Evidence map›Paper›PMID 23652796›Full record

ArticleThe Journal of investigative dermatology2013

Plakoglobin as a regulator of desmocollin gene expression.

Etienne Tokonzaba, Jiangli Chen, Xing Cheng, Zhining Den, Radhika Ganeshan, Eliane J Műller, Peter J Koch

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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

7 authors at 3 institutions in 2 countries.

Etienne TokonzabaDepartment of Dermatology, University of Colorado School of Medicine, Aurora, Colorado, USA.
Jiangli ChenDepartment of Dermatology, University of Colorado School of Medicine, Aurora, Colorado, USA.
Xing ChengDepartment of Dermatology, Baylor College of Medicine, Houston, Texas, USA.
Zhining DenDepartment of Dermatology, Baylor College of Medicine, Houston, Texas, USA.
Radhika GaneshanDepartment of Dermatology, University of Colorado School of Medicine, Aurora, Colorado, USA.
Eliane J MűllerMolecular Dermatology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Peter J KochDepartment of Dermatology, University of Colorado School of Medicine, Aurora, Colorado, USA; Department of Dermatology, Baylor College of Medicine, Houston, Texas, USA; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, Colorado, USA. Electronic address: Peter.Koch@ucdenver.edu.
University of Colorado Denver · USBaylor College of Medicine · USUniversity of Bern · CH

Funding

Cross-talk Between Desmosomal Proteins and Signaling Pathways in the SkinR01AR053892 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI KOCH, PETER J. · 2008 to 2012
$1.9M
Montagna Symposium on the Biology of SkinR13AR009431 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SANCY ANN LEACHMAN · 1986 to 2026
$785k
NIAMS NIH HHS 5R01AR053892NIAMS NIH HHS R01 AR053892NIAMS NIH HHS R13 AR009431
6 · The paper itself

Abstract

Desmosomes are cell adhesion junctions required for the normal development and maintenance of mammalian tissues and organs such as the skin, skin appendages, and the heart. The goal of this study was to investigate how desmocollins (DSCs), transmembrane components of desmosomes, are regulated at the transcriptional level. We hypothesized that differential expression of the Dsc2 and Dsc3 genes is a prerequisite for normal development of skin appendages. We demonstrate that plakoglobin (Pg) in conjunction with lymphoid enhancer-binding factor 1 (Lef-1) differentially regulates the proximal promoters of these two genes. Specifically, we found that Lef-1 acts as a switch activating Dsc2 and repressing Dsc3 in the presence of Pg. Interestingly, we also determined that NF-κB pathway components, the downstream effectors of the ectodysplasin-A (EDA)/ ectodysplasin-A receptor (EDAR)/NF-κB signaling cascade, can activate Dsc2 expression. We hypothesize that Lef-1 and EDA/EDAR/NF-κB signaling contribute to a shift in Dsc isoform expression from Dsc3 to Dsc2 in placode keratinocytes. It is tempting to speculate that this shift is required for the invasive growth of placode keratinocytes into the dermis, a crucial step in skin appendage formation.

Indexed as

Gene Expression RegulationAnimalsBinding SitesCell AdhesionDesmocollinsDogsEctodysplasinsgamma CateninKeratinocytesLymphoid Enhancer-Binding Factor 1Madin Darby Canine Kidney CellsMembrane GlycoproteinsMiceMice, TransgenicNF-kappa BPromoter Regions, GeneticDesmocollinsDsc2 protein, mouseDsc3 protein, mouseEctodysplasinsgamma CateninLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Membrane GlycoproteinsNF-kappa BReceptors, Ectodysplasin

Identifiers

PMID23652796
PMCPMC3760975
OpenAlexW2062133630

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.