Cited by 2,498Hippo pathway signaling and YAP/TAZCancer-related molecular mechanisms researchSignaling Pathways in Disease

TEAD mediates YAP-dependent gene induction and growth control

Open access
Zhao, Bin, Ye, Xin, Yu, Jindan, Li, Li, Li, Weiquan, Li, Siming, Yu, Jianjun, Lin, Jiandie D. +4 more·2008·Genes & Development

Abstract

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.

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Crossref · 10.1101/gad.1664408

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  • In a human study, the mRNA of Hippo pathway marker genes CYR61 and CTGF increased 14-fold and 2.5-fold, respectively, 30 min after exercise.

    “The mRNA of the Hippo pathway marker genes cysteine-rich angiogenic protein 61 (CYR61) and connective tissue growth factor (CTGF) (77, 164) increased 14- and 2.5-fold 30 min after exercise, respectively.”

    From The Hippo signal transduction network for exercise physiologists (2016) · cites this paper as [164]

    The citation follows the identification of CYR61 and CTGF as Hippo pathway marker genes, rather than the exercise result. In “CTGF is a direct YAP-TEAD target gene required for cell growth” (page unavailable), the paper establishes CTGF as a Hippo-pathway target, but our copy does not establish CYR61 as one. It does not report the human exercise measurements or their fold changes. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • YAP S94A, which cannot associate with TEAD family members, did not affect MRTX-849 response.

    “By contrast, YAP S94A , which encodes a mutant unable to associate with TEAD family members (39), did not affect MRTX-849 response”

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Authors
Zhao, B., Ye, X., Yu, J., Li, L., Li, W., Li, S., Yu, J., Lin, J. D., Wang, C.-Y., Chinnaiyan, A. M., Lai, Z.-C., & Guan, K.-L.
Affiliations
  • University of Michigan (US)
  • Pennsylvania State University (US)
  • University of California, Los Angeles (US)
  • University of California San Diego (US)
Venue
Genes & Development
Published
2008-06-25
Volume
22
Issue
14
Pages
1962-1971
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2167978765
Cited by
2,498
References
35
Citations by year
2026: 122 · 2025: 172 · 2024: 197 · 2023: 167 · 2022: 209 · 2021: 201 · 2020: 223 · 2019: 187 · 2018: 181 · 2017: 161 · 2016: 152 · 2015: 147 · 2014: 102 · 2013: 88 · 2012: 68
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Science Foundation
  • University of Michigan
  • National Institutes of Health
  • Horace H. Rackham School of Graduate Studies, University of Michigan
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
YAP, TEAD transcription factors, Hippo signaling pathway, cell growth regulation, oncogenic transformation, epithelial-mesenchymal transition, connective tissue growth factor, YAP phosphorylation, Scalloped, transcriptional coactivation
MeSH terms
YAP-Signaling Proteins, TEA Domain Transcription Factors, Animals, Breast Neoplasms, Carcinoma, Renal Cell, Cell Transformation, Neoplastic, Cells, Cultured, DNA-Binding Proteins, Epithelial Cells, Gene Expression Regulation, Humans, Kidney Neoplasms, Mesoderm, Nuclear Proteins, Phosphoproteins, Promoter Regions, Genetic, Transcription Factors, Transcription, Genetic, Signal Transduction, Transcriptional Activation, Trans-Activators, Cell Cycle Proteins, NIH 3T3 Cells, Adaptor Proteins, Signal Transducing, Cell Proliferation, Mice

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