Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration
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* Corresponding author: Olivier RY De Backer olivier.debacker@fundp.ac.be
1 URPHYM (Unité de Recherche en Physiologie Moléculaire), NARILIS (Namur Research Institute for Life Sciences), FUNDP school of Medicine, University of Namur, 21 rue de Bruxelles, Namur B-5000, Belgium
2 Molecular Signaling and Cell Death Unit, Department for Molecular Biomedical Research, VIB, 9052 Ghent, Belgium
3 Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium
4 Christian de Duve Institute of Cellular Pathology, Université Catholique de Louvain (UCL), Avenue Hippocrate 75, Brussels B-1200, Belgium
BMC Cell Biology 2010, 11:57 doi:10.1186/1471-2121-11-57
Published: 20 July 2010Additional files
Additional file 1:
Figure S1. Cell-cycle distribution of C2C12 myoblasts 12 h and 24 h after serum starvation. C2C12 myoblasts were induced to differentiate by serum starvation, and the fractions of cells in G1, S and G2/M were determined by FACS after staining with propidium iodide.
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Additional file 2:
Figure S2. MyoD activates the MAGED1 promoter in a dose-dependent manner. Increasing amounts of MyoD expression plasmid pEMSV-MyoD were cotransfected with pMAGED1-531+80-luc in 3T3 fibroblasts. Luc activity was measured 48 h after transfection. Results are presented as relative Luc activities with respect to the activity of pMAGED1-531+80-luc in absence of MyoD.
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Additional file 3:
Figure S3. Maged1 knockout myoblasts express normal levels of MyoD, MyoG and Mef2C. Wild-type and Maged1 knockout primary myoblasts were induced to differentiate by serum starvation. MyoD, MyoG and Mef2C RNA levels were quantified using qRT-PCR. GAPDH RNA was used for normalization. Data are presented as the ratio relative to the RNA levels of each analyzed gene in wild-type cells at the time of serum starvation (t = 0 h).
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