ArticleMolecular and cellular biology2010
Nuclear function of Smad7 promotes myogenesis.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- TEAD4 Promotes Myogenic Differentiation of Porcine Skeletal Muscle Satellite Cells.Animals : an open access journal from MDPI · 2026Article
- Aberrant expression of nuclear prothymosin α contributes to epithelial-mesenchymal transition in lung cancer.Molecular oncology · 2025Article
- Thrown for a loop: fibro-adipogenic progenitors in skeletal muscle fibrosis.American journal of physiology. Cell physiology · 2023Review
- Eutherian-Specific Functions of BetaM Acquired throughLife (Basel, Switzerland) · 2023Article
- Sulforaphane Enhanced Proliferation of Porcine Satellite Cells via Epigenetic Augmentation ofAnimals : an open access journal from MDPI · 2022Article
- Article
- 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
- Smad7:β-catenin complex regulates myogenic gene transcription.Cell death & disease · 2019Article
- Linc-smad7 promotes myoblast differentiation and muscle regeneration via sponging miR-125b.Epigenetics · 2018Article
- Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017Review
- Genome-Wide Association Study of Piglet Uniformity and Farrowing Interval.Frontiers in genetics · 2017Article
- SMAD7, an antagonist of TGF-beta signaling, is a candidate of prenatal skeletal muscle development and weaning weight in pigs.Molecular biology reports · 2016Article
- Genetic disruption of Smad7 impairs skeletal muscle growth and regeneration.The Journal of physiology · 2015Article
- Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ.Skeletal muscle · 2015Article
- Innate antiviral host defense attenuates TGF-β function through IRF3-mediated suppression of Smad signaling.Molecular cell · 2014Article
- Regulation of TGF-β Signal Transduction.Scientifica · 2014Review
- The dual role of Smad7 in the control of cancer growth and metastasis.International journal of molecular sciences · 2013Review
- The Scaffold attachment factor b1 (Safb1) regulates myogenic differentiation by facilitating the transition of myogenic gene chromatin from a repressed to an activated state.Nucleic acids research · 2013Article
- N-acetylcysteine attenuates cardiopulmonary bypass-induced lung injury in dogs.Journal of cardiothoracic surgery · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In the "canonical" view of transforming growth factor beta (TGF-beta) signaling, Smad7 plays an inhibitory role. While Smad7 represses Smad3 activation by TGF-beta, it does not reverse the inhibitory effect of TGF-beta on myogenesis, suggesting a different function in myogenic cells. We previously reported a promyogenic role of Smad7 mediated by an interaction with MyoD. Based on this association, we hypothesized a possible nuclear function of Smad7 independent of its role at the level of the receptor. We therefore engineered a chimera of Smad7 with a nuclear localization signal (NLS), which serves to prevent and therefore bypass binding to the TGF-beta receptor while concomitantly constitutively localizing Smad7 to the nucleus. This Smad7-NLS did not repress Smad3 activation by TGF-beta but did retain its ability to enhance myogenic gene activation and phenotypic myogenesis, indicating that the nuclear, receptor-independent function of Smad7 is sufficient to promote myogenesis. Furthermore, Smad7 physically interacts with MyoD and antagonizes the repressive effects of active MEK on MyoD. Reporter and myogenic conversion assays indicate a pivotal regulation of MyoD transcriptional properties by the balance between Smad7 and active MEK. Thus, Smad7 has a nuclear coactivator function that is independent of TGF-beta signaling and necessary to promote myogenic differentiation.
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Registered trials
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.