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Updated: Jun 4, 2026

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Smad7: not only a regulator, but also a cross-talk mediator of TGF-β signalling

Xiaohua Yan1, Ye-Guang Chen

  • 1The State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Tsinghua University, Beijing, China.

The Biochemical Journal
|January 29, 2011
PubMed

Insights

Transforming growth factor-β (TGF-β) signaling is regulated by Smad7, a key negative regulator. Smad7 antagonizes TGF-β actions and influences development, homeostasis, and diseases like cancer and fibrosis.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Biochemistry

Background:

  • Transforming growth factor-β (TGF-β) is a crucial cytokine involved in numerous cellular functions.
  • TGF-β exerts its effects via membrane receptors and downstream signaling molecules, including Smad proteins.
  • Smad7 is a well-established negative regulator of TGF-β signaling.

Purpose of the Study:

  • To elucidate the multifaceted roles of Smad7 in TGF-β signaling.
  • To understand Smad7's mechanisms of action in both the cytoplasm and nucleus.
  • To highlight Smad7's significance as a cross-talk mediator and its implications in human diseases.

Main Methods:

  • Analysis of Smad7's inhibitory mechanisms.
  • Investigation of Smad7's transcriptional regulation by TGF-β and other growth factors.
  • Review of Smad7's involvement in cellular processes and disease pathogenesis.

Main Results:

  • Smad7 effectively antagonizes TGF-β signaling through diverse cytoplasmic and nuclear mechanisms.
  • Smad7 expression is induced by TGF-β and other growth factors, indicating its role in pathway cross-talk.
  • Altered Smad7 expression is linked to various human diseases, including cancer, fibrosis, and inflammation.

Conclusions:

  • Smad7 is a pivotal negative regulator of TGF-β signaling with broad implications.
  • Smad7's regulatory functions are critical for embryonic development and adult homeostasis.
  • Dysregulation of Smad7 contributes to the pathogenesis of significant human diseases.

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