Evidence map›Paper›PMID 8830783›Full record

ArticleThe Journal of cell biology1996

Is plasminogen activator inhibitor-1 the molecular switch that governs urokinase receptor-mediated cell adhesion and release?

G Deng, S A Curriden, S Wang, S Rosenberg, D J Loskutoff

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
16.7field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 456 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. PAI-1 deficiency drives pulmonary vascular smooth muscle remodeling and pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  7. Senescence-Associated Alterations in Matrisome of Mesenchymal Stem Cells.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

51 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

5 authors at 1 institution in 1 country.

G DengDepartment of Vascular Biology, Scripps Research Institute, La Jolla, California 92037, USA.
S A Curriden
S Wang
S Rosenberg
D J Loskutoff
Scripps Research Institute · US

Funding

THROMBUS FORMATION IN BABOONSP01HL031950 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H · 1985 to 2015
$29.4M
BLOOD SYSTEMS IN COAGULATION AND VESSEL DISEASET32HL007195 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUF, WOLFRAM · 1985 to 2011
$5.1M
PLASMINOGEN ACTIVATOR INHIBITOR BINDING PROTEINSF32HL009400 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI DENG, GANG · 1995 to 1997
–
NHLBI NIH HHS HL07195-19NHLBI NIH HHS HL09400-01NHLBI NIH HHS HL31950
6 · The paper itself

Abstract

Induction of the urokinase type plasminogen activator receptor (uPAR) promotes cell adhesion through its interaction with vitronectin (VN) in the extracellular matrix, and facilitates cell migration and invasion by localizing uPA to the cell surface. We provide evidence that this balance between cell adhesion and cell detachment is governed by PA inhibitor-1 (PAI-1). First, we demonstrate that uPAR and PAI-1 bind to the same site in VN (i.e., the amino-terminal somatomedin B domain; SMB), and that PAI-1 competes with uPAR for binding to SMB. Domain swapping and mutagenesis studies indicate that the uPAR-binding sequence is located within the central region of the SMB domain, a region previously shown to contain the PAI-1-binding motif. Second, we show that PAI-1 dissociates bound VN from uPAR and detaches U937 cells from their VN substratum. This PAI-1 mediated release of cells from VN appears to occur independently of its ability to function as a protease inhibitor, and may help to explain why high PAI-1 levels indicate a poor prognosis for many cancers. Finally, we show that uPA can rapidly reverse this effect of PAI-1. Taken together, these results suggest a dynamic regulatory role for PAI-1 and uPA in uPAR-mediated cell adhesion and release.

Indexed as

Amino AcidsBinding SitesCell AdhesionDNA Mutational AnalysisHumansLeukemia, Promyelocytic, AcutePlasminogen Activator Inhibitor 1Plasminogen ActivatorsProtein Structure, TertiaryReceptors, Cell SurfaceReceptors, Urokinase Plasminogen ActivatorRecombinant ProteinsTumor Cells, CulturedVitronectinAmino AcidsPlasminogen Activator Inhibitor 1Plasminogen ActivatorsPLAUR protein, humanReceptors, Cell SurfaceReceptors, Urokinase Plasminogen ActivatorRecombinant ProteinsVitronectin

Identifiers

PMID8830783
PMCPMC2120994
OpenAlexW2102577298

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.