ArticlePloS one2014
Design and analysis of a Petri net model of the Von Hippel-Lindau (VHL) tumor suppressor interaction network.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Petri net modeling and simulation of post-transcriptional regulatory networks of human embryonic stem cell (hESC) differentiation to cardiomyocytes.Journal of integrative bioinformatics · 2025Article
- Mathematical modeling of the molecular switch of TNFR1-mediated signaling pathways applying Petri net formalism and in silico knockout analysis.PLoS computational biology · 2022Article
- The E3 ubiquitin-protein ligase MDM2 is a novel interactor of the von Hippel-Lindau tumor suppressor.Scientific reports · 2020Article
- Deciphering the expression dynamics of ANGPTL8 associated regulatory network in insulin resistance using formal modelling approaches.IET systems biology · 2020Article
- 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
- Manatee invariants reveal functional pathways in signaling networks.BMC systems biology · 2017Article
- In Silico Knockout Studies of Xenophagic Capturing of Salmonella.PLoS computational biology · 2016Article
- VHLdb: A database of von Hippel-Lindau protein interactors and mutations.Scientific reports · 2016Article
- Isoform-specific interactions of the von Hippel-Lindau tumor suppressor protein.Scientific reports · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Von Hippel-Lindau (VHL) syndrome is a hereditary condition predisposing to the development of different cancer forms, related to germline inactivation of the homonymous tumor suppressor pVHL. The best characterized function of pVHL is the ubiquitination dependent degradation of Hypoxia Inducible Factor (HIF) via the proteasome. It is also involved in several cellular pathways acting as a molecular hub and interacting with more than 200 different proteins. Molecular details of pVHL plasticity remain in large part unknown. Here, we present a novel manually curated Petri Net (PN) model of the main pVHL functional pathways. The model was built using functional information derived from the literature. It includes all major pVHL functions and is able to credibly reproduce VHL syndrome at the molecular level. The reliability of the PN model also allowed in silico knockout experiments, driven by previous model analysis. Interestingly, PN analysis suggests that the variability of different VHL manifestations is correlated with the concomitant inactivation of different metabolic pathways.
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