ArticleDevelopment (Cambridge, England)2016
Cooperative binding of AP-1 and TEAD4 modulates the balance between vascular smooth muscle and hemogenic cell fate.
Article in Development (Cambridge, England), 2016. 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.
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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
40 citing papers in PubMed, 59 citations in OpenAlex.
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- Nap1L4a Cooperates with Scl/Klf1 to Recruit H2A.Z in Mediating Interactions Among Cis-Regulatory Elements and Transcription Required for Primitive Erythropoiesis in Zebrafish.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting TAZ-TEAD in minimal residual disease enhances the duration of targeted therapy in melanoma models.Nature communications · 2025Article
- A feedback loop between Paxillin and Yorkie sustains Drosophila intestinal homeostasis and regeneration.Nature communications · 2025Article
- Regulation of developmentally controlled enhancer activity by extrinsic signals in normal and malignant cells: AP-1 at the centre.Frontiers in epigenetics and epigenomics · 2024Article
- Identification of resistance mechanisms to small-molecule inhibition of TEAD-regulated transcription.EMBO reports · 2024Article
- H3K4me1 facilitates promoter-enhancer interactions and gene activation during embryonic stem cell differentiation.Molecular cell · 2024Article
- Chromatin priming elements direct tissue-specific gene activity before hematopoietic specification.Life science alliance · 2024Article
- TEAD4 antagonizes cellular senescence by remodeling chromatin accessibility at enhancer regions.Cellular and molecular life sciences : CMLS · 2023Article
- A genome-wide relay of signalling-responsive enhancers drives hematopoietic specification.Nature communications · 2023Article
- Identification and characterization of enhancer elements controlling cell type-specific and signalling dependent chromatin programming during hematopoietic development.Stem cell investigation · 2023Review
- The SWI/SNF Complex: A Frequently Mutated Chromatin Remodeling Complex in Cancer.Cancer treatment and research · 2023Article
- Identifying a novel role for the master regulator Tal1 in the Endothelial to Hematopoietic Transition.Scientific reports · 2022Article
- Integrative epigenomic and transcriptomic analysis reveals the requirement of JUNB for hematopoietic fate induction.Nature communications · 2022Article
- Cell-intrinsic Aryl Hydrocarbon Receptor signalling is required for the resolution of injury-induced colonic stem cells.Nature communications · 2022Article
- TEAD4 as an Oncogene and a Mitochondrial Modulator.Frontiers in cell and developmental biology · 2022Review
- Sequences to Differences in Gene Expression: Analysis of RNA-Seq Data.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Efficient hemogenic endothelial cell specification by RUNX1 is dependent on baseline chromatin accessibility of RUNX1-regulated TGFβ target genes.Genes & development · 2021Article
- Review
- Integrative methylome-transcriptome analysis unravels cancer cell vulnerabilities in infant MLL-rearranged B cell acute lymphoblastic leukemia.The Journal of clinical investigation · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The transmission of extracellular signals into the nucleus involves inducible transcription factors, but how different signalling pathways act in a cell type-specific fashion is poorly understood. Here, we studied the regulatory role of the AP-1 transcription factor family in blood development using embryonic stem cell differentiation coupled with genome-wide transcription factor binding and gene expression analyses. AP-1 factors respond to MAP kinase signalling and comprise dimers of FOS, ATF and JUN proteins. To examine genes regulated by AP-1 and to examine how it interacts with other inducible transcription factors, we abrogated its global DNA-binding activity using a dominant-negative FOS peptide. We show that FOS and JUN bind to and activate a specific set of vascular genes and that AP-1 inhibition shifts the balance between smooth muscle and hematopoietic differentiation towards blood. Furthermore, AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signalling. Our bottom-up approach demonstrates that AP-1- and TEAD4-associated cis-regulatory elements form hubs for multiple signalling-responsive transcription factors and define the cistrome that regulates vascular and hematopoietic development by extrinsic signals.
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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.