ArticleCancer science2009
Promoter-wide analysis of Smad4 binding sites in human epithelial cells.
Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Bta-miR-146a Inhibits Proliferation and Promotes Apoptosis of Bovine Immature Sertoli Cells by Targeting SMAD4 via the TGF-β/MAPK Signaling Pathway.International journal of molecular sciences · 2026Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- Epithelial-intrinsic defects in TGFβR signaling drive local allergic inflammation manifesting as eosinophilic esophagitis.Science immunology · 2023Article
- Tumor: Stroma Interaction and Cancer.Experientia supplementum (2012) · 2022Article
- A pan-cancer analysis reveals nonstop extension mutations causing SMAD4 tumour suppressor degradation.Nature cell biology · 2020Article
- Comparative analysis of TTF-1 binding DNA regions in small-cell lung cancer and non-small-cell lung cancer.Molecular oncology · 2020Article
- Lessons learned from SMAD4 loss in squamous cell carcinomas.Molecular carcinogenesis · 2019Review
- Combined Inhibition of DYRK1A, SMAD, and Trithorax Pathways Synergizes to Induce Robust Replication in Adult Human Beta Cells.Cell metabolism · 2019Article
- Venous identity requires BMP signalling through ALK3.Nature communications · 2019Article
- Protein kinase CK2 activation is required for transforming growth factor β-induced epithelial-mesenchymal transition.Molecular oncology · 2018Article
- Transforming growth factor-β signaling in head and neck squamous cell carcinoma: Insights into cellular responses.Oncology letters · 2018Review
- SMAD transcription factors are altered in cell models of HD and regulate HTT expression.Cellular signalling · 2017Article
- Transcriptional Control by the SMADs.Cold Spring Harbor perspectives in biology · 2016Review
- Smad2 and Smad3 Regulate Chondrocyte Proliferation and Differentiation in the Growth Plate.PLoS genetics · 2016Article
- The proto-oncogenic protein TAL1 controls TGF-β1 signaling through interaction with SMAD3.Biochimie open · 2016Article
- TGF-β and the TGF-β Family: Context-Dependent Roles in Cell and Tissue Physiology.Cold Spring Harbor perspectives in biology · 2016Review
- Activation of TGF-β1-CD147 positive feedback loop in hepatic stellate cells promotes liver fibrosis.Scientific reports · 2015Article
- Basonuclin-1 modulates epithelial plasticity and TGF-β1-induced loss of epithelial cell integrity.Oncogene · 2015Article
- TGFβ signaling promotes juvenile granulosa cell tumorigenesis by suppressing apoptosis.Molecular endocrinology (Baltimore, Md.) · 2014Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smad4, the common partner Smad, is a key molecule in transforming growth factor-beta (TGF-beta) family signaling. Loss of Smad4 expression is found in several types of cancer, including pancreatic cancer and colon cancer, and is related to carcinogenesis. Here we identified Smad4 binding sites in the promoter regions of over 25 500 known genes by chromatin immunoprecipitation on a microarray (ChIP-chip) in HaCaT human keratinocytes. We identified 925 significant Smad4 binding sites. Approximately half of the identified sites overlapped the binding regions of Smad2 and Smad3 (Smad2/3, receptor-regulated Smads in TGF-beta signaling), while the rest of the regions appeared dominantly occupied by Smad4 even when a different identification threshold for Smad2/3 binding regions was used. Distribution analysis showed that Smad4 was found in the regions relatively distant from the transcription start sites, while Smad2/3 binding regions were more often present near the transcription start sites. Motif analysis also revealed that activator protein 1 (AP-1) sites were especially enriched in the sites common to Smad2/3 and Smad4 binding regions. In contrast, GC-rich motifs were enriched in Smad4-dominant binding regions. We further determined putative target genes of Smad4 whose expression was regulated by TGF-beta. Our findings revealed some general characteristics of Smad4 binding regions, and provide resources for examining the role of Smad4 in epithelial cells and cancer pathogenesis.
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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.