Evidence map›Paper›PMID 18089563›Full record

ArticleThe Journal of biological chemistry2008

Immediate-early signaling induced by E-cadherin engagement and adhesion.

Tomas D Perez, Masako Tamada, Michael P Sheetz, W James Nelson

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Adhesion-Based Self-Organization in Tissue Patterning.Annual review of cell and developmental biology · 2022
    Review
  6. Tension-dependent stabilization of E-cadherin limits cell-cell contact expansion in zebrafish germ-layer progenitor cells.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Changes in E-cadherin rigidity sensing regulate cell adhesion.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Review
  20. Review

2 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

4 authors.

Tomas D PerezDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, California 94305-5430, USA.
Masako Tamada
Michael P Sheetz
W James Nelson

Funding

Topogenesis of NA/K-ATPASE in Polarized Epithelial CellsR37GM035527 · NIGMS · STANFORD UNIVERSITY · PI NELSON, W. JAMES · 2003 to 2012
$7.4M
Topogenesis of Na/K-ATPase in Polarized MDCK Epithelial CellsR01GM035527 · NIGMS · STANFORD UNIVERSITY · PI NELSON, W. JAMES · 1986 to 2015
$3.3M
Howard Hughes Medical InstituteNIGMS NIH HHS GM35527NIGMS NIH HHS R01 GM035527NIGMS NIH HHS R37 GM035527
6 · The paper itself

Abstract

Epithelial cell-cell interactions require localized adhesive interactions between E-cadherin on opposing membranes and the activation of downstream signaling pathways that affect membrane and actin dynamics. However, it is not known whether E-cadherin engagement and activation of these signaling pathways are locally coordinated or whether signaling is sustained or locally down-regulated like other receptor-mediated pathways. To obtain high spatiotemporal resolution of immediate-early signaling events upon E-cadherin engagement, we used laser tweezers to place beads coated with functional E-cadherin extracellular domain on cells. We show that cellular E-cadherin accumulated rapidly around beads, reaching a sustained plateau level in 1-3 min. Phosphoinositides and Rac1 co-accumulated with E-cadherin, reached peak levels with E-cadherin, but then rapidly dispersed. Both E-cadherin and Rac1 accumulated independently of Rac1 GTP binding/hydrolysis, but these activities were required for Rac1 dispersal. E-cadherin accumulation was dependent on membrane dynamics and actin polymerization, but actin did not stably co-accumulate with E-cadherin; mathematical modeling showed that diffusion-mediated trapping could account for the initial E-cadherin accumulation. We propose that initial E-cadherin accumulation requires active membrane dynamics and involves diffusion-mediated trapping at contact sites; to propagate further contacts, phosphatidylinositol 3-kinase and Rac1 are transiently activated by E-cadherin engagement and initiate a new round of membrane dynamics, but they are subsequently suppressed at that site to allow maintenance of weak E-cadherin mediated adhesion.

Indexed as

ActinsAnimalsCadherinsCell AdhesionCell LineCell MembraneDogsEpithelial CellsMicrospheresOptical TweezersPhosphatidylinositol 3-KinasesPhosphatidylinositolsProtein Transportrac1 GTP-Binding ProteinSignal TransductionActinsCadherinsPhosphatidylinositol 3-KinasesPhosphatidylinositolsrac1 GTP-Binding Protein

Identifiers

PMID18089563
PMCPMC3372897

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.