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The p65 subunit of NF-κB and PARP1 assist Snail1 in activating fibronectin transcription
Author(s) -
Jelena Stanisavljević,
Montserrat Porta-de-la-Riva,
Raquel Batlle,
Antonio Garcı́a de Herreros,
Josep Baulida
Publication year - 2011
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.078824
Subject(s) - biology , protein subunit , repressor , transcription (linguistics) , promoter , microbiology and biotechnology , transcription factor , epithelial–mesenchymal transition , nf κb , fibronectin , mesenchymal stem cell , gene , gene expression , cancer research , downregulation and upregulation , genetics , signal transduction , extracellular matrix , linguistics , philosophy
Snail1 is a transcriptional repressor of E-cadherin that triggers epithelial-mesenchymal transition (EMT). Here, we report assisted Snail1 interaction with the promoter of a typical mesenchymal gene, fibronectin (FN1), both in epithelial cells undergoing EMT and in fibroblasts. Together with Snail1, the p65 subunit of NF-κB and PARP1 bound to the FN1 promoter. We detected nuclear interaction of these proteins and demonstrated the requirement of all three for FN1 transcription. Moreover, other genes involved in cell movement mimic FN1 expression induced by Snail1 or TGF-β1 treatment and recruit p65NF-κB and Snail1 to their promoters. The molecular cooperation between Snail1 and NF-κB in transcription activation provides a new insight into how Snail1 can modulate a variety of cell programs.

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