Evidence map›Paper›PMID 20388653›Full record

ArticleDevelopment (Cambridge, England)2010

Drosophila VHL tumor-suppressor gene regulates epithelial morphogenesis by promoting microtubule and aPKC stability.

Serena Duchi, Luca Fagnocchi, Valeria Cavaliere, Anita Hsouna, Giuseppe Gargiulo, Tien Hsu

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Comparative Expression Profiling of Wild TypeFrontiers in physiology · 2019
    Article
  7. Interaction between Nm23 and the tumor suppressor VHL.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Drosophila Mgr, a Prefoldin subunit cooperating with von Hippel Lindau to regulate tubulin stability.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  14. 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

6 authors at 3 institutions in 2 countries.

Serena DuchiDipartimento di Biologia Evoluzionistica Sperimentale, Università di Bologna, Via Selmi 3, 40126 Bologna, Italy.
Luca Fagnocchi
Valeria Cavaliere
Anita Hsouna
Giuseppe Gargiulo
Tien Hsu
University of Bologna · ITMedical University of South Carolina · USMUSC Hollings Cancer Center · US

Funding

THE ROLE OF FLI1 IN CELLULAR DIFFERENTIATION AND DEVELOPMENTP01CA078582 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2009
$9.1M
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
SIGNALING MECHANISMS IN FOLLICLE CELL FATE DETERMINATIONR01GM057843 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HSU, TIEN · 1999 to 2006
$1.6M
NCI NIH HHS P01 CA078582NCI NIH HHS P01CA78582NCI NIH HHS R01 CA109860NCI NIH HHS R01CA109860NIGMS NIH HHS R01 GM057843
6 · The paper itself

Abstract

Mutations in the human von Hippel-Lindau (VHL) genes are the cause of VHL disease, which displays multiple benign and malignant tumors. The VHL gene has been shown to regulate angiogenic potential and glycolic metabolism via its E3 ubiquitin ligase function against the alpha subunit of hypoxia-inducible factor (HIF). However, many other HIF-independent functions of VHL have been identified and recent evidence indicates that the canonical function cannot fully explain the VHL mutant cell phenotypes. Many of these functions have not been verified in genetically tractable systems. Using an established follicular epithelial model in Drosophila, we show that the Drosophila VHL gene is involved in epithelial morphogenesis via stabilizing microtubule bundles and aPKC. Microtubule defects in VHL mutants lead to mislocalization of aPKC and subsequent loss of epithelial integrity. Destabilizing microtubules in ex vivo culture of wild-type egg chambers can also result in aPKC mislocalization and epithelial defects. Importantly, paclitaxel-induced stabilization of microtubules can rescue the aPKC localization phenotype in Drosophila VHL mutant follicle cells. The results establish a developmental function of the VHL gene that is relevant to its tumor-suppressor activity.

Indexed as

AnimalsDrosophilaDrosophila ProteinsEnzyme StabilityEpitheliumFemaleImmunohistochemistryImmunoprecipitationIn Vitro TechniquesMaleMicroscopy, ConfocalMicrotubulesOvarian FollicleProtein Kinase C-alphaVon Hippel-Lindau Tumor Suppressor ProteinDrosophila ProteinsProtein Kinase C-alphaVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID20388653
PMCPMC2853850
OpenAlexW2062019745

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.