Evidence map›Paper›PMID 18751708›Full record

ReviewDer Pathologe2008

[Von-Hippel-Lindau (VHL) protein function by initiation and progression of renal cancer].

H Moch

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Der Pathologe, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 98% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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.

H MochInstitut für Klinische Pathologie, Departement Pathologie, Universitätsspital Zürich, Schmelzbergstr. 12, 8091 Zürich, Schweiz. holger.moch@usz.ch
Herzgefäss Medizin Klinik Im Park · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Germ line inactivation of the von-Hippel-Lindau (VHL) tumor suppressor gene causes von Hippel-Lindau hereditary cancer syndrome, and somatic mutations of this gene have been linked to the development of sporadic hemangioblastomas and clear cell renal carcinomas. The protein encoded by VHL, pVHL, has no known enzymatic activities but interacts with various partner proteins. In this review, various pVHL functions are highlighted. pVHL acts as a multi-purpose adaptor protein that controls different gene expression programs. Through its oxygen-dependent regulation of hypoxia-inducible factor alpha (HIFalpha), pVHL plays a central role in the oxygen-sensing pathway. In addition, many HIFalpha-independent functions of pVHL have recently been identified. These include microtubule-based processes, extracellular matrix assembly and suppression of kidney cyst formation. These complex pVHL functions can explain the diverse consequences of pVHL dysregulation in tumor formation and progression.

Indexed as

AllelesCarcinoma, Renal CellCell Transformation, NeoplasticDNA Mutational AnalysisGene Expression Regulation, NeoplasticHumansKidney Neoplasmsvon Hippel-Lindau DiseaseVon Hippel-Lindau Tumor Suppressor ProteinVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID18751708
OpenAlexW177448773

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.