Related Experiment Video
Updated: May 4, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
A new light on an old disease: adhesion signaling in pemphigus vulgaris
Arnaud Galichet1, Luca Borradori2, Eliane J Müller1
1Vetsuisse Faculty, Molecular Dermatology and Stem Cell Research, Institute of Animal Pathology, University Hospital of Bern, Bern, Switzerland; DermFocus University of Bern, University Hospital of Bern, Bern, Switzerland.
Abstract:
Disruption of desmosomal cadherin adhesion leads to the activation of intracellular signaling pathways that are responsible for blister formation in pemphigus vulgaris (PV). Recent studies corroborate the implication of the p38 mitogen-activated protein kinase in PV blistering via its downstream effector mitogen-activated protein kinase activated protein kinase 2. These insights highlight the key role of cadherins in tissue homeostasis and are expected to change pemphigus management.
Related Concept Videos
Immunoglobulin-like Cell Adhesion Molecules
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...
Intracellular Signaling Affects Focal Adhesions
Some...
Adherens Junctions
Adherens Junctions are Dynamic
Desmosomes
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
Anchoring Junctions

