Evidence map›Paper›PMID 23022961›Full record

ReviewCellular signalling2013

Beyond cell adhesion: the role of armadillo proteins in the heart.

David Swope, Jifen Li, Glenn L Radice

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Advances in VT ablation for arrhythmogenic cardiomyopathy: evidence, mapping and ablation strategies, and predictive factors.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Analyzing gene expression profiles in dilated cardiomyopathy via bioinformatics methods.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  15. Article
  16. Pathogenesis of Arrhythmogenic Cardiomyopathy.The Canadian journal of cardiology · 2015
    Review
  17. Article
  18. Nuclear signaling from cadherin adhesion complexes.Current topics in developmental biology · 2015
    Review
  19. Article
  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

3 authors at 1 institution in 1 country.

David SwopeCenter for Translational Medicine, Department of Medicine, Jefferson Medical College, Philadelphia, PA 19107, USA.
Jifen Li
Glenn L Radice
Jefferson College · US

Funding

Cadherin/Catenin Function in ArrhythmogenesisR01HL081569 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI RADICE, GLENN LAWRENCE · 2007 to 2011
$1.9M
Role of the cytoskeleton in cardiac regenerationR21HL111788 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI RADICE, GLENN LAWRENCE · 2012 to 2013
$417k
NHLBI NIH HHS HL081569NHLBI NIH HHS HL111788NHLBI NIH HHS R01 HL081569NHLBI NIH HHS R21 HL111788
6 · The paper itself

Abstract

Plakoglobin (PG, γ-Catenin, JUP), a member of the armadillo protein family and close homolog of β-catenin, functions to link cell surface cadherin molecules with the cytoskeleton. PG is the only junctional component found in both desmosomes and adherens junctions and thus plays a critical role in the regulation of cell-cell adhesion. Similar to β-catenin, PG is able to interact with components of the Wnt signaling pathway and directly affect gene expression by binding with LEF/TCF transcription factors. In addition, it has been proposed that PG functions primarily as a competitive inhibitor of β-catenin transcriptional activity by sequestering LEF/TCF. Compared to β-catenin, the contribution of PG as a transcriptional regulator in either physiological or pathological conditions is poorly understood. There is increasing clinical interest in PG as both a structural protein as well as a signaling molecule as mutations have been identified in the human PG gene that cause Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) and cutaneous syndromes. This review will discuss the connection between altered cell adhesion and gene expression and its contribution to disease pathogenesis.

Indexed as

Cell AdhesionAnimalsArmadillo Domain ProteinsArrhythmogenic Right Ventricular Dysplasiabeta Cateningamma CateninGene Expression RegulationHumansMyocardiumSignal TransductionArmadillo Domain Proteinsbeta Cateningamma Catenin

Identifiers

PMID23022961
PMCPMC3508382
OpenAlexW2058341029

What OpenQuestion holds

Textmetadata
LicenceTDM
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.