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Article

Expression of desmoglein 1 compensates for genetic loss of desmoglein 3 in keratinocyte adhesion.

The Journal of investigative dermatology - 1 Jul 2002

Hanakawa Yasushi, Matsuyoshi Norihisa, Stanley John R

Abstract excerpt

The desmoglein compensation hypothesis, namely that one desmoglein can compensate for loss of function of another, has been proposed to explain the tissue specificity of the autoantibody-induced loss of cell adhesion in pemphigus. To validate this hypothesis genetically, we used desmoglein-3 knockout mice (DSG3-/-) that lose their telogen hair prematurely due to loss of adhesion between keratinocytes of the...

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Source

Identifiers

PMID: 12164920
DOI: 10.1046/j.1523-1747.2002.01780.x

Genes

DSG3

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Expression of desmoglein 1 compensates for genetic loss of desmoglein 3 in keratinocyte adhesion.PMID 12164920Read ↗

Desmoglein 3 anchors telogen hair in the follicle.Semantic proximity Read ↗

Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) gene in mice causes loss of keratinocyte cell adhesion with a phenotype similar to pemphigus vulgaris.Semantic proximity Read ↗

Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.Semantic proximity Read ↗

Desmoglein 4 in hair follicle differentiation and epidermal adhesion: evidence from inherited hypotrichosis and acquired pemphigus vulgaris.Semantic proximity Read ↗

Loss of desmocollin 3 in mice leads to epidermal blistering.Semantic proximity Read ↗

Transgenic rescue of desmoglein 3 null mice with desmoglein 1 to develop a syngeneic mouse model for pemphigus vulgaris.Semantic proximity Read ↗

A spontaneous deletion within the desmoglein 3 extracellular domain of mice results in hypomorphic protein expression, immunodeficiency, and a wasting disease phenotype.Semantic proximity Read ↗

Ultrastructural changes in mice actively producing antibodies to desmoglein 3 parallel those in patients with pemphigus vulgaris.Semantic proximity Read ↗

Antibodies against keratinocyte antigens other than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions.Semantic proximity Read ↗

Epidermal transglutaminase (TGase 3) is required for proper hair development, but not the formation of the epidermal barrier.Semantic proximity Read ↗

Use of autoantigen-knockout mice in developing an active autoimmune disease model for pemphigus.Semantic proximity Read ↗

Delineation of diversified desmoglein distribution in stratified squamous epithelia: implications in diseasesSemantic proximity Read ↗

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