Evidence map›Paper›PMID 14517207›Full record

ArticleThe Journal of cell biology2003

EphA kinase activation regulates HGF-induced epithelial branching morphogenesis.

Hui Miao, Christian H Nickel, Lloyd G Cantley, Leslie A Bruggeman, Laura N Bennardo, Bingcheng Wang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

46 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Genes · 2022
    Article
  8. Review
  9. Approaches to Manipulate Ephrin-A:EphA Forward Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Eph- and ephrin-dependent mechanisms in tumor and stem cell dynamics.Cellular and molecular life sciences : CMLS · 2014
    Review
  18. Review
  19. 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

6 authors at 2 institutions in 1 country.

Hui MiaoRammelkamp Center for Research, MetroHealth Campus, Cleveland, OH 44109, USA.
Christian H Nickel
Lloyd G Cantley
Leslie A Bruggeman
Laura N Bennardo
Bingcheng Wang
MetroHealth · USYale University · US

Funding

EphA2 Agonists as Novel Inhibitors of Tumor ProgressionR01CA092259 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI WANG, BINGCHENG · 2002 to 2007
$1.4M
Eph Kinase Signaling in Prostate CancerR01CA096533 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI WANG, BINGCHENG · 2001 to 2004
$954k
SIGNALING BY GAB1 IN EPITHELIAL MORPHOGENESISR01DK054911 · NIDDK · YALE UNIVERSITY · PI CANTLEY, LLOYD G · 1999 to 2003
$840k
NCI NIH HHS CA92259NCI NIH HHS CA96533NCI NIH HHS R01 CA092259NCI NIH HHS R01 CA096533NIDDK NIH HHS DK54911
6 · The paper itself

Abstract

Eph kinases and their ephrin ligands are widely expressed in epithelial cells in vitro and in vivo. Our results show that activation of endogenous EphA kinases in Madin-Darby canine kidney (MDCK) cells negatively regulates hepatocyte growth factor/scatter factor (HGF)-induced branching morphogenesis in collagen gel. Cotreatment with HGF and ephrin-A1 reduced sprouting of cell protrusions, an early step in branching morphogenesis. Moreover, addition of ephrin-A1 after HGF stimulation resulted in collapse and retraction of preexisting cell protrusions. In a newly developed assay that simulates the localized interactions between Ephs and ephrins in vivo, immobilized ephrin-A1 suppressed HGF-induced MDCK cell scattering. Ephrin-A1 inhibited basal ERK1/2 mitogen-activated protein kinase activity; however, the ephrin-A1 effect on cell protrusion was independent of the mitogen-activated protein kinase pathway. Ephrin-A1 suppressed HGF-induced activation of Rac1 and p21-activated kinase, whereas RhoA activation was retained, leading to the preservation of stress fibers. Moreover, dominant-negative RhoA or inhibitor of Rho-associated kinase (Y27632) substantially negated the inhibitory effects of ephrin-A1. These data suggest that interfering with c-Met signaling to Rho GTPases represents a major mechanism by which EphA kinase activation inhibits HGF-induced MDCK branching morphogenesis.

Indexed as

AnimalsCell LineCell MovementCell SizeCollagenEphrin-A1Ephrin-A2Epithelial CellsGelsHepatocyte Growth FactorKidneyLigandsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinasesrac1 GTP-Binding ProteinCollagenEphrin-A1Ephrin-A2GelsHepatocyte Growth FactorLigandsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinasesrac1 GTP-Binding ProteinrhoA GTP-Binding Protein

Identifiers

PMID14517207
PMCPMC2173949
OpenAlexW2067818732

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.