ArticleNature communications2019
YAP1 subgroup supratentorial ependymoma requires TEAD and nuclear factor I-mediated transcriptional programmes for tumorigenesis.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 104 citations in OpenAlex.
- Chromosome 6q mediated loss of LATS1 tumour suppression as a targetable mechanism of ultra-high-risk posterior fossa A ependymoma.Acta neuropathologica · 2026Article
- Supratentorial ependymoma: a comprehensive review of molecular classification, management strategies, and clinical outcomes (Part II of pediatric ependymomas across compartments).Journal of neuro-oncology · 2026Review
- Patient-derived ependymoma and medulloblastoma tumoroids: generation, biobanking and drug screening.Nature protocols · 2026Review
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Communications biology · 2026Article
- A brief history of ependymoma.Neuro-oncology · 2026Review
- Ependymoma group-specific blood-brain barrier differences uncovered by a multi-omics approach.Scientific reports · 2026Article
- Article
- Developing an advanced risk stratification model for pediatric intracranial ependymoma based on the prospective trial E-HIT2000 and subsequent registries.Neuro-oncology · 2026Article
- Integrated transcriptomic landscape of medulloblastoma and ependymoma reveals novel tumor subtype-specific biology.Neuro-oncology · 2026Article
- Degradation of the TEAD•YAP/TAZ Transcription Factor Complex by Heterobifunctional Small Molecules that Bind to the TEAD Allosteric Lipid Pocket.bioRxiv : the preprint server for biology · 2026Article
- YAP-TEAD regulates the super-enhancer network to control early surface ectoderm commitment.Nucleic acids research · 2026Article
- Integrated ERK-PKA-YAP/TAZ-SHH Signaling Orchestrates Cortical Radial Glia Identity and Lineage Diversification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Investigation of a global mouse methylome atlas reveals subtype-specific copy number alterations in pediatric cancer models.Nature genetics · 2026Article
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Research square · 2025Article
- C-terminal fusion partner activity contributes to the oncogenic functions of YAP1::TFE3.Scientific reports · 2025Article
- Integrated transcriptomic landscape of medulloblastoma and ependymoma reveals novel tumor subtype-specific biology.bioRxiv : the preprint server for biology · 2025Article
- C-terminal fusion partner activity contributes to the oncogenic functions of YAP1::TFE3.bioRxiv : the preprint server for biology · 2025Article
- Advances in molecular prognostication and treatments in ependymoma.Journal of neuro-oncology · 2025Review
- Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
33 authors at 6 institutions in 5 countries.
Funding
Abstract
YAP1 fusion-positive supratentorial ependymomas predominantly occur in infants, but the molecular mechanisms of oncogenesis are unknown. Here we show YAP1-MAMLD1 fusions are sufficient to drive malignant transformation in mice, and the resulting tumors share histo-molecular characteristics of human ependymomas. Nuclear localization of YAP1-MAMLD1 protein is mediated by MAMLD1 and independent of YAP1-Ser127 phosphorylation. Chromatin immunoprecipitation-sequencing analyses of human YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and TEAD transcription factor binding site motifs in YAP1-bound regulatory elements, suggesting a role for these transcription factors in YAP1-MAMLD1-driven tumorigenesis. Mutation of the TEAD binding site in the YAP1 fusion or repression of NFI targets prevents tumor induction in mice. Together, these results demonstrate that the YAP1-MAMLD1 fusion functions as an oncogenic driver of ependymoma through recruitment of TEADs and NFIs, indicating a rationale for preclinical studies to block the interaction between YAP1 fusions and NFI and TEAD transcription factors.
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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.