of TET2. b Gene ontology (GO) analysis of differentially expressed genes (DEGs) between AMPK-/-:FLAG-BirA-TET2-S97E (TET2-S97E) and AMPK-/-:FLAG-BirA-TET2-WT (TET2-WT) C2C12 cells. c Myod1, Myog and Pax7 mRNA contents were detected by RT-qPCR. Results of two independent C2C12 clones of AMPK-/-:FLAG-BirA-TET2-S97E (TET2-S97E) and AMPK-/-:FLAG-BirA-TET2-WT (TET2-WT) are shown. d Increased myosin heavy chain (MHC) expression after eight days induction of differentiation in AMPK-/-:FLAG-BirA-TET2-S97E (TET2-S97E) cells compared to AMPK-/-:FLAG-BirA-TET2-WT (TET2-WT) cells. Representative Western blot results are shown

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