19
Views
215
CrossRef citations to date
0
Altmetric
Research Article

Tumor Suppressor Smad4 Is a Transforming Growth Factor β-Inducible DNA Binding Protein

, , , , &
Pages 7019-7028 | Received 08 Jul 1997, Accepted 22 Sep 1997, Published online: 29 Mar 2023

References

  • Attisano, L., and J. L. Wrana. 1996. Signal transduction by members of the transforming growth factor-β superfamily. Cytokine Growth Factor Rev. 7:327–339.
  • Baker, J., and R. Harland. 1996. A novel mesoderm inducer, Madr2, functions in the activin signal transduction pathway. Genes Dev. 10:1880–1889.
  • Bassing, C. H., J. M. Yingling, D. J. Howe, T. Wang, W. W. He, M. L. Gustafson, P. Shah, P. K. Donahoe, and X. F. Wang. 1994. A transforming growth factor β type I receptor that signals to activate gene expression. Science 263:87–89.
  • Chen, X., M. J. Rubock, and M. Whitman. 1996. A transcriptional partner for MAD proteins in TGF-β signalling. Nature 383:691–696.
  • Chen, X., E. Weisberg, V. Fridmacher, M. Watanabe, and M. Whitman. 1997. Smad4 and FAST-1 in the assembly of activin-responsive factor. Nature 389:85–89.
  • Chen, Y., J. J. Lebrun, and W. Vale. 1996. Regulation of transforming growth factor β- and activin-induced transcription by mammalian Mad proteins. Proc. Natl. Acad. Sci. USA 93:12992–12997.
  • Datto, M. B., Y. Yu, and X. F. Wang. 1995. Functional analysis of the transforming growth factor β responsive elements in the WAF1/Cip1/p21 promoter. J. Biol. Chem. 270:28623–28628.
  • de Caestecker, M. P., P. Hemmati, S. Larisch-Bloch, R. Ajmera, A. B. Roberts, and R. J. Lechleider. 1997. Characterization of functional domains within Smad4/DPC4. J. Biol. Chem. 271:13690–13696.
  • Derynck, R., W. M. Gelbart, R. M. Harland, C. H. Heldin, S. E. Kern, J. Massague, D. A. Melton, M. Mlodzik, R. W. Padgett, A. B. Roberts, J. Smith, G. H. Thomsen, B. Vogelstein, and X.-F. Wang. 1996. Nomenclature: vertebrate mediators of TGF-β family signals. Cell 87:173.
  • Eppert, K., S. W. Scherer, H. Ozcelik, R. Pirone, P. Hoodless, H. Kim, L. C. Tsui, B. Bapat, S. Gallinger, I. L. Andrulis, G. H. Thomsen, J. L. Wrana, and L. Attisano. 1996. MADR2 maps to 18q21 and encodes a TGFβeta-regulated MAD-related protein that is functionally mutated in colorectal carcinoma. Cell 86:543–552.
  • Franzen, P., P. ten Dijke, H. Ichijo, H. Yamashita, P. Schulz, C.-H. Heldin, and K. Miyazono. 1993. Cloning of a TGFβ type I receptor that forms a heteromeric complex with the TGFβ type II receptor. Cell 75:681–692.
  • Graff, J. M., A. Bansal, and D. A. Melton. 1996. Xenopus Mad proteins transduce distinct subsets of signals for the TGF β superfamily. Cell 85:479–487.
  • Hahn, S. A., M. Schutte, A. T. Hoque, C. A. Moskaluk, L. T. da Costa, E. Rozenblum, C. L. Weinstein, A. Fischer, C. J. Yeo, R. H. Hruban, and S. E. Kern. 1996. DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. Science 271:350–353.
  • Hata, A., R. S. Lo, D. Wotton, G. Lagna, and J. Massague. 1997. Mutations increasing autoinhibition inactivate tumour suppressors Smad2 and Smad4. Nature 388:82–87.
  • Hoodless, P. A., T. Haerry, S. Abdollah, M. Stapleton, M. B. O’Connor, L. Attisano, and J. L. Wrana. 1996. MADR1, a MAD-related protein that functions in BMP2 signaling pathways. Cell 85:489–500.
  • Keeton, M. R., S. A. Curriden, A. J. van Zonneveld, and D. J. Loskutoff. 1991. Identification of regulatory sequences in the type 1 plasminogen activator inhibitor gene responsive to transforming growth factor β. J. Biol. Chem. 266:23048–23052.
  • Kim, J., K. Johnson, H. J. Chen, S. Carroll, and A. Laughon. 1997. Drosophila MAD binds to DNA and directly mediates activation of vestigial by decapentaplegic. Nature 388:304–308.
  • Kretzschmar, M., F. Liu, A. Hata, J. Doody, and J. Massague. 1997. The TGF-β family mediator Smad1 is phosphorylated directly and activated functionally by the BMP receptor kinase. Genes Dev. 11:984–995.
  • Lagna, G., A. Hata, A. Hemmati-Brivanlou, and J. Massague. 1996. Partnership between DPC4 and SMAD proteins in TGF-β signalling pathways. Nature 383:832–836.
  • Lechleider, R. J., M. P. de Caestecker, A. Dehejia, M. H. Polymeropoulos, and A. B. Roberts. 1996. Serine phosphorylation, chromosomal localization, and transforming growth factor-β signal transduction by human bsp-1. J. Biol. Chem. 271:17617–17620.
  • Li, J.-M., and X. F. Wang. Submitted for publication.
  • Lin, H. Y., X. F. Wang, E. Ng-Eaton, R. A. Weinberg, and H. F. Lodish. 1992. Expression cloning of the TGF-β type II receptor, a functional transmembrane serine/threonine kinase. Cell 68:775–785.
  • Liu, F., A. Hata, J. C. Baker, J. Doody, J. Carcamo, R. M. Harland, and J. Massague. 1996. A human Mad protein acting as a BMP-regulated transcriptional activator. Nature 381:620–623.
  • Macias-Silva, M., S. Abdollah, P. Hoodless, R. Pirone, L. Attisano, and J. Wrana. 1996. MADR2 is a substrate of the TGF-β receptor and its phosphorylation is required for nuclear accumulation and signaling. Cell 87:1215–1224.
  • Massague, J. 1996. TGFβ signaling: receptors, transducers, and Mad proteins. Cell 85:947–50.
  • Massague, J. 1990. The transforming growth factor-β family. Annu. Rev. Cell Biol. 6:597–641.
  • Roberts, A. B., and M. B. Sporn. 1993. Physiological actions and clinical applications of transforming growth factor-β (TGF-β). Growth Factors 8:1–9.
  • Savage, C., P. Das, A. L. Finelli, S. R. Townsend, C. Y. Sun, S. E. Baird, and R. W. Padgett. 1996. Caenorhabditis elegans genes sma-2, sma-3, and sma-4 define a conserved family of transforming growth factor β pathway components. Proc. Natl. Acad. Sci. USA 93:790–794.
  • Sekelsky, J. J., S. J. Newfeld, L. A. Raftery, E. H. Chartoff, and W. M. Gelbart. 1995. Genetic characterization and cloning of mothers against dpp, a gene required for decapentaplegic function in Drosophila melanogaster. Genetics 139:1347–1358.
  • Shi, Y., A. Hata, R. S. Lo, J. Massague, and N. P. Pavletich. 1997. A structural basis for mutational inactivation of the tumour suppressor, Smad4. Nature 388:87–93.
  • Suzuki, A., C. Chang, J. M. Yingling, X.-F. Wang, and A. Hemmati-Brivanlou. 1997. Smad5 induces ventral fates in Xenopus embryo. Dev. Biol. 184:402–405.
  • Tanaka, M., and W. Herr. 1990. Differential transcriptional activation by Oct-1 and Oct-2: interdependent activation domains induce Oct-2 phosphorylation. Cell 60:375–386.
  • Thomsen, G. H. 1996. Xenopus mothers against decapentaplegic is an embryonic ventralizing agent that acts downstream of the BMP-2/4 receptor. Development 122:2359–2366.
  • Wrana, J. L., L. Attisano, J. Carcamo, A. Zentella, J. Doody, M. Laiho, X. F. Wang, and J. Massague. 1992. TGF β signals through a heteromeric protein kinase receptor complex. Cell 71:1003–1014.
  • Wrana, J. L., L. Attisano, R. Wieser, F. Ventura, and J. Massague. 1994. Mechanism of activation of the TGF-β receptor. Nature 370:341–347.
  • Wu, R. Y., Y. Zhang, X. H. Feng, and R. Derynck. 1997. Heteromeric and homomeric interactions correlate with signaling activity and functional cooperativity of Smad3 and Smad4/DPC4. Mol. Cell. Biol. 17:2521–2528.
  • Yingling, J. M., P. Das, C. Savage, M. Zhang, R. W. Padgett, and X. F. Wang. 1996. Mammalian dwarfins are phosphorylated in response to TGF-β and are implicated in control of cell growth. Proc. Natl. Acad. Sci. USA 93:8940–8944.
  • Zhang, Y., X. Feng, R. We, and R. Derynck. 1996. Receptor-associated Mad homologues synergize as effectors of the TGF-β response. Nature 383:168–172.
  • Zhang, Y., T. Musci, and R. Derynck. 1997. The tumor suppressor Smad4/ DPC 4 as a central mediator of Smad function. Curr. Biol. 7:270–276.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.