ReviewCurrent pharmaceutical design2009
The VHL tumor suppressor: master regulator of HIF.
Review in Current pharmaceutical design, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 176 citations in OpenAlex.
- UK kidney association clinical practice guideline: update of anaemia of chronic kidney disease.BMC nephrology · 2025Guideline
- The efficacy and safety of belzutifan inhibitor in patients with advanced or metastatic clear cell renal cell carcinoma: a meta-analysis.BMC pharmacology & toxicology · 2024Pooled it
- Belzutifan for von Hippel-Lindau disease-associated renal cell carcinoma and other neoplasms (LITESPARK-004): 50 months follow-up from a single-arm, phase 2 study.The Lancet. Oncology · 2025Trial
- Belzutifan for von Hippel-Lindau Disease: Pancreatic Lesion Population of the Phase 2 LITESPARK-004 Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Belzutifan for Renal Cell Carcinoma in von Hippel-Lindau Disease.The New England journal of medicine · 2021Trial
- Variants of SCARB1 and VDR Involved in Complex Genetic Interactions May Be Implicated in the Genetic Susceptibility to Clear Cell Renal Cell Carcinoma.BioMed research international · 2015Trial
- Review
- Von Hippel-Lindau disease: pathophysiological and clinical advances.Familial cancer · 2026Review
- VHL Suppresses Angiogenesis Through HIF-1a-Mediated Ang/Tie2/AMPK/VEGF Signaling Pathway in Tie-2 Expressed Macrophages (TEMs).Biochemical genetics · 2026Article
- Proteostasis sustains T cell differentiation potential and tumor-infiltrating lymphocyte function.Cell · 2026Article
- APP ubiquitination by VHL protein is essential for MVB sorting and lysosomal degradation.Journal of molecular cell biology · 2026Article
- A genome-scale single-cell CRISPRi map of trans gene regulation across human pluripotent stem cell lines.Cell genomics · 2026Article
- Proteostasis sustains T cell differentiation potential and tumor-infiltrating lymphocyte function.bioRxiv : the preprint server for biology · 2026Article
- Overcoming chemoresistance in esophageal cancer with synergistic strategies.Frontiers in immunology · 2026Review
- eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules.Cell reports · 2025Article
- From surgery to systemic therapy: long-term lessons of belzutifan in von Hippel-Lindau disease.Translational andrology and urology · 2025Article
- HIF1 activity in photoreceptors drives type 3 neovascularization and retinal atrophy in a new mouse model of age-related macular degeneration.Cell death & disease · 2025Article
- Connexin 41.8 governs timely haematopoietic stem and progenitor cell specification.Biology open · 2025Article
- The HIF axes in cancer: angiogenesis, metabolism, and immune-modulation.Trends in biochemical sciences · 2025Review
- Overexpression of BDNF and uPA Combined with the Suppression of Von Hippel-Lindau Tumor Suppressor Enhances the Neuroprotective Activity of the Secretome of Human Mesenchymal Stromal Cells in the Model of Intracerebral Hemorrhage.International journal of molecular sciences · 2025Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Hypoxia-Inducible Factors (HIFs) are heterodimeric oxygen-sensitive basic helix-loop-helix transcription factors that play central roles in cellular adaptation to low oxygen environments. The von-Hippel Lindau tumor suppressor (pVHL) is the substrate recognition component of an E3 ubiquitin ligase and functions as a master regulator of HIF activity by targeting the hydroxylated HIF-alpha subunit for ubiquitylation and rapid proteasomal degradation under normoxic conditions. Mutations in pVHL can be found in familial and sporadic hemangioblastomas, clear cell carcinomas of the kidney, pheochromocytomas and inherited forms of erythrocytosis, illustrating the importance of disrupted molecular oxygen sensing in the pathogenesis of these diseases. Tissue-specific gene targeting of pVHL in mice has demonstrated that efficient execution of HIF proteolysis is critically important for normal tissue physiology, and has provided novel insights into the functional consequences of HIF activation on the cellular and tissue level. Here we focus on the contribution of individual HIF transcription factors to the development of VHL phenotypes and discuss how the pVHL/HIF axis could be exploited pharmacologically.
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What OpenQuestion holds
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.