ArticleScientific reports2015
Isoform-specific interactions of the von Hippel-Lindau tumor suppressor protein.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mammalian Polycistronic mRNAs and Disease.Trends in genetics : TIG · 2017Pooled it
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- 5' UTR length shapes alternative N-terminal protein isoforms across cancers and in rare disease.EMBO reports · 2026Article
- 5' UTR length regulates alternative N-terminal protein isoform production in health and disease.bioRxiv : the preprint server for biology · 2026Article
- Mathematical modeling and simulation of tumor-induced angiogenesis in retinal hemangioblastoma.PLoS computational biology · 2025Article
- Nonstop mutations cause loss of renal tumor suppressor proteinsScience advances · 2025Article
- Structural Characterization of Hypoxia Inducible Factor α-Prolyl Hydroxylase Domain 2 Interaction through MD Simulations.International journal of molecular sciences · 2023Article
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- Lighting up Nobel Prize-winning studies with protein intrinsic disorder.Cellular and molecular life sciences : CMLS · 2022Review
- Characterization of the pVHL Interactome in Human Testis Using High-Throughput Library Screening.Cancers · 2022Article
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- VHL suppresses RAPTOR and inhibits mTORC1 signaling in clear cell renal cell carcinoma.Scientific reports · 2021Article
- The E3 ubiquitin-protein ligase MDM2 is a novel interactor of the von Hippel-Lindau tumor suppressor.Scientific reports · 2020Article
- The long form of pVHL is artifactually modified by serine protease inhibitor AEBSF.Protein science : a publication of the Protein Society · 2020Article
- Ancient Evolutionary Origin of Intrinsically Disordered Cancer Risk Regions.Biomolecules · 2020Article
- The pVHL neglected functions, a tale of hypoxia-dependent and -independent regulations in cancer.Open biology · 2020Review
- Algorithmic assessment of missense mutation severity in the Von-Hippel Lindau protein.PloS one · 2020Article
- Genotype-phenotype relations of the von Hippel-Lindau tumor suppressor inferred from a large-scale analysis of disease mutations and interactors.PLoS computational biology · 2019Article
- Article
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8 authors.
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Abstract
Deregulation of the von Hippel-Lindau tumor suppressor protein (pVHL) is considered one of the main causes for malignant renal clear-cell carcinoma (ccRCC) insurgence. In human, pVHL exists in two isoforms, pVHL19 and pVHL30 respectively, displaying comparable tumor suppressor abilities. Mutations of the p53 tumor suppressor gene have been also correlated with ccRCC insurgence and ineffectiveness of treatment. A recent proteomic analysis linked full length pVHL30 with p53 pathway regulation through complex formation with the p14ARF oncosuppressor. The alternatively spliced pVHL19, missing the first 53 residues, lacks this interaction and suggests an asymmetric function of the two pVHL isoforms. Here, we present an integrative bioinformatics and experimental characterization of the pVHL oncosuppressor isoforms. Predictions of the pVHL30 N-terminus three-dimensional structure suggest that it may exist as an ensemble of structured and disordered forms. The results were used to guide Yeast two hybrid experiments to highlight isoform-specific binding properties. We observed that the physical pVHL/p14ARF interaction is specifically mediated by the 53 residue long pVHL30 N-terminal region, suggesting that this N-terminus acts as a further pVHL interaction interface. Of note, we also observed that the shorter pVHL19 isoform shows an unexpected high tendency to form homodimers, suggesting an additional isoform-specific binding specialization.
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