学术探索
学术期刊
新闻热点
数据分析
智能评审

Negative feedback regulation of TGF-β signaling by the SnoN oncoprotein

被引：430
作者：
Stroschein, SL
Wang, W
Zhou, SL
Zhou, Q
Luo, KX
机构：
[1] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
来源：
SCIENCE | 1999年 / 286卷 / 5440期
关键词：
D O I：
10.1126/science.286.5440.771
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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.
引用
收藏
页码：771 / 774
页数：4
相关论文
共 49 条
  • [41] Smad-dependent transcriptional activation of human type VII collagen gene (COL7A1) promoter by transforming growth factor-β
    Vindevoghel, L
    Kon, A
    Lechleider, RJ
    Uitto, J
    Roberts, AB
    Mauviel, A
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (21) : 13053 - 13057
  • [42] Wong C, 1999, MOL CELL BIOL, V19, P1821
  • [43] Heteromeric and homomeric interactions correlate with signaling activity and functional cooperativity of Smad3 and Smad4/DPC4
    Wu, RY
    Zhang, Y
    Feng, XH
    Derynck, R
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (05) : 2521 - 2528
  • [44] Tumor suppressor Smad4 is a transforming growth factor beta-inducible DNA binding protein
    Yingling, JM
    Datto, MB
    Wong, C
    Frederick, JP
    Liberati, NT
    Wang, XF
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (12) : 7019 - 7028
  • [45] Human Smad3 and Smad4 are sequence-specific transcription activators
    Zawel, L
    Dai, JL
    Buckhaults, P
    Zhou, SB
    Kinzler, KW
    Vogelstein, B
    Kern, SE
    [J]. MOLECULAR CELL, 1998, 1 (04) : 611 - 617
  • [46] The tumor suppressor Smad4 DPC 4 as a central mediator of Smad function
    Zhang, Y
    Musci, T
    Derynck, R
    [J]. CURRENT BIOLOGY, 1997, 7 (04) : 270 - 276
  • [47] Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-β-induced transcription
    Zhang, Y
    Feng, XH
    Derynck, R
    [J]. NATURE, 1998, 394 (6696) : 909 - 913
  • [48] Receptor-associated Mad homologues synergize as effectors of the TGF-beta response
    Zhang, Y
    Feng, XH
    Wu, RY
    Derynck, R
    [J]. NATURE, 1996, 383 (6596) : 168 - 172
  • [49] Transcription elongation factor P-TEFb mediates Tat activation of HIV-1 transcription at multiple stages
    Zhou, Q
    Chen, D
    Pierstorff, E
    Luo, KX
    [J]. EMBO JOURNAL, 1998, 17 (13) : 3681 - 3691
12345