ArticleStructure (London, England : 1993)2015
Insights into Cullin-RING E3 ubiquitin ligase recruitment: structure of the VHL-EloBC-Cul2 complex.
Article in Structure (London, England : 1993), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 84 citations in OpenAlex.
- Recent advances in etiology and treatment of von Hippel-Lindau Disease (VHLD).Cancer metastasis reviews · 2026Review
- Structure of the E3 ligase CRL2Cell reports · 2026Article
- Article
- Article
- The E3 ubiquitin ligase mechanism specifying target-directed microRNA degradation.bioRxiv : the preprint server for biology · 2026Article
- Dysregulation of the ubiquitin-proteasome system in von Hippel-Lindau syndrome: molecular insights and clinical perspectives.Clinical and experimental medicine · 2025Review
- Targeted degradation of the HPV oncoprotein E6 reduces tumor burden in cervical cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- PHD3-VHL axis controls HIV-2 infection through oxygen-dependent hydroxylation and degradation of Vpx.PLoS pathogens · 2025Article
- Clinical and Prognostic Value of VHL in Korean Patients with Rectal Cancer.Medicina (Kaunas, Lithuania) · 2025Article
- Functional genomics pipeline identifies CRL4 inhibition for the treatment of ovarian cancer.Clinical and translational medicine · 2025Article
- Identification of novel 7-hydroxycoumarin derivatives as ELOC binders with potential to modulate CRL2 complex formation.Scientific reports · 2025Article
- Roles of E3 ubiquitin ligases and deubiquitinating enzymes in renal cell carcinoma.Frontiers in oncology · 2025Review
- A case report: identifying a novel variant in ELOC(Frontiers in oncology · 2025Article
- Mechanism of degrader-targeted protein ubiquitinability.Science advances · 2024Article
- Mechanism of Ψ-Pro/C-degron recognition by the CRL2Nature communications · 2024Article
- Elongin B promotes breast cancer progression by ubiquitinating tumor suppressor p14/ARF.Cell biology and toxicology · 2024Article
- Co-opting the E3 ligase KLHDC2 for targeted protein degradation by small molecules.Nature structural & molecular biology · 2024Article
- CAND1 inhibits Cullin-2-RING ubiquitin ligases for enhanced substrate specificity.Nature structural & molecular biology · 2024Article
- Computational analysis of protein-protein interactions of cancer drivers in renal cell carcinoma.FEBS open bio · 2024Article
- PIN1 and CDK1 cooperatively govern pVHL stability and suppressive functions.Cell death and differentiation · 2023Article
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5 authors at 1 institution in 1 country.
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Abstract
The von Hippel-Lindau tumor suppressor protein (VHL) recruits a Cullin 2 (Cul2) E3 ubiquitin ligase to downregulate HIF-1α, an essential transcription factor for the hypoxia response. Mutations in VHL lead to VHL disease and renal cell carcinomas. Inhibition of this pathway to upregulate erythropoietin production is a promising new therapy to treat ischemia and chronic anemia. Here, we report the crystal structure of VHL bound to a Cul2 N-terminal domain, Elongin B, and Elongin C (EloC). Cul2 interacts with both the VHL BC box and cullin box and a novel EloC site. Comparison with other cullin E3 ligase structures shows that there is a conserved, yet flexible, cullin recognition module and that cullin selectivity is influenced by distinct electrostatic interactions. Our structure provides a structural basis for the study of the pathogenesis of VHL disease and rationale for the design of novel compounds that may modulate cullin-substrate receptor interactions.
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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.