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. NMuMG parental clone or DSMAD1/5 Clone 1, untreated or treated with TGF-b for 48 hr, n=3 in each group.

转化生长因子-β（TGF-β）处理可诱导众多基因的转录调控。然而，其中依赖SMAD1/5的基因占比尚不明确。本研究对比了亲本克隆与经CRISPR/Cas9技术敲除SMAD1/5的克隆在TGF-β处理后的转录组谱，以鉴定依赖SMAD1/5的基因。实验分组如下：NMuMG亲本克隆或DSMAD1/5克隆1，分别设置未处理组与TGF-β处理48小时组，每组设置3个生物学重复。