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Gene Review

Tead1  -  TEA domain family member 1

Mus musculus

Synonyms: 2610024B07Rik, B230114H05Rik, Gtrgeo5, NTEF-1, Protein GT-IIC, ...
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Disease relevance of Tead1

  • TEF-1 transcription factors regulate activity of the mouse mammary tumor virus LTR [1].
  • Gel mobility shift assays revealed strong TEF-1 factor binding to one site using nuclear extracts from CV-1 cells and from the human breast cancer cell line MCF-7 [1].
  • Here we describe that VITO-1, a new SID (scalloped interaction domain)-containing protein, binds to TEF1 in vitro and strongly stimulates transcription of a MCAT reporter plasmid together with TEF-1 [2].
  • We demonstrated that TEF-1 represses hCS promoter activity in choriocarcinoma (BeWo) cells (Jiang, S.W., and Eberhardt, N.L. (1995) J. Biol. Chem. 270, 13609-13915), suggesting that TEF-1 interacts with basal transcription factors [3].
  • A TEF-1-element is required for activation of the promoter of pseudorabies virus glycoprotein X gene by IE180 [4].

High impact information on Tead1


Biological context of Tead1

  • In transient transfection assays, TEF-1 squelched the basal LTR activity and completely abrogated the response to the glucocorticoid dexamethasone [1].
  • Amino acid sequences deduced for ETFR-1 and -2 as well as those of other known proteins of the same family, TEF-1 and ETF, exhibited significant identity (63-75% overall) to each other not only in the TEA DNA binding domain but also in the C-terminal regions [9].
  • alpha(1)-Adrenergic signaling in cardiac myocytes activates the skeletal muscle alpha-actin gene through an MCAT cis-element, the binding site of the transcriptional enhancer factor-1 (TEF-1) family of transcription factors [10].
  • TEF1 itself is unable to activate reporter plasmids bearing TEF1-binding sites, suggesting that additional bridging or co-activating factors are necessary to allow interaction of TEF1 with the transcriptional machinery [2].
  • Both this interaction and sequence-specific DNA binding by TEAD were required for transcriptional activation in mouse cells [6].

Anatomical context of Tead1


Associations of Tead1 with chemical compounds

  • These TEF-1 factors also interfered with the response to dexamethasone [1].
  • Site-directed mutagenesis was used to inactivate eight serine residues of RTEF-1, not present in TEF-1, that are putative targets of alpha(1)-adrenergic-dependent kinases [15].
  • Chelation of nuclear but not cytosolic Ca(2+) increased TEAD activity two times above control [16].
  • Although the Sph element is similar in sequence to the SV40 element, the PLF Sph-binding factor is distinct from TEF-1, the factor that binds to the SV40 Sph motif [17].
  • Our findings demonstrate, for the first time, that the cell transformation and tumorigenesis induced by cadmium are due, at least in part, to the overexpression of TEF-1 delta, a novel cadmium-responsive proto-oncogene [18].
  • These effects could be reversed in vivo by mechanical overload, which decreased muscle creatine kinase-driven TEAD-1 transgene expression, and in cultured satellite cells by TEAD-1-specific small interfering RNA [19].

Physical interactions of Tead1


Regulatory relationships of Tead1

  • These results suggest that Tead activates the Foxa2 enhancer core element in the mouse node in cooperation with a second factor that binds to the 5' element, and that a similar mechanism also operates in the zebrafish shield [13].
  • However, the mechanism whereby Vgl-2 regulates TEF-1 factors and the requirement for Vgl-2 for muscle-specific gene expression were not known [21].
  • Functional analysis of this region reveals that the CCAAT box-binding protein nuclear factor Y (NF-Y) can substitute for TEF-1 in activating VSM alpha-actin transcription but that the TEF-1-binding site is essential for the maintenance of full transcriptional repression [22].

Other interactions of Tead1

  • Embryonic TEA domain-containing factor (ETF) belongs to the family of proteins structurally related to transcriptional enhancer factor-1 (TEF-1) and is implicated in neural development [23].
  • In contrast, alpha(1)-adrenergic stimulation did not alter, and phosphatase treatment increased, MCAT binding of TEF-1 and RTEF-1 [10].
  • Teads and their co-factor YAP65 activated the CE in P19 cells, and binding of Tead to CE was essential for enhancer activity [13].
  • These results suggest that the M-CAT binding factors consist of two different factors; the ubiquitous A2 is encoded by mTEF-1, but the muscle-specific A1 factor is distinct from mTEF-1 [20].
  • The objective was to determine if the newly discovered TEF1, MSY1, Puralpha and Purbeta VSM alpha-actin transcriptional reprogramming proteins (TRPs) were associated with development of chronic rejection histopathology in accepted murine cardiac allografts [24].

Analytical, diagnostic and therapeutic context of Tead1


  1. TEF-1 transcription factors regulate activity of the mouse mammary tumor virus LTR. Maeda, T., Maeda, M., Stewart, A.F. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  2. VITO-1 is an essential cofactor of TEF1-dependent muscle-specific gene regulation. Günther, S., Mielcarek, M., Krüger, M., Braun, T. Nucleic Acids Res. (2004) [Pubmed]
  3. TEF-1 transrepression in BeWo cells is mediated through interactions with the TATA-binding protein, TBP. Jiang, S.W., Eberhardt, N.L. J. Biol. Chem. (1996) [Pubmed]
  4. A TEF-1-element is required for activation of the promoter of pseudorabies virus glycoprotein X gene by IE180. Ou, C.J., Wong, M.L., Chang, T.J. Virus Genes (2002) [Pubmed]
  5. Cloning, expression, and transcriptional properties of the human enhancer factor TEF-1. Xiao, J.H., Davidson, I., Matthes, H., Garnier, J.M., Chambon, P. Cell (1991) [Pubmed]
  6. TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm. Vassilev, A., Kaneko, K.J., Shu, H., Zhao, Y., DePamphilis, M.L. Genes Dev. (2001) [Pubmed]
  7. Cardiomyocytes can be generated from marrow stromal cells in vitro. Makino, S., Fukuda, K., Miyoshi, S., Konishi, F., Kodama, H., Pan, J., Sano, M., Takahashi, T., Hori, S., Abe, H., Hata, J., Umezawa, A., Ogawa, S. J. Clin. Invest. (1999) [Pubmed]
  8. Transcription enhancer factor-1 (TEF-1) DNA binding sites can specifically enhance gene expression at the beginning of mouse development. Mélin, F., Miranda, M., Montreau, N., DePamphilis, M.L., Blangy, D. EMBO J. (1993) [Pubmed]
  9. A novel family of TEA domain-containing transcription factors with distinct spatiotemporal expression patterns. Yasunami, M., Suzuki, K., Ohkubo, H. Biochem. Biophys. Res. Commun. (1996) [Pubmed]
  10. Mouse DTEF-1 (ETFR-1, TEF-5) is a transcriptional activator in alpha 1-adrenergic agonist-stimulated cardiac myocytes. Maeda, T., Mazzulli, J.R., Farrance, I.K., Stewart, A.F. J. Biol. Chem. (2002) [Pubmed]
  11. Myocardin is a direct transcriptional target of Mef2, Tead and Foxo proteins during cardiovascular development. Creemers, E.E., Sutherland, L.B., McAnally, J., Richardson, J.A., Olson, E.N. Development (2006) [Pubmed]
  12. Identification of minimal enhancer elements sufficient for Pax3 expression in neural crest and implication of Tead2 as a regulator of Pax3. Milewski, R.C., Chi, N.C., Li, J., Brown, C., Lu, M.M., Epstein, J.A. Development (2004) [Pubmed]
  13. Tead proteins activate the Foxa2 enhancer in the node in cooperation with a second factor. Sawada, A., Nishizaki, Y., Sato, H., Yada, Y., Nakayama, R., Yamamoto, S., Nishioka, N., Kondoh, H., Sasaki, H. Development (2005) [Pubmed]
  14. Identification of a murine TEF-1-related gene expressed after mitogenic stimulation of quiescent fibroblasts and during myogenic differentiation. Hsu, D.K., Guo, Y., Alberts, G.F., Copeland, N.G., Gilbert, D.J., Jenkins, N.A., Peifley, K.A., Winkles, J.A. J. Biol. Chem. (1996) [Pubmed]
  15. Identification of the functional domain in the transcription factor RTEF-1 that mediates alpha 1-adrenergic signaling in hypertrophied cardiac myocytes. Ueyama, T., Zhu, C., Valenzuela, Y.M., Suzow, J.G., Stewart, A.F. J. Biol. Chem. (2000) [Pubmed]
  16. Inhibition of the TEF/TEAD transcription factor activity by nuclear calcium and distinct kinase pathways. Thompson, M., Andrade, V.A., Andrade, S.J., Pusl, T., Ortega, J.M., Goes, A.M., Leite, M.F. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
  17. Characterization of a delayed early serum response region. Groskopf, J.C., Linzer, D.I. Mol. Cell. Biol. (1994) [Pubmed]
  18. Oncogenic potential of mouse translation elongation factor-1 delta, a novel cadmium-responsive proto-oncogene. Joseph, P., Lei, Y.X., Whong, W.Z., Ong, T.M. J. Biol. Chem. (2002) [Pubmed]
  19. Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype. Tsika, R.W., Schramm, C., Simmer, G., Fitzsimons, D.P., Moss, R.L., Ji, J. J. Biol. Chem. (2008) [Pubmed]
  20. Both a ubiquitous factor mTEF-1 and a distinct muscle-specific factor bind to the M-CAT motif of the myosin heavy chain beta gene. Shimizu, N., Smith, G., Izumo, S. Nucleic Acids Res. (1993) [Pubmed]
  21. Transcription cofactor Vgl-2 is required for skeletal muscle differentiation. Chen, H.H., Maeda, T., Mullett, S.J., Stewart, A.F. Genesis (2004) [Pubmed]
  22. Negative regulation of the vascular smooth muscle alpha-actin gene in fibroblasts and myoblasts: disruption of enhancer function by sequence-specific single-stranded-DNA-binding proteins. Sun, S., Stoflet, E.S., Cogan, J.G., Strauch, A.R., Getz, M.J. Mol. Cell. Biol. (1995) [Pubmed]
  23. Structural organization and chromosomal assignment of the mouse embryonic TEA domain-containing factor (ETF) gene. Suzuki, K., Yasunami, M., Matsuda, Y., Maeda, T., Kobayashi, H., Terasaki, H., Ohkubo, H. Genomics (1996) [Pubmed]
  24. Reprogramming of vascular smooth muscle alpha-actin gene expression as an early indicator of dysfunctional remodeling following heart transplant. Subramanian, S.V., Kelm, R.J., Polikandriotis, J.A., Orosz, C.G., Strauch, A.R. Cardiovasc. Res. (2002) [Pubmed]
  25. A novel family of developmentally regulated mammalian transcription factors containing the TEA/ATTS DNA binding domain. Jacquemin, P., Hwang, J.J., Martial, J.A., Dollé, P., Davidson, I. J. Biol. Chem. (1996) [Pubmed]
  26. Vgl-4, a novel member of the vestigial-like family of transcription cofactors, regulates alpha1-adrenergic activation of gene expression in cardiac myocytes. Chen, H.H., Mullett, S.J., Stewart, A.F. J. Biol. Chem. (2004) [Pubmed]
  27. Cloning of human RTEF-1, a transcriptional enhancer factor-1-related gene preferentially expressed in skeletal muscle: evidence for an ancient multigene family. Stewart, A.F., Richard, C.W., Suzow, J., Stephan, D., Weremowicz, S., Morton, C.C., Adra, C.N. Genomics (1996) [Pubmed]
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