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Updated: Feb 17, 2026

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Published on: October 27, 2020
Crosstalk between TGF-β signaling and epigenome
Jianbo Bai1,2, Qiaoran Xi1
1Ministry of Education Key Laboratory of Protein Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
The transforming growth factor beta (TGF-β) signaling pathway regulates gene expression through epigenetic mechanisms. This review highlights how R-SMAD interactions with epigenetic regulators impact development and disease, especially cancer.
Area of Science:
- Molecular Biology
- Developmental Biology
- Epigenetics
Background:
- The transforming growth factor beta (TGF-β) signaling pathway is crucial for embryonic development, tissue homeostasis, immunity, and repair.
- Dysregulation of TGF-β signaling is linked to severe diseases, including cancer.
- Epigenetic regulation plays a key role in mediating cellular responses to TGF-β signaling.
Purpose of the Study:
- To review epigenetic regulatory mechanisms within the TGF-β signaling pathway during mammalian development and disease.
- To elucidate the central role of receptor-activated SMAD (R-SMAD) interactions with epigenetic regulators.
- To discuss the implications of TGF-β signaling and epigenome crosstalk in transcriptional regulation.
Main Methods:
- Literature review focusing on epigenetic mechanisms in TGF-β signaling.
- Analysis of R-SMAD interactions with epigenetic modifiers.
- Examination of studies on mammalian development and disease models.
Main Results:
- TGF-β signaling utilizes epigenetic regulation for cell context-dependent responses.
- R-SMAD proteins recruit epigenetic regulators to modulate gene expression.
- Crosstalk between TGF-β signaling and the epigenome fine-tunes transcription.
Conclusions:
- Epigenetic regulation is integral to TGF-β signaling, influencing development and disease.
- The interaction between R-SMAD and epigenetic regulators is critical for shaping the transcriptome.
- Understanding this crosstalk offers insights into developmental processes and cancer progression.
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