ArticleThe Journal of clinical investigation1999
Synthetic peptides define critical contacts between elongin C, elongin B, and the von Hippel-Lindau protein.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 112 citations in OpenAlex.
- The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer.Molecular oncology · 2026Review
- Deubiquitinase-Targeting Chimeras Mediated Stabilization of Tumor Suppressive E3 Ligase Proteins as a Strategy for Cancer Therapy.Journal of the American Chemical Society · 2025Article
- Molecular dynamics reveal potential effects of novel VHL variants on VHL-Elongin C binding in ccRCC patients from Eastern India.Scientific reports · 2025Article
- Review
- Ubiquitin-specific proximity labeling for the identification of E3 ligase substrates.Nature chemical biology · 2024Article
- Homozygous EPRS1 missense variant causing hypomyelinating leukodystrophy-15 alters variant-distal mRNA mNature communications · 2024Article
- CircSTX6 promotes pancreatic ductal adenocarcinoma progression by sponging miR-449b-5p and interacting with CUL2.Molecular cancer · 2022Article
- Review
- Algorithmic assessment of missense mutation severity in the Von-Hippel Lindau protein.PloS one · 2020Article
- Arginine refolds, stabilizes, and restores function of mutant pVHL proteins in animal model of the VHL cancer syndrome.Oncogene · 2019Article
- Renal Cell Carcinoma: Molecular Aspects.Indian journal of clinical biochemistry : IJCB · 2018Review
- Single SNP- and pathway-based genome-wide association studies for beak deformity in chickens using high-density 600K SNP arrays.BMC genomics · 2018Article
- BC-Box Motif-Mediated Neuronal Differentiation of Somatic Stem Cells.International journal of molecular sciences · 2018Article
- VHL promotes immune response against renal cell carcinoma via NF-κB-dependent regulation of VCAM-1.The Journal of cell biology · 2017Article
- VHL missense mutations in the p53 binding domain show different effects on p53 signaling and HIFα degradation in clear cell renal cell carcinoma.Oncotarget · 2017Article
- William Kaelin, Peter Ratcliffe, and Gregg Semenza receive the 2016 Albert Lasker Basic Medical Research Award.The Journal of clinical investigation · 2016Article
- Molecular Characterization of a Novel Germline VHL Mutation by Extensive In Silico Analysis in an Indian Family with Von Hippel-Lindau Disease.Genetics research international · 2016Article
- E2-EPF UCP regulates stability and functions of missense mutant pVHL via ubiquitin mediated proteolysis.BMC cancer · 2015Article
- Computational and experimental characterization of dVHL establish a Drosophila model of VHL syndrome.PloS one · 2014Article
- Hereditary kidney cancer syndromes.Advances in chronic kidney disease · 2014Review
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The von Hippel-Lindau tumor suppressor protein (pVHL) negatively regulates hypoxia-inducible mRNAs such as the mRNA encoding vascular endothelial growth factor (VEGF). This activity has been linked to its ability to form multimeric complexes that contain elongin C, elongin B, and Cul2. To understand this process in greater detail, we performed a series of in vitro binding assays using pVHL, elongin B, and elongin C variants as well as synthetic peptide competitors derived from pVHL or elongin C. A subdomain of elongin C (residues 17-50) was necessary and sufficient for detectable binding to elongin B. In contrast, elongin B residues required for binding to elongin C were not confined to a discrete colinear domain. We found that the pVHL (residues 157-171) is necessary and sufficient for binding to elongin C in vitro and is frequently mutated in families with VHL disease. These mutations preferentially involve residues that directly bind to elongin C and/or alter the conformation of pVHL such that binding to elongin C is at least partially diminished. These results are consistent with the view that diminished binding of pVHL to the elongins plays a causal role in VHL disease.
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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.