Inhibition of MEK signaling leads to the resaturation of differentiation in cells with Brd2 overexpression.

<p>3T3-L1 cells transfected with pmBrd2 were induced to differentiate in the presence of UO126 or dimethylsulfoxide (DMSO) as a vehicle, and WT 3T3-L1 as a control. (A) Adipogenic differentiation of 3T3-L1 adipocytes from pre-adipocytes was performed and on day +8, cells were fixed, and then stained with Oil Red O. (B) Quantification of lipid content in transfected 3T3-L1 cells after adipogenic differentiation. (C) Adipogenic differentiation of 3T3-L1 adipocytes from pre-adipocytes was performed and on day +8, Western blotting was performed with p-PPARγ, PPARγ, 422/aP2 and β-actin antibodies. (D) 422/aP2 expression levels were quantified by densitometry in arbitrary units (AU) using ImageJ software, normalized to the amount of β-actin. All data are expressed as mean ± SEM and representative results of at least three experiments are shown. **<i>P</i> < 0.01, Student <i>t</i>-test.