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MOESM1 of Phosphorylation of TET2 by AMPK is indispensable in myogenic differentiation

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posted on 04.06.2019, 05:00 authored by Ting Zhang, Xiaowen Guan, Un Choi, Qiang Dong, Melody Lam, Jianming Zeng, Jun Xiong, Xianju Wang, Terence Poon, Hongjie Zhang, Xuanjun Zhang, Hailin Wang, Ruiyu Xie, Bing Zhu, Gang Li
Additional file 1. Fig. S1. SDS-PAGE analysis of the recombinant N-terminus of murine TET2 (aa 1-181) and its mutant. Fig. S2. AMPK knockout impaired the differentiation of C2C12 cells. Fig. S3. Gene ontology analysis of upregulated genes between AMPK-KO and wild-type C2C12 cells at myoblast- (differentiation d0, A) or myotube- stage (differentiation d8, B). Fig. S4. Increased DNA methylation at a potential intragenic enhancer of Pax7. Fig. S5. CRISPR/Cas9-mediated deletion of the Pax7 intragenic enhancer in C2C12 cells. Fig. S6. Knocking in (KI) the pS97E mutation of Tet2 in AMPK-/- C2C12 cells. Fig. S7. S97E mutation of TET2 partly rescues the differentiation defect of the AMPK-/- C2C12 cells. Fig. S8. Increased myosin heavy chain (MHC) expression in AMPK-/- C1C12 cells rescued with TET2 harboring S97E. Table S1. ELISA analysis of pTET2 [Ser99 (h); Ser97(m)] antibodies*. Table S3. Antibodies. Table S4: Primers and Oligos.