Evidence map›Paper›PMID 16505488›Full record

ArticleThe Journal of biological chemistry2006

Endocytic function of von Hippel-Lindau tumor suppressor protein regulates surface localization of fibroblast growth factor receptor 1 and cell motility.

Tien Hsu, Yair Adereth, Nurgun Kose, Vincent Dammai

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. The 'known-knowns', and 'known-unknowns' of extracellular Nm23-H1/NDPK proteins.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  12. The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  13. The pVHLOncotarget · 2017
    Article
  14. Review
  15. Article
  16. Dynamin controls extracellular level of Awd/Nme1 metastasis suppressor protein.Naunyn-Schmiedeberg's archives of pharmacology · 2016
    Article
  17. Article
  18. Interaction between Nm23 and the tumor suppressor VHL.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Article
  19. Janus-faces of NME-oncoprotein interactions.Naunyn-Schmiedeberg's archives of pharmacology · 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

4 authors at 1 institution in 1 country.

Tien HsuDepartment of Pathology and Laboratory Medicine and Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Yair Adereth
Nurgun Kose
Vincent Dammai
Medical University of South Carolina · 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

The tumor suppressor VHL (von Hippel-Lindau protein) serves as a negative regulator of hypoxia-inducible factor-alpha subunits. However, accumulated evidence indicates that VHL may play additional roles in other cellular functions. We report here a novel hypoxia-inducible factor-independent function of VHL in cell motility control via regulation of fibroblast growth factor receptor 1 (FGFR1) endocytosis. In VHL null tumor cells or VHL knock-down cells, FGFR1 internalization is defective, leading to surface accumulation and abnormal activation of FGFR1. The enhanced FGFR1 activity directly correlates with increased cell migration. VHL disease mutants, in two of the mutation hot spots favoring development of renal cell carcinoma, failed to rescue the above phenotype. Interestingly, surface accumulation of the chemotactic receptor appears to be selective in VHL mutant cells, since other surface proteins such as epidermal growth factor receptor, platelet-derived growth factor receptor, IGFR1, and c-Met are not affected. We demonstrate that 1) FGFR1 endocytosis is defective in the VHL mutant and is rescued by reexpression of wild-type VHL, 2) VHL is recruited to FGFR1-containing, but not EGFR-containing, endosomal vesicles, 3) VHL exhibits a functional relationship with Rab5a and dynamin 2 in FGFR1 internalization, and 4) the endocytic function of VHL is mediated through the metastasis suppressor Nm23, a protein known to regulate dynamin-dependent endocytosis.

Indexed as

Cell MovementEndocytosisCarcinoma, Renal CellCells, Culturedc-Mer Tyrosine KinaseDynamin IIErbB ReceptorsHumansHypoxia-Inducible Factor 1KidneyKidney NeoplasmsMutationNM23 Nucleoside Diphosphate KinasesNucleoside-Diphosphate KinaseProto-Oncogene Proteinsrab5 GTP-Binding Proteinsc-Mer Tyrosine KinaseDynamin IIErbB ReceptorsHypoxia-Inducible Factor 1MERTK protein, humanNM23 Nucleoside Diphosphate KinasesNME1 protein, humanNucleoside-Diphosphate KinaseProto-Oncogene Proteinsrab5 GTP-Binding ProteinsReceptor, Fibroblast Growth Factor, Type 1Receptor, IGF Type 1Receptor Protein-Tyrosine KinasesReceptors, Platelet-Derived Growth FactorVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID16505488
PMCPMC2367321
OpenAlexW2015107954

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.