Evidence map›Paper›PMID 18219317›Full record

ReviewCell death and differentiation2008

The VHL tumor suppressor and HIF: insights from genetic studies in mice.

P P Kapitsinou, V H Haase

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

88 citing papers in PubMed, 147 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Low expression of MKRN1 promotes leukemia cell proliferation.European journal of medical research · 2025
    Article
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  8. Distinct Stress Regulators in the CRL Family: Emerging Roles of F-Box Proteins: Cullin-RING Ligases and Stress-Sensing.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  9. Review
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  16. Review
  17. Article
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  20. Studying Kidney Diseases Using Organoid Models.Frontiers in cell and developmental biology · 2022
    Review

28 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

P P KapitsinouDepartment of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
V H Haase
University of Pennsylvania · US

Funding

Hypoxia VHL nad HIF in Renal Tumor DevelopmentR01CA100787 · NCI · VANDERBILT UNIVERSITY · PI HAASE, VOLKER HANS · 2004 to 2008
$1.3M
VHL FUNCTION BY CONDITIONAL GENE TARGETINGK08DK002668 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HAASE, VOLKER H. · 1999 to 2003
$502k
Hypoxic signaling in hepatocytesR21DK073467 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HAASE, VOLKER H. · 2006 to 2007
$427k
Molecular mechanisms of renal injuryR21DK072037 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HAASE, VOLKER H. · 2006 to 2007
$310k
NCI NIH HHS R01 CA100787NIDDK NIH HHS K08 DK002668NIDDK NIH HHS R21 DK072037NIDDK NIH HHS R21 DK073467
6 · The paper itself

Abstract

The von Hippel-Lindau tumor suppressor gene product, pVHL, functions as the substrate recognition component of an E3-ubiquitin ligase, which targets the oxygen-sensitive alpha-subunit of hypoxia-inducible factor (HIF) for rapid proteasomal degradation under normoxic conditions and as such plays a central role in molecular oxygen sensing. Mutations in pVHL can be found in familial and sporadic clear cell carcinomas of the kidney, hemangioblastomas of the retina and central nervous system, and pheochromocytomas, underscoring its gatekeeper function in the pathogenesis of these tumors. Tissue-specific gene targeting of VHL in mice has demonstrated that efficient execution of pVHL-mediated HIF proteolysis under normoxia is fundamentally important for survival, proliferation, differentiation and normal physiology of many cell types, and has provided novel insights into the biological function of individual HIF transcription factors. In this review, we discuss the role of HIF in the development of the VHL phenotype.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCarcinoma, Renal CellEndothelial PAS Domain-Containing Protein 1Gene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGenotypeGerm-Line MutationHumansHypoxia-Inducible Factor 1, alpha SubunitKidney NeoplasmsMiceMice, KnockoutNeoplasmsPhenotypeUbiquitin-Protein LigasesBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Hypoxia-Inducible Factor 1, alpha SubunitUbiquitin-Protein LigasesVHL protein, mouseVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID18219317
PMCPMC3799983
OpenAlexW2073422719

What OpenQuestion holds

Textmetadata
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.