ArticleThe Journal of biological chemistry2008
Pemphigus vulgaris IgG-induced desmoglein-3 endocytosis and desmosomal disassembly are mediated by a clathrin- and dynamin-independent mechanism.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- What protein kinases are crucial for acantholysis and blister formation in pemphigus vulgaris? A systematic review.Journal of cellular physiology · 2022Pooled it
- Gingival Response to Dental Implant: Comparison Study on the Effects of New Nanopored Laser-Treated vs. Traditional Healing Abutments.International journal of molecular sciences · 2020Trial
- Caspase-activation powers anti-Desmoglein 3-induced acantholysis in human epidermis.Cell death discovery · 2026Article
- Genistein in autoimmune diseases: from experimental evidence to emerging clinical data.Frontiers in immunology · 2026Review
- Dihydroartemisinin attenuates pemphigus vulgaris by regulating Dsg3 and the TLR9/NF-κB pathway.American journal of translational research · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Desmosomes at a glance.Journal of cell science · 2024Review
- Role of auto-antibodies in the mechanisms of dengue pathogenesis and its progression: a comprehensive review.Archives of microbiology · 2024Review
- Treatment-naïve pemphigus patients showing IgG tissue deposits have serum IgG antibodies against desmoglein 1 detected more often than those against desmoglein 3: a monocentre laboratory experience.Postepy dermatologii i alergologii · 2023Article
- Apoptolysis: a less understood concept in the pathogenesis of Pemphigus Vulgaris.Apoptosis : an international journal on programmed cell death · 2022Review
- Article
- Cortical tension regulates desmosomal morphogenesis.Frontiers in cell and developmental biology · 2022Article
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Cadherin Signaling in Cancer and Autoimmune Diseases.International journal of molecular sciences · 2021Review
- Exploration and insights into the cellular internalization and intracellular fate of amphiphilic polymeric nanocarriers.Acta pharmaceutica Sinica. B · 2021Review
- The desmosomal cadherin desmoglein-3 acts as a keratinocyte anti-stress protein via suppression of p53.Cell death & disease · 2019Article
- Immortalized Human hTert/KER-CT Keratinocytes a Model System for Research on Desmosomal Adhesion and Pathogenesis of Pemphigus Vulgaris.International journal of molecular sciences · 2019Article
- The desmosome is a mesoscale lipid raft-like membrane domain.Molecular biology of the cell · 2019Article
- RPGRIP1L is required for stabilizing epidermal keratinocyte adhesion through regulating desmoglein endocytosis.PLoS genetics · 2019Article
- Role of PKC and ERK Signaling in Epidermal Blistering and Desmosome Regulation in Pemphigus.Frontiers in immunology · 2019Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Pemphigus vulgaris (PV) is a life-threatening autoimmune disease characterized by oral mucosal erosions and epidermal blistering. The autoantibodies generated target the desmosomal cadherin desmoglein-3 (Dsg3). Previous studies demonstrate that upon PV IgG binding, Dsg3 is internalized and enters an endo-lysosomal pathway where it is degraded. To define the endocytic machinery involved in PV IgG-induced Dsg3 internalization, human keratinocytes were incubated with PV IgG, and various tools were used to perturb distinct endocytic pathways. The PV IgG.Dsg3 complex failed to colocalize with clathrin, and inhibitors of clathrin- and dynamin-dependent pathways had little or no effect on Dsg3 internalization. In contrast, cholesterol binding agents such as filipin and nystatin and the tyrosine kinase inhibitor genistein dramatically inhibited Dsg3 internalization. Furthermore, the Dsg3 cytoplasmic tail specified sensitivity to these inhibitors. Moreover, inhibition of Dsg3 endocytosis with genistein prevented disruption of desmosomes and loss of adhesion in the presence of PV IgG. Altogether, these results suggest that PV IgG-induced Dsg3 internalization is mediated through a clathrin- and dynamin-independent pathway and that Dsg3 endocytosis is tightly coupled to the pathogenic activity of PV IgG.
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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.