ArticleMolecular biology of the cell2004
Induction of vascular smooth muscle alpha-actin gene transcription in transforming growth factor beta1-activated myofibroblasts mediated by dynamic interplay between the Pur repressor proteins and Sp1/Smad coactivators.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Epigenetic alteration of smooth muscle cells regulates endothelin-dependent blood pressure and hypertensive arterial remodeling.The Journal of clinical investigation · 2025Article
- The writing on the arterial wall: epigenetic control of blood pressure and vascular remodeling.The Journal of clinical investigation · 2025Article
- DUSP8 induces TGF-β-stimulated IL-9 transcription and Th9-mediated allergic inflammation by promoting nuclear export of Pur-α.The Journal of clinical investigation · 2023Article
- Six Shades of Vascular Smooth Muscle Cells Illuminated by KLF4 (Krüppel-Like Factor 4).Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Purine-rich element binding protein B attenuates the coactivator function of myocardin by a novel molecular mechanism of smooth muscle gene repression.Molecular and cellular biochemistry · 2021Article
- The Molecular Function of PURA and Its Implications in Neurological Diseases.Frontiers in genetics · 2021Review
- Methylation in pericytes after acute injury promotes chronic kidney disease.The Journal of clinical investigation · 2020Article
- Myofibroblasts and Fibrosis: Mitochondrial and Metabolic Control of Cellular Differentiation.Circulation research · 2020Review
- Structural and functional analysis of single-nucleotide polymorphic variants of purine-rich element-binding protein B.Journal of cellular biochemistry · 2019Article
- Ascorbic acid promotes a TGFPhysiological reports · 2017Article
- Electrostatic and Hydrophobic Interactions Mediate Single-Stranded DNA Recognition and Acta2 Repression by Purine-Rich Element-Binding Protein B.Biochemistry · 2016Article
- Effects of Tongmai oral liquid in femoral ateriovenous fistula.BMC complementary and alternative medicine · 2015Article
- Article
- Activation of MRTF-A-dependent gene expression with a small molecule promotes myofibroblast differentiation and wound healing.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Structural basis of multisite single-stranded DNA recognition and ACTA2 repression by purine-rich element binding protein B (Purβ).Biochemistry · 2013Article
- Article
- Loss-of-function thrombospondin-1 mutations in familial pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Myocardin-related transcription factors A and B are key regulators of TGF-β1-induced fibroblast to myofibroblast differentiation.The Journal of investigative dermatology · 2011Article
- Delayed stress fiber formation mediates pulmonary myofibroblast differentiation in response to TGF-β.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro-inflammatory factors in vivo and in vitro.British journal of pharmacology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The mouse vascular smooth muscle alpha-actin (SMA) gene enhancer is activated in fibroblasts by transforming growth factor beta1 (TGFbeta1), a potent mediator of myofibroblast differentiation and wound healing. The SMA enhancer contains tandem sites for the Sp1 transcriptional activator protein and Puralpha and beta repressor proteins. We have examined dynamic interplay between these divergent proteins to identify checkpoints for possible control of myofibroblast differentiation during chronic inflammatory disease. A novel element in the SMA enhancer named SPUR was responsible for both basal and TGFbeta1-dependent transcriptional activation in fibroblasts and capable of binding Sp1 and Pur proteins. A novel Sp1:Pur:SPUR complex was dissociated when SMA enhancer activity was increased by TGFbeta1 or Smad protein overexpression. Physical association of Pur proteins with Smad2/3 was observed as was binding of Smads to an upstream enhancer region that undergoes DNA duplex unwinding in TGFbeta1-activated myofibroblasts. Purbeta repression of the SMA enhancer could not be relieved by TGFbeta1, whereas repression mediated by Puralpha was partially rescued by TGFbeta1 or overexpression of Smad proteins. Interplay between Pur repressor isoforms and Sp1 and Smad coactivators may regulate SMA enhancer output in TGFbeta1-activated myofibroblasts during episodes of wound repair and tissue remodeling.
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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.