ArticleNature communications2018
Eya3 partners with PP2A to induce c-Myc stabilization and tumor progression.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 59 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
59 citing papers in PubMed, 81 citations in OpenAlex.
- Genetic and Pharmacologic Targeting of Eya3 in Macrophages Drives Anti-Tumor Immunity in Triple-Negative Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
- Article
- Switching of the c-Myc protein degradation pathway depending on the PP2A-B55α complex levels.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting Musashi-2 to counteract senescence and resistance in chronic myeloid leukemia: enhancing the efficacy of imatinib therapy.BMC cancer · 2025Article
- TAM family kinases are potential candidate targets for therapeutic intervention in chronic myeloid leukemia.Discover oncology · 2025Article
- PR55α subunit of protein phosphatase 2A supports KRASOncogene · 2025Article
- Cryo-EM structures of PP2A:B55 with p107 and Eya3 define substrate recruitment.Nature structural & molecular biology · 2025Article
- PP2A Promotes the Symmetric Division of MUC1-Dominant Cancer Stem-Like Cells in Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- EYA3 regulation of NF-κB and CCL2 suppresses cytotoxic NK cells in the premetastatic niche to promote TNBC metastasis.Science advances · 2025Article
- Targeting protein synthesis pathways in MYC-amplified medulloblastoma.Discover oncology · 2025Review
- Phosphorylation determines the glucose metabolism reprogramming and tumor-promoting activity of sine oculis homeobox 1.Signal transduction and targeted therapy · 2024Article
- EYA3 promotes the tumorigenesis of gastric cancer through activation of the mTORC1 signaling pathway and inhibition of autophagy.Scientific reports · 2024Article
- Sex-specific regulation of the cardiac transcriptome by the protein phosphatase 2A regulatory subunit B55α.npj metabolic health and disease · 2024Article
- Substrate recognition principles for the PP2A-B55 protein phosphatase.Science advances · 2024Article
- Effects of imidazole derivatives on cellular proliferation and apoptosis in myeloid leukemia.BMC cancer · 2024Article
- Biochemical characterization of the Eya and PP2A-B55α interaction.The Journal of biological chemistry · 2024Article
- A multi-omics approach for biomarker discovery in neuroblastoma: a network-based framework.NPJ systems biology and applications · 2024Article
- All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- Article
- B56δ long-disordered arms form a dynamic PP2A regulation interface coupled with global allostery and Jordan's syndrome mutations.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Eya genes encode a unique family of multifunctional proteins that serve as transcriptional co-activators and as haloacid dehalogenase-family Tyr phosphatases. Intriguingly, the N-terminal domain of Eyas, which does not share sequence similarity to any known phosphatases, contains a separable Ser/Thr phosphatase activity. Here, we demonstrate that the Ser/Thr phosphatase activity of Eya is not intrinsic, but arises from its direct interaction with the protein phosphatase 2A (PP2A)-B55α holoenzyme. Importantly, Eya3 alters the regulation of c-Myc by PP2A, increasing c-Myc stability by enabling PP2A-B55α to dephosphorylate pT58, in direct contrast to the previously described PP2A-B56α-mediated dephosphorylation of pS62 and c-Myc destabilization. Furthermore, Eya3 and PP2A-B55α promote metastasis in a xenograft model of breast cancer, opposing the canonical tumor suppressive function of PP2A-B56α. Our study identifies Eya3 as a regulator of PP2A, a major cellular Ser/Thr phosphatase, and uncovers a mechanism of controlling the stability of a critical oncogene, c-Myc.
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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.