ArticleCell death & disease2019
Smad7:β-catenin complex regulates myogenic gene transcription.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Copper Promotes Myogenic Differentiation of Bovine Skeletal Muscle-Derived Cells by Activating the HIF-1α/β-catenin Signaling Axis.Biological trace element research · 2026Article
- SMAD7 regulates the canonical Wnt signaling through TGF-β cascade crosstalk and SMAD7/β-CATENIN transcription factor complex formation during tooth regeneration.International journal of oral science · 2026Article
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- Emerging regulatory mechanisms and functions of biomolecular condensates: implications for therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Liquid-liquid phase separation of membrane-less condensates: from biogenesis to function.Frontiers in cell and developmental biology · 2025Review
- FoxP1 Represses MEF2A in Striated Muscle.Molecular and cellular biology · 2024Article
- Dynamic chromatin architectures provide insights into the genetics of cattle myogenesis.Journal of animal science and biotechnology · 2023Article
- Temporal mechanisms of myogenic specification in human induced pluripotent stem cells.Science advances · 2021Article
- Potential roles of mediator Complex Subunit 13 in Cardiac Diseases.International journal of biological sciences · 2021Review
- Maintenance of the Undifferentiated State in Myogenic Progenitor Cells by TGFβ Signaling is Smad Independent and Requires MEK Activation.International journal of molecular sciences · 2020Article
- UBE2M promotes cell proliferation via the β-catenin/cyclin D1 signaling in hepatocellular carcinoma.Aging · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Recent reports indicate that Smad7 promotes skeletal muscle differentiation and growth. We previously documented a non-canonical role of nuclear Smad7 during myogenesis, independent of its role in TGF-β signaling. Here further characterization of the myogenic function of Smad7 revealed β-catenin as a Smad7 interacting protein. Biochemical analysis identified a Smad7 interaction domain (SID) between aa575 and aa683 of β-catenin. Reporter gene analysis and chromatin immunoprecipitation demonstrated that Smad7 and β-catenin are cooperatively recruited to the extensively characterized ckm promoter proximal region to facilitate its muscle restricted transcriptional activation in myogenic cells. Depletion of endogenous Smad7 and β-catenin in muscle cells reduced ckm promoter activity indicating their role during myogenesis. Deletion of the β-catenin SID substantially reduced the effect of Smad7 on the ckm promoter and exogenous expression of SID abolished β-catenin function, indicating that SID functions as a trans dominant-negative regulator of β-catenin activity. β-catenin interaction with the Mediator kinase complex through its Med12 subunit led us to identify MED13 as an additional Smad7-binding partner. Collectively, these studies document a novel function of a Smad7-MED12/13-β-catenin complex at the ckm locus, indicating a key role of this complex in the program of myogenic gene expression underlying skeletal muscle development and regeneration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.