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Therefore, it is plausible that ecdysone regulates Mad expression cell autonomously via chromatin modifications.
We therefore suggest that Mad expression is closely associated with epithelial cell differentiation, and that this association is retained in epithelial tumours of the skin.
We hypothesised that MAD expression would be repressed in the progression of oesophageal adenocarcinoma in a reciprocal pattern to c-MYC.
However, Mad expression was lost in palisading basal carcinoma cells and poorly differentiated squamous cell carcinomas, which lacked the epithelial differentiation marker syndecan-1.
Furthermore, we show that Brat represses Mad expression in the embryo, demonstrating that antagonism between Brat repression and BMP signalling also exists in other developmental contexts.
Mad expression and ID2 down-regulation are important events in the TGFβ1 cytostatic program in epithelial cells and ID2 suppression by TGFβ1 is essential for EMT to occur [ 28, 29].
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Moreover, P-Mad expression is also reduced.
In the central region the activation of P-Mad expression by Dpp/BMP2 signalling represses brk transcription to yield a nested pattern of Sal and Omb [3].
Similar to what it was observed for Sal and Omb, P-Mad expression is decreased but not completely eliminated in these clones (Fig. 6A, arrowheads in green channel; Fig. S1).
Since brk downregulation requires P-Mad expression and P-Mad levels are reduced in dTIEGS14 cells, it was investigate whether dTIEG might also regulate the expression of brk repressor.
As expected, 35-day-old GSCs exhibited decreased p-Mad expression (Fig. 4D and E).
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