ReviewFEBS letters2012
Systemic VHL gene functions and the VHL disease.
Review in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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
44 citing papers in PubMed, 80 citations in OpenAlex.
- Review
- From surgery to systemic therapy in von Hippel-Lindau disease: insights from extended follow-up of LITESPARK-004.Translational andrology and urology · 2025Article
- Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025Review
- Construction of a risk and prognostic model for migrasome-associated lncRNAs in renal cell carcinoma.Scientific reports · 2025Article
- Mandarin fish von Hippel-Lindau protein regulates the NF-κB signaling pathway via interaction with IκB to promote fish ranavirus replication.Zoological research · 2024Article
- Article
- When rare diseases crisscross within the same patient: von Hippel-Lindau and type 1 gastric neuroendocrine tumor.Hormones (Athens, Greece) · 2024Review
- Metabolic and proteostatic differences in quiescent and active neural stem cells.Neural regeneration research · 2024Review
- Physiological and pathophysiological mechanisms of the molecular and cellular biology of angiogenesis and inflammation in moyamoya angiopathy and related vascular diseases.Frontiers in neurology · 2023Review
- Article
- Review
- The Role of Propranolol as a Repurposed Drug in Rare Vascular Diseases.International journal of molecular sciences · 2022Review
- Blockade of β2-Adrenergic Receptor Reduces Inflammation and Oxidative Stress in Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2022Article
- Impact of RSUME Actions on Biomolecular Modifications in Physio-Pathological Processes.Frontiers in endocrinology · 2022Review
- Deletion ofFrontiers in immunology · 2022Article
- GZ17-6.02 and axitinib interact to kill renal carcinoma cells.Oncotarget · 2022Article
- Erythrocytosis: genes and pathways involved in disease development.Blood transfusion = Trasfusione del sangue · 2021Review
- Modeling Neoplastic Growth in Renal Cell Carcinoma and Polycystic Kidney Disease.International journal of molecular sciences · 2021Review
- Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases.The application of clinical genetics · 2021Review
- Targeting β2-Adrenergic Receptors Shows Therapeutical Benefits in Clear Cell Renal Cell Carcinoma from Von Hippel-Lindau Disease.Journal of clinical medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The von Hippel-Lindau tumor suppressor gene (VHL) is best known as an E3 ubiquitin ligase that negatively regulates the hypoxia inducible factor (HIF). VHL mutations are the genetic defects underlying several human diseases including polycythemia, familial VHL tumor syndrome and sporadic renal cell carcinoma. VHL mutations can lead to cell-autonomous phenotypes in the tumor cells. However, non-tumor cell-autonomous functions of VHL have also been noted. VHL tumor-derived cytokines can promote inflammation and induce mobilization of endothelial progenitor cells. Up-regulation of HIF caused by VHL loss-of-function mutants, including heterozygotes, has been shown to increase the activities of hematopoietic stem cells, endothelial cells and myeloid cells. As such, systemic functions of VHL likely play important roles in the development of VHL disease.
Indexed as
Identifiers
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.