ArticleMolecular and cellular biology1999
Smad3-Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by transforming growth factor beta.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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
86 citing papers in PubMed, 261 citations in OpenAlex.
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- Present and Future Perspectives in the Treatment of Liver Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- PRDM16 functions as a co-repressor in the BMP pathway to suppress neural stem cell proliferation.eLife · 2025Article
- TGFβ in Pancreas and Colorectal Cancer: Opportunities to Overcome Therapeutic Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- 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
- SALL1 enforces microglia-specific DNA binding and function of SMADs to establish microglia identity.Nature immunology · 2023Article
- TGF-beta signal transduction: biology, function and therapy for diseases.Molecular biomedicine · 2022Review
- Delineating chromatin accessibility re-patterning at single cell level during early stage of direct cardiac reprogramming.Journal of molecular and cellular cardiology · 2022Article
- Smad4 controls signaling robustness and morphogenesis by differentially contributing to the Nodal and BMP pathways.Nature communications · 2021Article
- Article
- Chronic Wound Healing by Amniotic Membrane: TGF-β and EGF Signaling Modulation in Re-epithelialization.Frontiers in bioengineering and biotechnology · 2021Review
- GPR50-Ctail cleavage and nuclear translocation: a new signal transduction mode for G protein-coupled receptors.Cellular and molecular life sciences : CMLS · 2020Article
- AP-1 and TGFß cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma.Nature communications · 2020Article
- TGFβ-induced fibroblast activation requires persistent and targeted HDAC-mediated gene repression.Journal of cell science · 2019Article
- Activin A regulates the epidermal growth factor receptor promoter by activating the PI3K/SP1 pathway in oral squamous cell carcinoma cells.Scientific reports · 2019Article
- Chalcone flavokawain A attenuates TGF-β1-induced fibrotic pathology via inhibition of ROS/Smad3 signaling pathways and induction of Nrf2/ARE-mediated antioxidant genes in vascular smooth muscle cells.Journal of cellular and molecular medicine · 2019Article
- Cholesterol depletion enhances TGF-β Smad signaling by increasing c-Jun expression through a PKR-dependent mechanism.Molecular biology of the cell · 2018Article
- An IL-15 superagonist/IL-15Rα fusion complex protects and rescues NK cell-cytotoxic function from TGF-β1-mediated immunosuppression.Cancer immunology, immunotherapy : CII · 2018Article
- Sirt1 interaction with active Smad2 modulates transforming growth factor-β regulated transcription.Cell communication and signaling : CCS · 2017Article
- Article
26 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
7 authors at 1 institution in 1 country.
Funding
Abstract
Transcriptional regulation by transforming growth factor beta (TGF-beta) is a complex process which is likely to involve cross talk between different DNA responsive elements and transcription factors to achieve maximal promoter activation and specificity. Here, we describe a concurrent requirement for two discrete responsive elements in the regulation of the c-Jun promoter, one a binding site for a Smad3-Smad4 complex and the other an AP-1 binding site. The two elements are located 120 bp apart in the proximal c-Jun promoter, and each was able to independently bind its corresponding transcription factor complex. The effects of independently mutating each of these elements were nonadditive; disruption of either sequence resulted in complete or severe reductions in TGF-beta responsiveness. This simultaneous requirement for two distinct and independent DNA binding elements suggests that Smad and AP-1 complexes function synergistically to mediate TGF-beta-induced transcriptional activation of the c-Jun promoter.
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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.