GSE103372
TGF-b utilizes a novel receptor activation mechanism to phosphorylate SMAD1/5 and regulate epithelial-to-mesenchymal transition
TGF-b treatment leads to the transcriptional regulation of many genes. However, the proportion of those that are dependent on SMAD1/5 is unknown. Here, we compared the transcriptional profile after TGF-b treatment in a parental clone and one in which SMAD1/5 had been deleted by CRISPR/Cas9 to identify SMAD1/5 dependent genes. Overall design: NMuMG parental clone or DSMAD1/5 Clone 1, untreated or treated with TGF-b for 48 hr, n=3 in each group.