The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.
Targeted Disruption of Smad3 Reveals an Essential Role in Transforming Growth Factor β-Mediated Signal Transduction
Open accessAbstract
The Smads are a family of nine related proteins which function as signaling intermediates for the transforming growth factor beta (TGF-beta) superfamily of ligands. To discern the in vivo functions of one of these Smads, Smad3, we generated mice harboring a targeted disruption of this gene. Smad3 null mice, although smaller than wild-type littermates, are viable, survive to adulthood, and exhibit an early phenotype of forelimb malformation. To study the cellular functions of Smad3, we generated Smad3 null mouse embryonic fibroblasts (MEFs) and dermal fibroblasts. We demonstrate that null MEFs have lost the ability to form Smad-containing DNA binding complexes and are unable to induce transcription from the TGF-beta-responsive promoter construct, p3TP-lux. Using the primary dermal fibroblasts, we also demonstrate that Smad3 is integral for induction of endogenous plasminogen activator inhibitor 1. We subsequently demonstrate that Smad3 null MEFs are partially resistant to TGF-beta's antiproliferative effect, thus firmly establishing a role for Smad3 in TGF-beta-mediated growth inhibition. We next examined cells in which Smad3 is most highly expressed, specifically cells of immune origin. Although no specific developmental defect was detected in the immune system of the Smad3 null mice, a functional defect was observed in the ability of TGF-beta to inhibit the proliferation of splenocytes activated by specific stimuli. In addition, primary splenocytes display defects in TGF-beta-mediated repression of cytokine production. These data, taken together, establish a role for Smad3 in mediating the antiproliferative effects of TGF-beta and implicate Smad3 as a potential effector for TGF-beta in modulating immune system function.
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Cites
Massagué, J. (1998) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.67.1.753 · Cited by 7,556
TGF-β signalling from cell membrane to nucleus through SMAD proteins
Heldin, C.-H., Miyazono, K., & ten Dijke, P. (1997) · Nature · doi:10.1038/37284 · Cited by 3,696
The Transforming Growth Factor-beta Family
Massague, J. (1990) · Annual Review of Cell Biology · doi:10.1146/annurev.cb.06.110190.003121 · Cited by 3,015
DPC4 , A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1
Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., da Costa, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., et al. (1996) · Science · doi:10.1126/science.271.5247.350 · Cited by 2,337
Mechanism of activation of the TGF-β receptor
Wrana, J. L., Attisano, L., Wieser, R., Ventura, F., & Massagué, J. (1994) · Nature · doi:10.1038/370341a0 · Cited by 2,337
Kulkarni, A. B., Huh, C. G., Becker, D., Geiser, A., Lyght, M., Flanders, K. C., Roberts, A. B., Sporn, M. B., Ward, J. M., & Karlsson, S. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.2.770 · Cited by 1,967
Dennler, S. (1998) · The EMBO Journal · doi:10.1093/emboj/17.11.3091 · Cited by 1,793
Kehrl, J. H., Wakefield, L. M., Roberts, A. B., Jakowlew, S., Alvarez-Mon, M., Derynck, R., Sporn, M. B., & Fauci, A. S. (1986) · The Journal of experimental medicine · doi:10.1084/jem.163.5.1037 · Cited by 1,582
TGFβ signals through a heteromeric protein kinase receptor complex
Wrana, J. L., Attisano, L., Cárcamo, J., Zentella, A., Doody, J., Laiho, M., Wang, X.-F., & Massague, J. (1992) · Cell · doi:10.1016/0092-8674(92)90395-s · Cited by 1,526
Self-citationNeonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene
Tybulewicz, V. L. J., Crawford, C. E., Jackson, P. K., Bronson, R. T., & Mulligan, R. C. (1991) · Cell · doi:10.1016/0092-8674(91)90011-m · Cited by 1,281
Cited by
TGF-β Signaling in Tumor Suppression and Cancer Progression
Derynck, R., Akhurst, R. J., & Balmain, A. (2001) · Nature Genetics · doi:10.1038/ng1001-117 · Cited by 2,275
Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response
Ashcroft, G. S., Yang, X., Glick, A. B., Weinstein, M., Letterio, J. J., Mizel, D. E., Anzano, M., Greenwell-Wild, T., Wahl, S. M., Deng, C., et al. (1999) · Nature Cell Biology · doi:10.1038/12971 · Cited by 911
Genetic Analysis of the Mammalian Transforming Growth Factor-β Superfamily
Chang, H., Brown, C. W., & Matzuk, M. M. (2002) · Endocrine Reviews · doi:10.1210/er.2002-0003 · Cited by 787
Protection from obesity and diabetes by blockade of TGF-β/smad3 signaling
Yadav, H., Quijano, C., Kamaraju, A. K., Gavrilova, O., Malek, R., Chen, W., Zerfas, P., Zhigang, D., Wright, E. C., Stuelten, C., et al. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.04.013 · Cited by 709
Transforming Growth Factor-β1 to the Bone
Janssens, K., ten Dijke, P., Janssens, S., & Van Hul, W. (2005) · Endocrine Reviews · doi:10.1210/er.2004-0001 · Cited by 710
Metadata
- Authors
- Datto, M. B., Frederick, J. P., Pan, L., Borton, A. J., Zhuang, Y., & Wang, X.-F.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1999-04-01
- Volume
- 19
- Issue
- 4
- Pages
- 2495-2504
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W1897269170
- Cited by
- 473
- References
- 69
- FWCI
- 11.20
- Type
- journal article
- Language
- en
- Open access
- green
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- Datto, M. B., Frederick, J. P., Pan, L., Borton, A. J., Zhuang, Y., & Wang, X.-F. (1999). Targeted Disruption of Smad3 Reveals an Essential Role in Transforming Growth Factor β-Mediated Signal Transduction. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.19.4.2495
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