The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Transforming Growth Factor β-Mediated Transcriptional Repression of c-myc Is Dependent on Direct Binding of Smad3 to a Novel Repressive Smad Binding Element
Open accessAbstract
Smad proteins are the most well-characterized intracellular effectors of the transforming growth factor beta (TGF-beta) signal. The ability of the Smads to act as transcriptional activators via TGF-beta-induced recruitment to Smad binding elements (SBE) within the promoters of TGF-beta target genes has been firmly established. However, the elucidation of the molecular mechanisms involved in TGF-beta-mediated transcriptional repression are only recently being uncovered. The proto-oncogene c-myc is repressed by TGF-beta, and this repression is required for the manifestation of the TGF-beta cytostatic program in specific cell types. We have shown that Smad3 is required for both TGF-beta-induced repression of c-myc and subsequent growth arrest in keratinocytes. The transcriptional repression of c-myc is dependent on direct Smad3 binding to a novel Smad binding site, termed a repressive Smad binding element (RSBE), within the TGF-beta inhibitory element (TIE) of the c-myc promoter. The c-myc TIE is a composite element, comprised of an overlapping RSBE and a consensus E2F site, that is capable of binding at least Smad3, Smad4, E2F-4, and p107. The RSBE is distinct from the previously defined SBE and may partially dictate, in conjunction with the promoter context of the overlapping E2F site, whether the Smad3-containing complex actively represses, as opposed to transactivates, the c-myc promoter.
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Cites
pl5INK4B is a potentia| effector of TGF-β-induced cell cycle arrest
Hannon, G. J., & Beach, D. (1994) · Nature · doi:10.1038/371257a0 · Cited by 1,950
Cited by
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 Family Signaling in the Control of Cell Proliferation and Survival
Zhang, Y., Alexander, P. B., & Wang, X.-F. (2017) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022145 · Cited by 626
Self-citationMYC: Connecting selective transcriptional control to global RNA production
Kress, T. R., Sabò, A., & Amati, B. (2015) · Nature reviews. Cancer · doi:10.1038/nrc3984 · Cited by 521
Cyclin-dependent kinases regulate the antiproliferative function of Smads
Matsuura, I., Denissova, N. G., Wang, G., He, D., Long, J., & Liu, F. (2004) · Nature · doi:10.1038/nature02650 · Cited by 503
PPM1A Functions as a Smad Phosphatase to Terminate TGFβ Signaling
Lin, X., Duan, X., Liang, Y.-Y., Su, Y., Wrighton, K. H., Long, J., Hu, M., Davis, C. M., Wang, J., Brunicardi, F. C., et al. (2006) · Cell · doi:10.1016/j.cell.2006.03.044 · Cited by 485
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Metadata
- Authors
- Frederick, J. P., Liberati, N. T., Waddell, D. S., Shi, Y., & Wang, X.-F.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2004-03-01
- Volume
- 24
- Issue
- 6
- Pages
- 2546-2559
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2162937786
- Cited by
- 221
- References
- 1
- FWCI
- 6.34
- Type
- journal article
- Language
- en
- Open access
- green
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- Frederick, J. P., Liberati, N. T., Waddell, D. S., Shi, Y., & Wang, X.-F. (2004). Transforming Growth Factor β-Mediated Transcriptional Repression of c-myc Is Dependent on Direct Binding of Smad3 to a Novel Repressive Smad Binding Element. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.24.6.2546-2559.2004
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