ArticleNature communications2024
The RNF214-TEAD-YAP signaling axis promotes hepatocellular carcinoma progression via TEAD ubiquitylation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- RNF214 silencing attenuates prostate cancer progression and modulates mTOR signaling through CAV1 ubiquitination.Cell & bioscience · 2026Article
- The role of e3 ubiquitin ligases and deubiquitinating enzymes in hepatocellular carcinoma.Cell biology and toxicology · 2026Review
- Research on the Hippo Pathway in Cancer.Cells · 2026Review
- ZFP36 Alleviates MASLD Through Facilitating TEAD4 mRNA Degradation After Sleeve Gastrectomy.International journal of molecular sciences · 2026Article
- Arginine Methylation Antagonizes TEAD3-Mediated Repression to Promote Osteogenic Differentiation by Disrupting RUNX2-Sequestrating Condensates.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structure-guided analysis and prediction of human E2-E3 ligase pairing specificity.bioRxiv : the preprint server for biology · 2026Article
- Ubiquitination mediated by RING-type E3 ligases in the progression of digestive system tumors: mechanistic insights and potential therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Roles of TEAD Transcription Factors and their Coactivators in the Progression and Metastasis of Cancers.Recent patents on anti-cancer drug discovery · 2026Review
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Molecular mechanisms mediated by liquid-liquid phase separation in chronic liver disease progression.iScience · 2025Review
- Bacterial effector screening reveals RNF214 as a virus restriction factor in mammals.PLoS pathogens · 2025Article
- Review
- Inc/GFP chimera protein-based interactomics reveals host cellular interactions of Cps0558, a novel Chlamydia psittaci inclusion protein.Pathogens and disease · 2025Article
- Proteomic Characterization of Liver Cancer Cells Treated with Clinical Targeted Drugs for Hepatocellular Carcinoma.Biomedicines · 2025Article
- Transcriptional enhanced associate domain factor 1 regulates cortactin-binding protein 2 N-terminal-like to control cell apoptosis in thyroid cancer.CytoJournal · 2025Article
- Atypical Hippo signaling network: uncovering novel insights into head and neck cancer biology and advancements in precision intervention.Frontiers in cell and developmental biology · 2025Review
- YAP activity protects against ventilator-induced lung injury.Frontiers in physiology · 2025Article
- Bacterial Effector Screening Reveals RNF214 as a Virus Restriction Factor in Mammals.bioRxiv : the preprint server for biology · 2024Article
- The RNF214-TEAD-YAP signaling axis promotes hepatocellular carcinoma progression via TEAD ubiquitylation.Nature communications · 2024Article
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21 authors.
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Abstract
RNF214 is an understudied ubiquitin ligase with little knowledge of its biological functions or protein substrates. Here we show that the TEAD transcription factors in the Hippo pathway are substrates of RNF214. RNF214 induces non-proteolytic ubiquitylation at a conserved lysine residue of TEADs, enhances interactions between TEADs and YAP, and promotes transactivation of the downstream genes of the Hippo signaling. Moreover, YAP and TAZ could bind polyubiquitin chains, implying the underlying mechanisms by which RNF214 regulates the Hippo pathway. Furthermore, RNF214 is overexpressed in hepatocellular carcinoma (HCC) and inversely correlates with differentiation status and patient survival. Consistently, RNF214 promotes tumor cell proliferation, migration, and invasion, and HCC tumorigenesis in mice. Collectively, our data reveal RNF214 as a critical component in the Hippo pathway by forming a signaling axis of RNF214-TEAD-YAP and suggest that RNF214 is an oncogene of HCC and could be a potential drug target of HCC therapy.
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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.