c-Jun N-terminal kinase 1 promotes transforming growth factor-β1-induced epithelial-to-mesenchymal transition via control of linker phosphorylation and transcriptional activity of Smad3

Transforming growth factor (TGF)-β1 is a key mediator of lung remodeling and fibrosis. Epithelial cells are both a source of and can respond to TGF-β1 with epithelial-to-mesenchymal transition (EMT). We recently determined that TGF-β1-induced EMT in lung epithelial cells requires the presence of c-J...

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Veröffentlicht in:	American journal of respiratory cell and molecular biology 2011-04, Vol.44 (4), p.571-581
Hauptverfasser:	Velden, Jos L J van der, Alcorn, John F, Guala, Amy S, Badura, Elsbeth C H L, Janssen-Heininger, Yvonne M W
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Binding Sites Epithelial Cells - drug effects Epithelial Cells - enzymology Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation - drug effects Humans JNK Mitogen-Activated Protein Kinases - metabolism Lung - cytology Mice Mutant Proteins - metabolism Phosphorylation - drug effects Protein Binding - drug effects Recombinant Fusion Proteins - metabolism Smad3 Protein - genetics Smad3 Protein - metabolism Smad4 Protein - metabolism Transcriptional Activation - drug effects Transforming Growth Factor beta1 - pharmacology
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