ArticleNucleic acids research2003
Smad proteins regulate transcriptional induction of the SM22alpha gene by TGF-beta.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 109 citations in OpenAlex.
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- Asparagine endopeptidase protects podocytes in adriamycin-induced nephropathy by regulating actin dynamics through cleaving transgelin.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Transgelin exacerbates pulmonary artery smooth muscle cell dysfunction in shunt-related pulmonary arterial hypertension.ESC heart failure · 2022Article
- The actin depolymerizing factor destrin serves as a negative feedback inhibitor of smooth muscle cell differentiation.American journal of physiology. Heart and circulatory physiology · 2021Article
- A 3D Renal Proximal Tubule on Chip Model Phenocopies Lowe Syndrome and Dent II Disease Tubulopathy.International journal of molecular sciences · 2021Article
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
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- Transgelin is a poor prognostic factor associated with advanced colorectal cancer (CRC) stage promoting tumor growth and migration in a TGFβ-dependent manner.Cell death & disease · 2020Article
- TGF-β1 induces VEGF expression in human granulosa-lutein cells: a potential mechanism for the pathogenesis of ovarian hyperstimulation syndrome.Experimental & molecular medicine · 2020Article
- Transgelins: Cytoskeletal Associated Proteins Implicated in the Metastasis of Colorectal Cancer.Frontiers in cell and developmental biology · 2020Review
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- TGF-β-induced transgelin promotes bladder cancer metastasis by regulating epithelial-mesenchymal transition and invadopodia formation.EBioMedicine · 2019Article
- Lineage-specific events underlie aortic root aneurysm pathogenesis in Loeys-Dietz syndrome.The Journal of clinical investigation · 2019Article
- TGFβ, smooth muscle cells and coronary artery disease: a review.Cellular signalling · 2019Review
- Mesenchyme homeobox 1 mediates transforming growth factor-β (TGF-β)-induced smooth muscle cell differentiation from mouse mesenchymal progenitors.The Journal of biological chemistry · 2018Article
- Loss of heme oxygenase-1 accelerates mesodermal gene expressions during embryoid body development from mouse embryonic stem cells.Redox biology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Smad proteins transduce signals from transforming growth factor-beta (TGF-beta) receptors and regulate transcription of target genes. TGF-beta is implicated in the regulation of the smooth muscle cell specific gene SM22alpha, but little is known about how Smads are involved in SM22alpha gene transcription. In this report, we demonstrate that TGF-beta activation of the SM22alpha promoter is Smad dependent in C3H10T1/2 cells, BALB 3T3 cells and neural crest Monc-1 cells. We find that the promoter region from -162 to +41 is sufficient to up-regulate the reporter gene upon TGF-beta induction. Smad3, Smad1 and Smad4 are found in TGF-beta inducible complexes that bind to a region containing a Smad binding site (SBS) and a medea box. Both the SBS and medea box are necessary for complex formation and are functionally important. Smad4 is limiting for TGF-beta induction, and Smad3, but not Smad1, significantly contributes to maximal activation. Time course luciferase assays and time course gel mobility shift assays reveal that the Smad3/4 complex is largely responsible for the immediate response of the SM22alpha promoter to TGF-beta induction, and also contributes to the maximal promoter activity. We further demonstrate that AP-1 elements contribute to induction of the SM22alpha promoter by TGF-beta.
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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.