Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A new ex vivo human oral mucosa model reveals that p38 MAPK inhibition is not effective in preventing autoantibody‐induced mucosal blistering in pemphigus

20 Jun 2019

Abstract excerpt

BACKGROUND: Pemphigus vulgaris (PV) is an autoimmune disease characterized by blister formation in the epidermis and oral mucosa due to loss of keratinocyte cohesion. Autoantibodies present in patients with PV (PV-IgG) are known to primarily target desmoglein (Dsg)1 and Dsg3 in desmosomes. The mucosal-dominant subtype of PV (mdPV) is caused by PV-IgG autoantibodies against the cadherin-type adhesion molecule...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autoimmune Bullous Skin Diseases
Share to Sympathectomy and Hyperhidrosis Treatments
Share to Urticaria and Related Conditions

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31218663
DOI: 10.1111/bjd.18237

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A new ex vivo human oral mucosa model reveals that p38 MAPK inhibition is not effective in preventing autoantibody‐induced mucosal blistering in pemphigusPMID 31218663Read ↗

Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated ModelSemantic proximity Read ↗

Different signaling patterns contribute to loss of keratinocyte cohesion dependent on autoantibody profile in pemphigusSemantic proximity Read ↗

Pemphigus-A Disease of Desmosome Dysfunction Caused by Multiple Mechanisms.Semantic proximity Read ↗

Pemphigus vulgaris: recent advances in our understanding of its pathogenesis.Semantic proximity Read ↗

In Vitro, Ex Vivo, and In Vivo Models for the Study of PemphigusSemantic proximity Read ↗

Immune response in pemphigus and beyond: progresses and emerging concepts.Semantic proximity Read ↗

Preclinical Studies Identify Non-Apoptotic Low-Level Caspase-3 as Therapeutic Target in Pemphigus VulgarisSemantic proximity Read ↗

Evolving Mechanisms in the Pathophysiology of Pemphigus Vulgaris: A Review Emphasizing the Role of Desmoglein 3 in Regulating p53 and the Yes-Associated ProteinSemantic proximity Read ↗

In pemphigus, cell detachment, but not autoantibody binding, induces cell-wide, long-lasting transcriptomic and proteomic changesSemantic proximity Read ↗

Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in PemphigusSemantic proximity Read ↗

Mucosal pemphigus vulgaris anti-Dsg3 IgG is pathogenic to the oral mucosa of humanized Dsg3 mice.Semantic proximity Read ↗

The impact of signaling pathways on the desmosome ultrastructure in pemphigusSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.