NDLI: Plakophilin-1 protects keratinocytes from pemphigus vulgaris IgG by forming calcium-independent desmosomes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tucker, Dana K. Stahley, Sara N. Kowalczyk, Andrew P.
Description	Country affiliation: United States Author Affiliation: Tucker DK ( 1] Department of Cell Biology, Emory University, Atlanta, Georgia, USA [2] Graduate Program in Biochemistry, Cell, and Developmental Biology, Emory University, Atlanta, Georgia, USA.); Stahley SN ( 1] Department of Cell Biology, Emory University, Atlanta, Georgia, USA [2] Graduate Program in Biochemistry, Cell, and Developmental Biology, Emory University, Atlanta, Georgia, USA.); Kowalczyk AP ( 1] Department of Cell Biology, Emory University, Atlanta, Georgia, USA [2] Department of Dermatology, Emory University, Atlanta, Georgia, USA [3] Winship Cancer Institute, Emory University, Atlanta, Georgia, USA.)
Abstract	Plakophilin-1 (PKP-1) is an armadillo family protein critical for desmosomal adhesion and epidermal integrity. In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodies (IgG) target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cell adhesion. Here, we report that enhanced expression of PKP-1 protects keratinocytes from PV IgG-induced loss of cell-cell adhesion. PKP-1 prevents loss of Dsg3 and other desmosomal proteins from cell-cell borders and prevents alterations in desmosome ultrastructure in keratinocytes treated with PV IgG. Using a series of Dsg3 chimeras and deletion constructs, we find that PKP-1 clusters Dsg3 with the desmosomal plaque protein desmoplakin in a manner dependent on the plakoglobin-binding domain of the Dsg3 tail. Furthermore, PKP-1 expression transforms desmosome adhesion from a calcium-dependent to a calcium-independent and hyperadhesive state. These results demonstrate that manipulating the expression of a single desmosomal plaque protein can block the pathogenic effects of PV IgG on keratinocyte adhesion.
File Format	HTM / HTML
ISSN	0022202X
e-ISSN	15231747
DOI	10.1038/jid.2013.401
Journal	Journal of Investigative Dermatology
Issue Number	4
Volume Number	134
Language	English
Publisher	Elsevier
Publisher Date	2014-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Dermatology Calcium Chemistry Desmosomes Metabolism Immunoglobulin G Keratinocytes Cytology Pemphigus Plakophilins Cell Adhesion Cells, Cultured Chelating Agents Desmoglein 3 Detergents Endocytosis Epidermis Gene Expression Regulation Immunology Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology Dermatology

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Plakophilin-1 protects keratinocytes from pemphigus vulgaris IgG by forming calcium-independent desmosomes

Desmosome disassembly in response to pemphigus vulgaris IgG occurs in distinct phases and can be reversed by expression of exogenous Dsg3.

Pemphigus vulgaris IgG-induced desmoglein-3 endocytosis and desmosomal disassembly are mediated by a clathrin- and dynamin-independent mechanism.

Plakophilins, desmogleins, and pemphigus: the tail wagging the dog.

Disruption of desmosome assembly by monovalent human pemphigus vulgaris monoclonal antibodies.

Loss of the desmosomal protein perp enhances the phenotypic effects of pemphigus vulgaris autoantibodies.

Differential IgG recognition of desmoglein 3 by paraneoplastic pemphigus and pemphigus vulgaris sera.

IgG autoantibody response against keratinocyte cadherins in endemic pemphigus foliaceus (fogo selvagem).

Super-Resolution Microscopy Reveals Altered Desmosomal Protein Organization in Tissue from Patients with Pemphigus Vulgaris.

Plakophilin-1 protects keratinocytes from pemphigus vulgaris IgG by forming calcium-independent desmosomes.

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Plakophilin-1 protects keratinocytes from pemphigus vulgaris IgG by forming calcium-independent desmosomes

Desmosome disassembly in response to pemphigus vulgaris IgG occurs in distinct phases and can be reversed by expression of exogenous Dsg3.

Pemphigus vulgaris IgG-induced desmoglein-3 endocytosis and desmosomal disassembly are mediated by a clathrin- and dynamin-independent mechanism.

Plakophilins, desmogleins, and pemphigus: the tail wagging the dog.

Disruption of desmosome assembly by monovalent human pemphigus vulgaris monoclonal antibodies.

Loss of the desmosomal protein perp enhances the phenotypic effects of pemphigus vulgaris autoantibodies.

Differential IgG recognition of desmoglein 3 by paraneoplastic pemphigus and pemphigus vulgaris sera.

IgG autoantibody response against keratinocyte cadherins in endemic pemphigus foliaceus (fogo selvagem).

Super-Resolution Microscopy Reveals Altered Desmosomal Protein Organization in Tissue from Patients with Pemphigus Vulgaris.

Plakophilin-1 protects keratinocytes from pemphigus vulgaris IgG by forming calcium-independent desmosomes.