ArticleProceedings of the National Academy of Sciences of the United States of America1999
Smads bind directly to the Jun family of AP-1 transcription factors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
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Who cites it
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 325 citations in OpenAlex.
- Meta-analysis of expression signatures of muscle atrophy: gene interaction networks in early and late stages.BMC genomics · 2008Pooled it
- Spatially resolved profiling of steroid nuclear receptors reveals a role for the disordered N-terminal domains in genome targeting and AP-1 interaction.Genome research · 2026Article
- Inhibition of runt related transcription factor 1 with Ro24-7429 improves lung function in experimental models of idiopathic pulmonary fibrosis.Scientific reports · 2026Article
- SMAD3 and p300 complex scaffolding by long non-coding RNA LIMD1-AS1 promotes TGF-β-induced breast cancer cell plasticity.Nucleic acids research · 2025Article
- A TBX2-driven signaling switch from androgen receptor to glucocorticoid receptor confers therapeutic resistance in prostate cancer.Oncogene · 2025Article
- ModelingJournal of the American Heart Association · 2025Article
- Uncovering the role of aquaporin and chromobox family members as potential biomarkers in head and neck squamous cell carcinoma via integrative multiomics and in silico approach.Journal of applied genetics · 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
- Positive and negative feedback regulation of the TGF-β1 explains two equilibrium states in skin aging.iScience · 2024Article
- Injury-induced cooperation of InhibinβA and JunB is essential for cell proliferation in Xenopus tadpole tail regeneration.Scientific reports · 2024Article
- TGF-β broadly modifies rather than specifically suppresses reactivated memory CD8 T cells in a dose-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A TGF-β-responsive enhancer regulates SRC expression and epithelial-mesenchymal transition-associated cell migration.Journal of cell science · 2023Article
- SALL1 enforces microglia-specific DNA binding and function of SMADs to establish microglia identity.Nature immunology · 2023Article
- A micropeptide JunBP regulated by TGF-β promotes hepatocellular carcinoma metastasis.Oncogene · 2023Article
- Survivin promotes a glycolytic switch in CD4iScience · 2022Article
- ACell genomics · 2022Article
- Verapamil inhibited the development of ureteral stricture by blocking CaMK II-mediated STAT3 and Smad3/JunD pathways.International urology and nephrology · 2022Article
- PCfun: a hybrid computational framework for systematic characterization of protein complex function.Briefings in bioinformatics · 2022Article
- Efficient hemogenic endothelial cell specification by RUNX1 is dependent on baseline chromatin accessibility of RUNX1-regulated TGFβ target genes.Genes & development · 2021Article
- Targeting Runt-Related Transcription Factor 1 Prevents Pulmonary Fibrosis and Reduces Expression of Severe Acute Respiratory Syndrome Coronavirus 2 Host Mediators.The American journal of pathology · 2021Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Smad3 and Smad4 are sequence-specific DNA-binding factors that bind to their consensus DNA-binding sites in response to transforming growth factor beta (TGFbeta) and activate transcription. Recent evidence implicates Smad3 and Smad4 in the transcriptional activation of consensus AP-1 DNA-binding sites that do not interact with Smads directly. Here, we report that Smad3 and Smad4 can physically interact with AP-1 family members. In vitro binding studies demonstrate that both Smad3 and Smad4 bind all three Jun family members: JunB, cJun, and JunD. The Smad interacting region of JunB maps to a C-terminal 20-amino acid sequence that is partially conserved in cJun and JunD. We show that Smad3 and Smad4 also associate with an endogenous form of cJun that is rapidly phosphorylated in response to TGFbeta. Providing evidence for the importance of this interaction between Smad and Jun proteins, we demonstrate that Smad3 is required for the activation of concatamerized AP-1 sites in a reporter construct that has previously been characterized as unable to bind Smad proteins directly. Together, these data suggest that TGFbeta-mediated transcriptional activation through AP-1 sites may involve a regulated interaction between Smads and AP-1 transcription factors.
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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.