Philipp rochard
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In parallel, RXR expression, through the synthesis of its truncated form addressed into mitochondria, could potentiate the activity of p43, a mitochondrial T3-dependent transcription factor. In addition, inhibition of TPA-inducible AP-1 activity induces the expression of BTG1, a potent coactivator of myogenic factors transcriptional activity.
PHILIPP ROCHARD FULL
At the onset of myoblast differentiation, RXR dissociates the TR/c-Jun/MyoD complex, thus restoring a full MyoD transcriptional activity in addition, it allows the liganded T3 nuclear receptor to inhibit TPA-inducible AP-1 activity, an event favouring c-Jun/ATF2 formation, a complex stimulating myogenin expression. In proliferating cells, it inhibits cell cycle arrest through sequestration of MyoD in a TR/c-Jun/MyoD complex in parallel, high levels of Jun/Fos AP-1 complexes inhibit MyoD and myogenin expression. Whereas c-Myc efficiently represses myoblast withdrawal from the cell cycle and terminal differentiation, c-Jun exerts a dual myogenic influence. Indeed, functional interactions between these proteins are deeply involved in the shift from proliferation to differentiation. Interestingly, their expression and/or activity are regulated by ligand-dependent transcription factors. Through their ability to repress irreversible cell cycle arrest, some transcription factors such as cellular oncogenes are considered as potent repressors of myoblast differentiation.