2024年12月25日 · SMAD7 (SMAD Family Member 7) is a Protein Coding gene. Diseases associated with SMAD7 include Colorectal Cancer 3 and Breast Cancer. Among its related pathways are Gene expression (Transcription) and Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer.

1997年10月9日 · Transfection of Smad7 blocks responses mediated by TGF-β in mammalian cells, and injection of Smad7 RNA into Xenopus embryos blocks activin/TGF-β signalling. Smad7 associates stably with the...

In this review, we discuss advances in research of Smad7, a member of the I-Smads family and a negative regulator of TGF-β signaling, and mainly review the expression and its function in diseases. Smad7 inhibits the activation of the NF-κB and TGF-β signaling pathways and plays a pivotal role in the prevention and treatment of various diseases.

Inhibitory Smads, including Smad6 and Smad7, are key regulators of TGF-beta/bone morphogenetic protein (BMP) signaling by negative feedback loops. They can form stable complexes with activated type I receptors and thereby blocking the phosphorylation of R-Smads, or recruit ubiquitin E3 ligases, such as Smurf1/2, resulting in the ubiquitination ...

2019年5月16日 · Reporter gene analysis and chromatin immunoprecipitation demonstrated that Smad7 and β-catenin are cooperatively recruited to the extensively characterized ckm promoter proximal region to...

2011年2月15日 · Smad7 has been well established to be a key negative regulator of TGF-β signalling. It antagonizes TGF-β signalling through multiple mechanisms in the cytoplasm and in the nucleus.

Smad7 is an inhibitory Smad protein that blocks Transforming Growth Factor-beta (TGF-β) signaling through a negative feedback loop, also capable of mediating the crosstalk between TGF-β and other signaling pathways.

2002年8月1日 · Smad7 is a major inhibitory regulator of transforming growth factor (TGF)-β signaling. Smad7 expression is induced by TGF-β itself and other signaling pathways, indicating a key role for Smad7 in feedback or cross-talk control of TGF-β signaling.

In this study we report a novel mechanism whereby Smad7 antagonizes TGF-β signaling at the Smad level. Smad7 oligomerized with R-Smad proteins upon TGF-β signaling and directly inhibited R-Smad activity, as assessed by Gal4-luciferase reporter assays.

Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity. Smad7 appears to be upregulated in endometrial cancers compared to normal endometrium.