ArticleOncogene2017
DNA-binding mechanism of the Hippo pathway transcription factor TEAD4.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 67 citations in OpenAlex.
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Coupling Vgll4b/Yap-regulated posterior cell addition with anterior vacuolation enables robust notochord elongation.Development (Cambridge, England) · 2026Article
- VGLL4-driven TEAD4 multimerization orchestrates DNA binding and YAP recruitment.Nature communications · 2026Article
- Regulation of YAP activity by nuclear G-actin binding.Nucleic acids research · 2026Article
- LINC01198 activates Hippo signaling to stimulate IL-1β autocrine for driving vemurafenib resistance by associating with TAOK1/2 in melanoma.Cell death discovery · 2025Article
- Structural insight into the substrate binding of the AMT complex via an inhibitor-trapped state.Protein science : a publication of the Protein Society · 2025Article
- Predicting nucleic acid binding sites by attention map-guided graph convolutional network with protein language embeddings and physicochemical information.Briefings in bioinformatics · 2025Article
- Disrupting bile acid metabolism by suppressing Fxr causes hepatocellular carcinoma induced by YAP activation.Nature communications · 2025Article
- Interpreting regulatory mechanisms of Hippo signaling through a deep learning sequence model.Cell genomics · 2025Article
- Ferroptosis: insight into the treatment of hepatocellular carcinoma.Cancer cell international · 2024Review
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
- Hippo Pathway Activation in Aged Mesenchymal Stem Cells Contributes to the Dysregulation of Hepatic Inflammation in Aged Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- YAP antagonizes TEAD-mediated AR signaling and prostate cancer growth.The EMBO journal · 2023Article
- TEAD Proteins Associate With DNA Repair Proteins to Facilitate Cellular Recovery From DNA Damage.Molecular & cellular proteomics : MCP · 2023Article
- Cross-lineage potential of Ascl1 uncovered by comparing diverse reprogramming regulatomes.Cell stem cell · 2022Article
- RBFOX2-regulated TEAD1 alternative splicing plays a pivotal role in Hippo-YAP signaling.Nucleic acids research · 2022Article
- CK2-induced cooperation of HHEX with the YAP-TEAD4 complex promotes colorectal tumorigenesis.Nature communications · 2022Article
- Hippo in Gastric Cancer: From Signalling to Therapy.Cancers · 2022Review
- TEAD4 as an Oncogene and a Mitochondrial Modulator.Frontiers in cell and developmental biology · 2022Review
- Single-cell sequencing reveals the cell map and transcriptional network of sporadic vestibular schwannoma.Frontiers in molecular neuroscience · 2022Article
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
No grant is acknowledged in the PubMed record.
Abstract
TEA domain (TEAD) family transcription factors are key regulators in development, tissue homeostasis and cancer progression. TEAD4 acts as a critical downstream effector of the evolutionarily conserved Hippo signaling pathway. The well-studied oncogenic protein YAP forms a complex with TEAD4 to regulate gene transcription; so does the tumor suppressor VGLL4. Although it is known that TEAD proteins can bind promoter regions of target genes through the TEA domain, the specific and detailed mechanism of DNA recognition by the TEA domain remains partially understood. Here, we report the crystal structure of TEAD4 TEA domain in complex with a muscle-CAT DNA element. The structure revealed extensive interactions between the TEA domain and the DNA duplex involving both the major and minor grooves of DNA helix. The DNA recognition helix, α3 helix, determines the specificity of the TEA domain binding to DNA sequence. Structure-guided biochemical analysis identified two major binding sites on the interface of the TEA domain-DNA complex. Mutation of TEAD4 at either site substantially decreases its occupancy on the promoter region of target genes, and largely impaired YAP-induced TEAD4 transactivation and target gene transcription, leading to inhibition of growth and colony formation of gastric cancer cell HGC-27. Collectively, our work provides a structural basis for understanding the regulatory mechanism of TEAD-mediated gene transcription.
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.