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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
20
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pubmed:dateCreated |
2009-5-11
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pubmed:abstractText |
The TAZ transcription co-activator has been shown to promote cell proliferation and to induce epithelial-mesenchymal transition. Recently we have demonstrated that TAZ is phosphorylated and inhibited by the Hippo tumor suppressor pathway, which is altered in human cancer. The mechanism of TAZ-mediated transcription is unclear. We demonstrate here that TEAD is a key downstream transcription factor mediating the function of TAZ. Disruption of TEAD-TAZ binding or silencing of TEAD expression blocked the function of TAZ to promote cell proliferation and to induce epithelial-mesenchymal transition, demonstrating TEAD as a key downstream effector of TAZ. We also identified CTGF, a gene that regulates cell adhesion, proliferation, and migration, as a direct target of TAZ and TEAD. Our study establishes a functional partnership between TAZ and TEAD under negative regulation by the Hippo signaling pathway.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-11118213,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-12202036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-14970209,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-15749018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-15766530,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-15782212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16099986,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16204178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16300735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16332960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16341207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16397409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-16740721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-17170128,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-17251353,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-17384585,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18227151,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18413727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18485877,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18568018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18579750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19324877-18622762
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
284
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13355-62
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pubmed:dateRevised |
2010-9-22
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pubmed:meshHeading |
pubmed-meshheading:19324877-Cell Adhesion,
pubmed-meshheading:19324877-Cell Line,
pubmed-meshheading:19324877-Cell Movement,
pubmed-meshheading:19324877-Cell Proliferation,
pubmed-meshheading:19324877-Connective Tissue Growth Factor,
pubmed-meshheading:19324877-Epithelium,
pubmed-meshheading:19324877-Gene Silencing,
pubmed-meshheading:19324877-Humans,
pubmed-meshheading:19324877-Mesoderm,
pubmed-meshheading:19324877-Phosphorylation,
pubmed-meshheading:19324877-Signal Transduction,
pubmed-meshheading:19324877-Transcription Factors,
pubmed-meshheading:19324877-Tumor Suppressor Proteins
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pubmed:year |
2009
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pubmed:articleTitle |
TEAD transcription factors mediate the function of TAZ in cell growth and epithelial-mesenchymal transition.
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pubmed:affiliation |
Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences, School of Life Science, Fudan University, Shanghai, China 200032.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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