ArticleNature communications2017
Structural basis for genome wide recognition of 5-bp GC motifs by SMAD transcription factors.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 128 citations in OpenAlex.
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- Structural basis for genome-wide site-specific DNA recognition by Nuclear Factor IA.Nature communications · 2025Article
- Proteomic analysis of 7-octenoic acid antifibrotic effects in TGF-β1 activated hepatic stellate cells.Scientific reports · 2025Article
- Development of a functional assay for the characterisation ofJournal of medical genetics · 2025Article
- Structural basis of Nuclear Factor 1-X DNA recognition provides prototypic insight into the NFI family.Nature communications · 2025Article
- Identification of methylation-related genes and the potential regulatory mechanism of SLAMF6 in CMS4 colorectal cancer.Clinical epigenetics · 2025Article
- Dual transcriptional activities of PAX3 and PAX7 spatially encode spinal cell fates through distinct gene networks.PLoS biology · 2025Article
- 3-Hydroxy-β-ionone Suppresses Breast Cancer Progression by Inducing Apoptosis and Blocking EMT Through the TGF-β/Smad Signaling Pathway.International journal of molecular sciences · 2025Article
- Gastrula-Premarked Posterior Enhancer Primes Posterior Tissue Development Through Cross-Talk with TGF-β Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PRDM16 functions as a co-repressor in the BMP pathway to suppress neural stem cell proliferation.eLife · 2025Article
- Regulation of the lncRNANAR molecular medicine · 2025Article
- Autocrine GDF10 Inhibits Hepatic Stellate Cell Activation via BMPR2/ALK3 Receptor to Prevent Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Article
- The Cyclin-Dependent Kinase 8 Inhibitor E966-0530-45418 Attenuates Pulmonary FibrosisInternational journal of biological sciences · 2025Article
- Genome-wide characterization and expression divergence of voltage-dependent anion channel (VDAC) in upland cotton (Frontiers in plant science · 2025Article
- ELK1 regulates BMPR1B transcriptional activity in ovine granulosa cells.Frontiers in cell and developmental biology · 2025Article
- TGF-β regulates the release of breast cancer cell-derived extracellular vesicles and the sorting of their protein cargo by downregulating RAB27B expression.Journal of extracellular vesicles · 2024Article
- Analysis of the DNA-binding properties of TGF-β-activated Smad complexes unveils a possible molecular basis for cellular context-dependent signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
18 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
14 authors at 5 institutions in 4 countries.
Funding
Abstract
Smad transcription factors activated by TGF-β or by BMP receptors form trimeric complexes with Smad4 to target specific genes for cell fate regulation. The CAGAC motif has been considered as the main binding element for Smad2/3/4, whereas Smad1/5/8 have been thought to preferentially bind GC-rich elements. However, chromatin immunoprecipitation analysis in embryonic stem cells showed extensive binding of Smad2/3/4 to GC-rich cis-regulatory elements. Here, we present the structural basis for specific binding of Smad3 and Smad4 to GC-rich motifs in the goosecoid promoter, a nodal-regulated differentiation gene. The structures revealed a 5-bp consensus sequence GGC(GC)|(CG) as the binding site for both TGF-β and BMP-activated Smads and for Smad4. These 5GC motifs are highly represented as clusters in Smad-bound regions genome-wide. Our results provide a basis for understanding the functional adaptability of Smads in different cellular contexts, and their dependence on lineage-determining transcription factors to target specific genes in TGF-β and BMP pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.