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Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration

Tuan HN Nguyen1, Mathieu JM Bertrand23, Christiane Sterpin1, Younes Achouri4 and Olivier RY De Backer1*

Author Affiliations

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

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BMC Cell Biology 2010, 11:57  doi:10.1186/1471-2121-11-57

Published: 20 July 2010

Additional 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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