ArticleNature communications2018
NUAK2 is a critical YAP target in liver cancer.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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.
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.
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Who cites it
85 citing papers in PubMed, 133 citations in OpenAlex.
- Identification of a NUAK1/2 Inhibitor as a Macrophage-Polarizing Compound by a Machine Learning-Based Phenotypic Cell Painting Screen.International journal of molecular sciences · 2026Article
- NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.Circulation research · 2026Article
- Article
- Phyllanthus niruri potentiates apoptosis in Huh-7 cells and mitigates diethylnitrosamine-induced hepatocarcinogenesis via Hippo-YAP pathway modulation.Medical oncology (Northwood, London, England) · 2026Article
- Gitogenin impedes tumorigenesis in hepatocellular carcinomaFrontiers in oncology · 2026Article
- AC005034.3/hsa-miR-126-5p/EIF3H axis: bioinformatics analysis, expression validation, and association with prognosis and immunosuppressive microenvironment in pancreatic adenocarcinoma.Frontiers in cell and developmental biology · 2026Article
- The oncogenic potential of YAP requires Y357 phosphorylation in cholangiocytes but not in hepatocytes.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Enhancing kinase-inhibitor activity and selectivity prediction through contrastive learning.Nature communications · 2025Article
- Development of Purine and Pyrrolopyrimidine Scaffolds as Potent, Selective, and Brain Penetrant NUAK1 Inhibitors.ACS medicinal chemistry letters · 2025Article
- NUAK2 is a therapeutically tractable regulator of RNA splicing and tumor progression in neuroendocrine prostate cancer.bioRxiv : the preprint server for biology · 2025Article
- Morphological regulation of wound repair astrocytes by leucine zipper-bearing kinase-AKT signaling after spinal cord injury.Experimental neurology · 2025Article
- Targeting the Hippo pathway in cancer.Nature reviews. Drug discovery · 2025Review
- A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.EMBO molecular medicine · 2025Article
- Integrative High-Throughput RNAi Screening Identifies BRSK1, STK32C and STK40 as Novel Activators of YAP/TAZ.International journal of molecular sciences · 2025Article
- Direct pharmacological AMPK activation inhibits mucosal SARS-CoV-2 infection by reducing lipid metabolism, restoring autophagy flux and the type I IFN response.Journal of virology · 2025Article
- Review
- Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- D-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.Journal of hematology & oncology · 2025Article
- A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- YAP/TAZ-associated cell signaling - at the crossroads of cancer and neurodevelopmental disorders.Frontiers in cell and developmental biology · 2025Review
25 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
10 authors at 5 institutions in 3 countries.
Funding
Abstract
The Hippo-YAP signaling pathway is a critical regulator of proliferation, apoptosis, and cell fate. The main downstream effector of this pathway, YAP, has been shown to be misregulated in human cancer and has emerged as an attractive target for therapeutics. A significant insufficiency in our understanding of the pathway is the identity of transcriptional targets of YAP that drive its potent growth phenotypes. Here, using liver cancer as a model, we identify NUAK2 as an essential mediator of YAP-driven hepatomegaly and tumorigenesis in vivo. By evaluating several human cancer cell lines we determine that NUAK2 is selectively required for YAP-driven growth. Mechanistically, we found that NUAK2 participates in a feedback loop to maximize YAP activity via promotion of actin polymerization and myosin activity. Additionally, pharmacological inactivation of NUAK2 suppresses YAP-dependent cancer cell proliferation and liver overgrowth. Importantly, our work here identifies a specific, potent, and actionable target for YAP-driven malignancies.
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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.