[HTML][HTML] p38 MAPK activation is downstream of the loss of intercellular adhesion in pemphigus vulgaris

X Mao, Y Sano, JM Park, AS Payne - Journal of Biological Chemistry, 2011 - ASBMB
Pemphigus vulgaris (PV) is a potentially fatal blistering disease characterized by
autoantibodies against the desmosomal adhesion protein desmoglein (Dsg) 3. Whether
autoantibody steric hindrance or signaling through pathways such as p38 MAPK is primary
in disease pathogenesis is controversial. PV mAbs that cause endocytosis of Dsg3 but do
not dissociate keratinocytes because of compensatory adhesion by Dsg1 do not activate
p38. The same mAbs plus exfoliative toxin to inactivate Dsg1 but not exfoliative toxin alone …