Dataset Information


TGF-beta signalling through SMAD1/5 is required for epithelial-to-mesenchymal transition

ABSTRACT: TGF-beta treatment leads to SMAD1/5 phosphorylation. However, the ability of SMAD1/5 to bind chromatin downstream of TGF-beta signalling is unknown. We performed ChIP-sequencing for pSMAD1/5 and SMAD3 to identify binding sites for pSMAD1/5 upon TGF-beta stimulation and identified preferential pSMAD1/5 binding at SMAD1/5:SMAD4 consensus sites. Overall design: MDA-MB-231 cells untreated or treated with TGF-beta for 1 h and then examined with a SMAD3 or pSMAD1/5 antibody. The SMAD3 acts as a control as it is well known that SMAD3 is required for transcriptional regulation of many TGF-beta target genes.

INSTRUMENT(S): Illumina HiSeq 2500 (Homo sapiens)

SUBMITTER: Caroline S Hill  

PROVIDER: GSE92443 | GEO | 2018-02-16


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TGF-β uses a novel mode of receptor activation to phosphorylate SMAD1/5 and induce epithelial-to-mesenchymal transition.

Ramachandran Anassuya A   Vizán Pedro P   Das Debipriya D   Chakravarty Probir P   Vogt Janis J   Rogers Katherine W KW   Müller Patrick P   Hinck Andrew P AP   Sapkota Gopal P GP   Hill Caroline S CS  

eLife 20180129

The best characterized signaling pathway downstream of transforming growth factor β (TGF-β) is through SMAD2 and SMAD3. However, TGF-β also induces phosphorylation of SMAD1 and SMAD5, but the mechanism of this phosphorylation and its functional relevance is not known. Here, we show that TGF-β-induced SMAD1/5 phosphorylation requires members of two classes of type I receptor, TGFBR1 and ACVR1, and establish a new paradigm for receptor activation where TGFBR1 phosphorylates and activates ACVR1, wh  ...[more]

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