ArticleThe EMBO journal2006
Smads orchestrate specific histone modifications and chromatin remodeling to activate transcription.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
90 citing papers in PubMed, 158 citations in OpenAlex.
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- A single-cell sequence analysis of mouse subcutaneous white adipose tissue reveals dynamic changes during weaning.Communications biology · 2024Article
- No time to die: Epigenetic regulation of natural killer cell survival.Immunological reviews · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
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- Suppression of preadipocyte determination by SOX4 limits white adipocyte hyperplasia in obesity.iScience · 2023Article
- A microbiota-epigenetic circuit controls systematic circadian programs in the gut epithelium.Frontiers in systems biology · 2023Article
- Effect of pilose antler polypeptide on the mechanism of bone homeostasis in osteoporosis.Frontiers in medicine · 2023Review
- Type IV Collagen and SOX9 Are Molecular Targets of BET Inhibition in Experimental Glomerulosclerosis.International journal of molecular sciences · 2022Article
- TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022Review
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- Localization Matters: Epigenetic Regulation of Natural Killer Cells in Different Tissue Microenvironments.Frontiers in immunology · 2022Review
- Gene expression analysis in endometriosis: Immunopathology insights, transcription factors and therapeutic targets.Frontiers in immunology · 2022Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smads are intracellular transducers for TGF-beta superfamily ligands, but little is known about the mechanism by which complexes of receptor-phosphorylated Smad2 and Smad4 regulate transcription. Using an in vitro transcription system, we have discovered that, unlike most transcription factors that are sufficient to recruit the basal transcription machinery and therefore activate transcription on both naked DNA and chromatin templates, the Smads only activate transcription from chromatin templates. We demonstrate that Smad2-mediated transcription requires the histone acetyltransferase, p300. Smad2-recruited p300 exhibits an altered substrate specificity, specifically acetylating nucleosomal histone H3 at lysines 9 and 18, and these modifications are also detected on an endogenous Smad2-dependent promoter in a ligand-induced manner. Furthermore, we show that endogenous Smad2 interacts with the SWI/SNF ATPase, Brg1, in a TGF-beta-dependent manner, and demonstrate that Brg1 is recruited to Smad2-dependent promoters and is specifically required for TGF-beta-induced expression of endogenous Smad2 target genes. Our data indicate that the Smads define a new class of transcription factors that absolutely require chromatin to assemble the basal transcription machinery and activate transcription.
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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.