ArticleNature structural & molecular biology2013
Structure-function analyses of the human SIX1-EYA2 complex reveal insights into metastasis and BOR syndrome.
Article in Nature structural & molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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Who cites it
72 citing papers in PubMed, 117 citations in OpenAlex.
- SIX1 branchio-oto-renal syndrome variants have different effects on embryonic craniofacial gene expression and cartilage formation.Development (Cambridge, England) · 2026Article
- EYA4 promotes cellular senescence by enhancing P21 transcription through interaction with SIX2.Advanced biotechnology · 2026Article
- A Novel EYA1 Splicing Mutation in a Chinese Family With Branchio-Oto Syndrome: A Functional Analysis and Reproductive Intervention.Clinical and experimental otorhinolaryngology · 2025Article
- Deubiquitinase-dependent transcriptional silencing controls inflammation.Cell research · 2025Article
- Identification of renal stem cells in zebrafish.Science advances · 2025Article
- Sine oculis homeobox homolog family function in gastrointestinal cancer: Progression and comprehensive analysis.World journal of clinical oncology · 2025Review
- Article
- Cytoplasmatic Localization of Six1 in Male Testis and Spermatogonial Stem Cells.International journal of stem cells · 2024Article
- Biochemical characterization of the Eya and PP2A-B55α interaction.The Journal of biological chemistry · 2024Article
- Targeting sine oculis homeoprotein 1 (SIX1): A review of oncogenic roles and potential natural product therapeutics.Heliyon · 2024Review
- Using Xenopus to discover new candidate genes involved in BOR and other congenital hearing loss syndromes.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2024Review
- All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- EYA2 tyrosine phosphatase inhibition reduces MYC and prevents medulloblastoma progression.Neuro-oncology · 2023Article
- SIX1 amplification modulates stemness and tumorigenesis in breast cancer.Journal of translational medicine · 2023Article
- A Novel EYA1 Mutation Causing Alternative RNA Splicing in a Chinese Family With Branchio-Oto Syndrome: Implications for Molecular Diagnosis and Clinical Application.Clinical and experimental otorhinolaryngology · 2023Article
- Phenotypic and molecular basis of SIX1 variants linked to non-syndromic deafness and atypical branchio-otic syndrome in South Korea.Scientific reports · 2023Article
- Overlapping functions of SIX homeoproteins during embryonic myogenesis.PLoS genetics · 2023Article
- The value of EYA1/3/4 in clear cell renal cell carcinoma: a study from multiple databases.Scientific reports · 2023Article
- Making a head: Neural crest and ectodermal placodes in cranial sensory development.Seminars in cell & developmental biology · 2023Review
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
SIX1 interacts with EYA to form a bipartite transcription factor essential for mammalian development. Loss of function of this complex causes branchio-oto-renal (BOR) syndrome, whereas re-expression of SIX1 or EYA promotes metastasis. Here we describe the 2.0-Å structure of SIX1 bound to EYA2, which suggests a new DNA-binding mechanism for SIX1 and provides a rationale for the effect of BOR syndrome mutations. The structure also reveals that SIX1 uses predominantly a single helix to interact with EYA. Substitution of a single amino acid in this helix is sufficient to disrupt SIX1-EYA interaction, SIX1-mediated epithelial-mesenchymal transition and metastasis in mouse models. Given that SIX1 and EYA are overexpressed in many tumor types, our data indicate that targeting the SIX1-EYA complex may be a potent approach to inhibit tumor progression in multiple cancer types.
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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.