Evidence map›Paper›PMID 22280890›Full record

ArticleDevelopmental cell2012

The cell adhesion molecule echinoid functions as a tumor suppressor and upstream regulator of the Hippo signaling pathway.

Tao Yue, Aiguo Tian, Jin Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. The tumor suppressor RASSF8: A WAVE interaction partner controlling migration and cohesion of invasive border cells inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The wing imaginal disc.Genetics · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Hippo-Independent Regulation of Yki/Yap/Taz: A Non-canonical View.Frontiers in cell and developmental biology · 2021
    Review
  16. Neuronal immunoglobulin superfamily cell adhesion molecules in epithelial morphogenesis: insights fromPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. Article

8 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

3 authors at 1 institution in 1 country.

Tao YueDepartment of Developmental Biology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Aiguo Tian
Jin Jiang
The University of Texas Southwestern Medical Center · US

Funding

REGULATION OF HEDGEHOG SIGNALING IN DROSOPHILAR01GM061269 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI JIANG, JIN · 2000 to 2016
$4.2M
Regulation of Hh/Ci signaling by Cos2 and its partnersR01GM067045 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI JIANG, JIN · 2003 to 2015
$4.0M
NIGMS NIH HHS GM61269NIGMS NIH HHS GM67045NIGMS NIH HHS R01 GM061269NIGMS NIH HHS R01 GM067045
6 · The paper itself

Abstract

The Hippo (Hpo) signaling pathway controls tissue growth and organ size in species ranging from Drosophila to mammals and is deregulated in a wide range of human cancers. The core pathway consists of the Hpo/Warts (Wts) kinase cassette that phosphorylates and inactivates the transcriptional coactivator Yorkie (Yki). Here, we report that Echinoid (Ed), an immunoglobulin domain-containing cell adhesion molecule, acts as an upstream regulator of the Hpo pathway. Loss of Ed compromises Yki phosphorylation, resulting in elevated Yki activity that increases Hpo target gene expression and drives tissue overgrowth. Ed physically interacts with and stabilizes the Hpo-binding partner Salvador (Sav) at adherens junctions. Ed/Sav interaction is promoted by cell-cell contact and requires dimerization of Ed cytoplasmic domain. Overexpression of Sav or dimerized Ed cytoplasmic domain suppressed loss-of-Ed phenotypes. We propose that Ed may link cell-cell contact to Hpo signaling through binding and stabilizing Sav, thus modulating the Hpo kinase activity.

Indexed as

Cell AdhesionAnimalsAnimals, Genetically ModifiedBlotting, WesternCell Adhesion MoleculesCell Cycle ProteinsDrosophila melanogasterDrosophila ProteinsHippo KinasesImmunoenzyme TechniquesImmunoprecipitationIntracellular Signaling Peptides and ProteinsMutationNuclear ProteinsPhenotypePhosphorylationCell Adhesion MoleculesCell Cycle ProteinsDrosophila ProteinsED protein, DrosophilaHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsNuclear ProteinsProtein Serine-Threonine KinasesRepressor Proteinssav protein, DrosophilaTrans-ActivatorsTumor Suppressor ProteinsYAP-Signaling ProteinsYki protein, Drosophila

Identifiers

PMID22280890
PMCPMC3288783
OpenAlexW2005482521

What OpenQuestion holds

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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.