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TEAD mediates YAP-dependent gene induction and growth control.

Genes & development | Jul 15, 2008

The YAP transcription coactivator has been implicated as an oncogene and is amplified in human cancers. Recent studies have established that YAP is phosphorylated and inhibited by the Hippo tumor suppressor pathway. Here we demonstrate that the TEAD family transcription factors are essential in mediating YAP-dependent gene expression. TEAD is also required for YAP-induced cell growth, oncogenic transformation, and epithelial-mesenchymal transition. CTGF is identified as a direct YAP target gene important for cell growth. Moreover, the functional relationship between YAP and TEAD is conserved in Drosophila Yki (the YAP homolog) and Scalloped (the TEAD homolog). Our study reveals TEAD as a new component in the Hippo pathway playing essential roles in mediating biological functions of YAP.

Pubmed ID: 18579750 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Animals | Breast Neoplasms | Carcinoma, Renal Cell | Cell Proliferation | Cell Transformation, Neoplastic | Cells, Cultured | DNA-Binding Proteins | Epithelial Cells | Gene Expression Regulation | Humans | Kidney Neoplasms | Mesoderm | Mice | NIH 3T3 Cells | Nuclear Proteins | Phosphoproteins | Promoter Regions, Genetic | Signal Transduction | Trans-Activators | Transcription Factors | Transcription, Genetic | Transcriptional Activation

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