[HTML][HTML] Desmosome signaling: inhibition of p38MAPK prevents pemphigus vulgaris IgG-induced cytoskeleton reorganization
P Berkowitz, P Hu, Z Liu, LA Diaz, JJ Enghild… - Journal of Biological …, 2005 - ASBMB
In the human autoimmune blistering disease pemphigus vulgaris (PV) pathogenic
antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell
detachment (acantholysis). Pathogenic PV dsg3 autoantibodies were used to initiate
desmosome signaling in human keratinocyte cell cultures. Heat shock protein 27 (HSP27)
and p38MAPK were identified as proteins rapidly phosphorylated in response to PV IgG.
Inhibition of p38MAPK activity prevented PV IgG-induced HSP27 phosphorylation, keratin …
antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell
detachment (acantholysis). Pathogenic PV dsg3 autoantibodies were used to initiate
desmosome signaling in human keratinocyte cell cultures. Heat shock protein 27 (HSP27)
and p38MAPK were identified as proteins rapidly phosphorylated in response to PV IgG.
Inhibition of p38MAPK activity prevented PV IgG-induced HSP27 phosphorylation, keratin …