Evidence map›Paper›PMID 21996733›Full record

ReviewOncogene2012

Complex cellular functions of the von Hippel-Lindau tumor suppressor gene: insights from model organisms.

T Hsu

Abstract readReview
In one paragraph

Review in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Comparative Expression Profiling of Wild TypeFrontiers in physiology · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. von Hippel-Lindau gene plays a role during zebrafish pronephros development.In vitro cellular & developmental biology. Animal · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Nucleoside diphosphate kinases (NDPKs) in animal development.Cellular and molecular life sciences : CMLS · 2015
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

T HsuDepartment of Medicine, Boston University School of Medicine, Boston, MA 02118, USA. tienh@bu.edu
Boston University · US

Funding

VHL tumor suppressor gene and the initiation of renal cell carcinomaR01CA109860 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HSU, TIEN · 2004 to 2015
$3.2M
NCI NIH HHS R01 CA109860NCI NIH HHS R01CA109860
6 · The paper itself

Abstract

The von Hippel-Lindau tumor suppressor gene (VHL) has attracted intensive interest not only because its mutations predispose carriers to devastating tumors, but also because it is involved in oxygen sensing under physiological conditions. VHL loss-of-function mutations result in organ-specific tumors, such as hemangioblastoma of the central nervous system and renal cell carcinoma, both untreatable with conventional chemotherapies. The VHL protein is best known as an E3 ubiquitin ligase that targets hypoxia-inducible factor-α (HIF-α), but many diverse, non-canonical cellular functions have also been assigned to VHL, mainly based on studies in cell culture systems. As such, although the HIF-dependent role of VHL is critical, the full spectrum of pathophysiological functions of VHL is still unresolved. Such understanding requires careful cross-referencing with physiologically relevant experimental models. Studies in model systems, such as Caenorhabditis elegans, Drosophila, zebrafish and mouse have provided critical in vivo confirmation of the VHL-HIF pathway, and verification of potentially important cellular functions including microtubule stabilization and epithelial morphogenesis. More recently, animal models have also suggested systemic roles of VHL in hematopoiesis, metabolic homeostasis and inflammation. In this review, the studies performed in model organisms will be summarized and placed in context with existing clinical and in vitro data.

Indexed as

Gene Expression RegulationModels, AnimalAnimalsCaenorhabditis elegansDrosophilaHematopoiesisHypoxia-Inducible Factor 1, alpha SubunitInflammationMiceMorphogenesisNeoplasmsOxygenVon Hippel-Lindau Tumor Suppressor ProteinZebrafishHypoxia-Inducible Factor 1, alpha SubunitOxygenVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID21996733
PMCPMC3343179
OpenAlexW2167427959

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.