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Science 22 October 1999:
Vol. 286. no. 5440, pp. 771 - 774
DOI: 10.1126/science.286.5440.771
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Reports

Negative Feedback Regulation of TGF-beta Signaling by the SnoN Oncoprotein

Shannon L. Stroschein, 12 Wei Wang, 1 Sharleen Zhou, 2 Qiang Zhou, 2 Kunxin Luo 12*

Smad proteins mediate transforming growth factor-beta (TGF-beta ) signaling to regulate cell growth and differentiation. The SnoN oncoprotein was found to interact with Smad2 and Smad4 and to repress their abilities to activate transcription through recruitment of the transcriptional corepressor N-CoR. Immediately after TGF-beta stimulation, SnoN is rapidly degraded by the nuclear accumulation of Smad3, allowing the activation of TGF-beta target genes. By 2 hours, TGF-beta induces a marked increase in SnoN expression, resulting in termination of Smad-mediated transactivation. Thus, SnoN maintains the repressed state of TGF-beta -responsive genes in the absence of ligand and participates in negative feedback regulation of TGF-beta signaling.

1 Life Sciences Division, Lawrence Berkeley National Laboratory, and
2 Department of Molecular and Cell Biology, University of California, Berkeley, 229 Stanley Hall, Mail Code 3206, Berkeley, CA 94720, USA.
*   To whom correspondence should be addressed. E-mail: k_luo{at}ux5.lbl.gov

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The corepressor CtBP interacts with Evi-1 to repress transforming growth factor {beta} signaling.
K. Izutsu, M. Kurokawa, Y. Imai, K. Maki, K. Mitani, and H. Hirai (2001)
Blood 97, 2815-2822
   Abstract »    Full Text »    PDF »
Human T-cell leukemia virus type I oncoprotein Tax represses Smad-dependent transforming growth factor {beta} signaling through interaction with CREB-binding protein/p300.
N. Mori, M. Morishita, T. Tsukazaki, C.-Z. Giam, A. Kumatori, Y. Tanaka, and N. Yamamoto (2001)
Blood 97, 2137-2144
   Abstract »    Full Text »    PDF »
Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling.
H. Kaji, L. Canaff, J.-J. Lebrun, D. Goltzman, and G. N. Hendy (2001)
PNAS
   Abstract »    Full Text »
SMAD3 Represses Androgen Receptor-mediated Transcription.
S. A. Hayes, M. Zarnegar, M. Sharma, F. Yang, D. M. Peehl, P. t. Dijke, and Z. Sun (2001)
Cancer Res. 61, 2112-2118
   Abstract »    Full Text »
The hepatitis B virus encoded oncoprotein pX amplifies TGF-{beta} family signaling through direct interaction with Smad4: potential mechanism of hepatitis B virus-induced liver fibrosis.
D. K. Lee, S. H. Park, Y. Yi, S.-G. Choi, C. Lee, W. T. Parks, H. Cho, M. P. de Caestecker, Y. Shaul, A. B. Roberts, et al. (2001)
Genes & Dev. 15, 455-466
   Abstract »    Full Text »
Ski represses bone morphogenic protein signaling in Xenopus and mammalian cells.
W. Wang, F. V. Mariani, R. M. Harland, and K. Luo (2000)
PNAS 97, 14394-14399
   Abstract »    Full Text »    PDF »
Transforming Growth Factor beta -Independent Shuttling of Smad4 between the Cytoplasm and Nucleus.
C. E. Pierreux, F. J. Nicolás, and C. S. Hill (2000)
Mol. Cell. Biol. 20, 9041-9054
   Abstract »    Full Text »
Co-repressors 2000.
L. J. BURKE and A. BANIAHMAD (2000)
FASEB J 14, 1876-1888
   Abstract »    Full Text »
Role of Transforming Growth Factor-{beta} Signaling in Cancer.
M. P. de Caestecker, E. Piek, and A. B. Roberts (2000)
J Natl Cancer Inst 92, 1388-1402
   Abstract »    Full Text »    PDF »
BF-1 Interferes with Transforming Growth Factor beta Signaling by Associating with Smad Partners.
C. Dou, J. Lee, B. Liu, F. Liu, J. Massague, S. Xuan, and E. Lai (2000)
Mol. Cell. Biol. 20, 6201-6211
   Abstract »    Full Text »
Vitamin D3 Up-Regulated Protein 1 Mediates Oxidative Stress Via Suppressing the Thioredoxin Function.
E. Junn, S. H. Han, J. Y. Im, Y. Yang, E. W. Cho, H. D. Um, D. K. Kim, K. W. Lee, P. L. Han, S. G. Rhee, et al. (2000)
J. Immunol. 164, 6287-6295
   Abstract »    Full Text »    PDF »
Roles of Autocrine TGF-{beta} Receptor and Smad Signaling in Adipocyte Differentiation.
L. Choy, J. Skillington, and R. Derynck (2000)
J. Cell Biol. 149, 667-682
   Abstract »    Full Text »    PDF »
Controlling TGF-beta signaling.
J. Massagué and Y.-G. Chen (2000)
Genes & Dev. 14, 627-644
   Full Text »


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