ArticleFrontiers in immunology2017
Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 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
- Pemphigus Vulgaris Autoantibodies Induce an Endoplasmic Reticulum Stress Response.The Journal of investigative dermatology · 2025Article
- Autoimmune pemphigus: difficulties in diagnosis and the molecular mechanisms underlying the disease.Frontiers in immunology · 2025Review
- Microarray Gene Expression Analysis of Lesional Skin in Canine Pemphigus Foliaceus.Veterinary sciences · 2024Article
- Deep pemphigus (pemphigus vulgaris, pemphigus vegetans and paraneoplastic pemphigus) in dogs, cats and horses: a comprehensive review.BMC veterinary research · 2020Review
- Endoplasmic reticulum stress promotes inflammation-mediated proteolytic activity at the ocular surface.Scientific reports · 2020Article
- Complementary Chinese Herbal Medicine Therapy Improves Survival in Patients With Pemphigus: A Retrospective Study From a Taiwan-Based Registry.Frontiers in pharmacology · 2020Article
- Condemned or Not to Die? Gene Polymorphisms Associated With Cell Death in Pemphigus Foliaceus.Frontiers in immunology · 2019Article
- Insights into the role of endoplasmic reticulum stress in skin function and associated diseases.The FEBS journal · 2019Review
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
Abstract
Pemphigus consists of a group of chronic blistering skin diseases mediated by autoantibodies (autoAbs). The dogma that pemphigus is caused by keratinocyte dissociation (acantholysis) as a distinctive and direct consequence of the presence of autoAb targeting two main proteins of the desmosome-desmoglein (DSG) 1 and/or DSG3-has been put to the test. Several outside-in signaling events elicited by pemphigus autoAb in keratinocytes have been described, among which stands out p38 mitogen-activated protein kinase (p38 MAPK) engagement and its apoptotic effect on keratinocytes. The role of apoptosis in the disease is, however, debatable, to an extent that it may not be a determinant event for the occurrence of acantholysis. Also, it has been verified that compromised DSG trans-interaction does not lead to keratinocyte dissociation when p38 MAPK is inhibited. These examples of conflicting results have been followed by recent work revealing an important role for endoplasmic reticulum (ER) stress in pemphigus' pathogenesis. ER stress is known to activate the p38 MAPK pathway, and
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