ReviewCellular and molecular life sciences : CMLS2013
The Eyes Absent proteins in development and disease.
Review in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed.
- Genetic and Pharmacologic Targeting of Eya3 in Macrophages Drives Anti-Tumor Immunity in Triple-Negative Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
- Potent synthetic lethality between PLK1 and EYA family inhibitors in tumors of the central and peripheral nervous systems.Genes & development · 2026Article
- Single-cell RNA sequencing reveals a putative lncRNA-associated ceRNA network in high-grade serous ovarian cancer.Genes & genomics · 2025Article
- Smurf2 knockdown attenuates the progression of diabetic nephropathy by inhibiting mesangial cell proliferation and fibrosis through suppressing EYA2 ubiquitination.Renal failure · 2025Article
- The role of SIX6 gene in juvenile open-angle glaucoma: a subtle contributor to the mutational landscape.Japanese journal of ophthalmology · 2025Article
- Inhibition of EYA family tyrosine phosphatase activity reveals a therapeutic vulnerability and enhances Menin and DOT1L inhibitor efficacy in KMT2A-rearranged leukemia.Experimental hematology & oncology · 2025Article
- EYA3 regulation of NF-κB and CCL2 suppresses cytotoxic NK cells in the premetastatic niche to promote TNBC metastasis.Science advances · 2025Article
- Methylseq, single-nuclei RNAseq, and discovery proteomics identify pathways associated with nephron-deficit CKD in the HSRA rat model.American journal of physiology. Renal physiology · 2025Article
- Article
- Endosomal chemokine receptor signalosomes regulate central mechanisms underlying cell migration.eLife · 2025Article
- Protein phosphatase EYA1 regulates the dephosphorylation and turnover of BCL2L12 to promote glioma development.International journal of biological sciences · 2025Article
- PROSER1 modulates DNA demethylation through dual mechanisms to prevent syndromic developmental malformations.Genes & development · 2024Article
- EYA3 promotes the tumorigenesis of gastric cancer through activation of the mTORC1 signaling pathway and inhibition of autophagy.Scientific reports · 2024Article
- Identification of a novel EYA4 likely pathogenic variant in a Chinese family with postlingual non-syndromic hearing loss and analysis of molecular epidemiology of EYA4 variants.BMC medical genomics · 2024Article
- Biochemical characterization of the Eya and PP2A-B55α interaction.The Journal of biological chemistry · 2024Article
- All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- A Benzarone Derivative Inhibits EYA to Suppress Tumor Growth in SHH Medulloblastoma.Cancer research · 2024Article
- RBFOX2 regulated EYA3 isoforms partner with SIX4 or ZBTB1 to control transcription during myogenesis.iScience · 2023Article
- Stem Cell Bioengineering with Bioportides: Inhibition of Planarian Head Regeneration with Peptide Mimetics of Eyes Absent Proteins.Pharmaceutics · 2023Article
- Tripartite motif containing 69 elicits ERK2-dependent EYA4 turnover to impart pancreatic tumorigenesis.Journal of Cancer · 2023Article
33 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
2 authors.
Funding
Abstract
The Eyes Absent (EYA) proteins, first described in the context of fly eye development, are now implicated in processes as disparate as organ development, innate immunity, DNA damage repair, photoperiodism, angiogenesis, and cancer metastasis. These functions are associated with an unusual combination of biochemical activities: tyrosine phosphatase and threonine phosphatase activities in separate domains, and transactivation potential when associated with a DNA-binding partner. EYA mutations are linked to multiorgan developmental disorders, as well as to adult diseases ranging from dilated cardiomyopathy to late-onset sensorineural hearing loss. With the growing understanding of EYA biochemical and cellular activity, biological function, and association with disease, comes the possibility that the EYA proteins are amenable to the design of targeted therapeutics. The availability of structural information, direct links to disease states, available animal models, and the fact that they utilize unconventional reaction mechanisms that could allow specificity, suggest that EYAs are well-positioned for drug discovery efforts. This review provides a summary of EYA structure, activity, and function, as they relate to development and disease, with particular emphasis on recent findings.
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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.