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Transforming Growth Factor β-Induced Smad1/5 Phosphorylation in Epithelial Cells Is Mediated by Novel Receptor Complexes and Is Essential for Anchorage-Independent Growth
Open accessAbstract
Transforming growth factor beta (TGF-beta) signals predominantly through a receptor complex comprising ALK5 and TbetaRII to activate receptor-regulated Smads (R-Smads) Smad2 and Smad3. In endothelial cells, however, TGF-beta can additionally activate Smad1 and Smad5. Here, we report that TGF-beta also strongly induces phosphorylation of Smad1/5 in many different normal epithelial cells, epithelium-derived tumor cells, and fibroblasts. We demonstrate that TbetaRII and ALK5, as well as ALK2 and/or ALK3, are required for TGF-beta-induced Smad1/5 phosphorylation. We show that the simultaneous activation of the R-Smads Smad2/3 and Smad1/5 by TGF-beta results in the formation of mixed R-Smad complexes, containing, for example, phosphorylated Smad1 and Smad2. The prevalence of these mixed R-Smad complexes explains why TGF-beta-induced Smad1/5 phosphorylation does not result in transcriptional activation via bone morphogenetic protein (BMP)-responsive elements, which bind activated Smad1/5-Smad4 complexes that are induced by BMP stimulation. Thus, TGF-beta induces two parallel pathways: one signaling via Smad2-Smad4 or Smad3-Smad4 complexes and the other signaling via mixed R-Smad complexes. Finally, we assess the function of the novel arm of TGF-beta signaling and show that TGF-beta-induced Smad1/5 activation is not required for the growth-inhibitory effects of TGF-beta but is specifically required for TGF-beta-induced anchorage-independent growth.
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Cites
SPECIFICITY AND VERSATILITY IN TGF-β SIGNALING THROUGH SMADS
Feng, X.-H., & Derynck, R. (2005) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.21.022404.142018 · Cited by 1,869
TGF-β inhibits p70 S6 kinase via protein phosphatase 2A to induce G1 arrest
Petritsch, C., Beug, H., Balmain, A., & Oft, M. (2000) · Genes & Development · doi:10.1101/gad.854200 · Cited by 223
Cited by
TGF-β Activation and Function in Immunity
Travis, M. A., & Sheppard, D. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120257 · Cited by 856
Specificity, versatility, and control of TGF-β family signaling
Derynck, R., & Budi, E. H. (2019) · Science Signaling · doi:10.1126/scisignal.aav5183 · Cited by 785
TGF-β Superfamily Signaling in Embryonic Development and Homeostasis
Wu, M. Y., & Hill, C. S. (2009) · Developmental Cell · doi:10.1016/j.devcel.2009.02.012 · Cited by 746
Self-citationSignaling Receptors for TGF-β Family Members
Heldin, C.-H., & Moustakas, A. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022053 · Cited by 711
Transforming growth factor‐β in stem cells and tissue homeostasis
Xu, X., Zheng, L., Yuan, Q., Zhen, G., Crane, J. L., Zhou, X., & Cao, X. (2018) · Bone Research · doi:10.1038/s41413-017-0005-4 · Cited by 414
Metadata
- Authors
- Daly, A. C., Randall, R. A., & Hill, C. S.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2008-11-01
- Volume
- 28
- Issue
- 22
- Pages
- 6889-6902
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2124784029
- Cited by
- 277
- References
- 2
- FWCI
- 9.55
- Type
- journal article
- Language
- en
- Open access
- green
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- Daly, A. C., Randall, R. A., & Hill, C. S. (2008). Transforming Growth Factor β-Induced Smad1/5 Phosphorylation in Epithelial Cells Is Mediated by Novel Receptor Complexes and Is Essential for Anchorage-Independent Growth. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.01192-08
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