ArticleThe Journal of investigative dermatology2009
Loss of the desmosomal protein perp enhances the phenotypic effects of pemphigus vulgaris autoantibodies.
Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Caspase-activation powers anti-Desmoglein 3-induced acantholysis in human epidermis.Cell death discovery · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Mutations in PERP Cause Dominant and Recessive Keratoderma.The Journal of investigative dermatology · 2019Article
- Desmosomes: regulators of cellular signaling and adhesion in epidermal health and disease.Cold Spring Harbor perspectives in medicine · 2014Review
- Transmembrane protein PERP is a component of tessellate junctions and of other junctional and non-junctional plasma membrane regions in diverse epithelial and epithelium-derived cells.Cell and tissue research · 2013Article
- Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer.Breast cancer research : BCR · 2012Article
- Pemphigus autoimmunity: hypotheses and realities.Autoimmunity · 2012Review
- Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts.Cell communication & adhesion · 2011Article
- Experimental human cell and tissue models of pemphigus.Dermatology research and practice · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pemphigus vulgaris (PV) is an autoimmune bullous disease in which autoantibodies against proteins of the desmosomal adhesion complex perturb desmosomal function, leading to intercellular adhesion defects in the oral mucosa and skin. Previous studies have demonstrated a central role for downregulation of the desmosomal cadherin desmoglein 3 (DSG3) in the pathogenesis of PV. However, the effects of non-cadherin desmosomal proteins in modulating the cellular manifestations of PV remain poorly understood. Here, we characterize the expression and functional importance of Perp, a newly discovered tetraspan desmosomal protein, in PV. Our data demonstrate that PV autoantibodies disrupt Perp expression at the membrane and trigger its internalization along with DSG3 into the endosomal pathway, where it is ultimately targeted to the lysosome for degradation. We further show that Perp deficiency exacerbates the pathogenic effects of PV autoantibodies on keratinocytes by enhancing both the depletion of desmosomal DSG3 and intercellular adhesion defects. Together, our findings highlight the importance of non-cadherin desmosomal proteins in modulating PV phenotypes and provide new insight into Perp's role in the desmosome.
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Registered trials
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.