Possible therapeutic target MKK3 in blister formation in pemphigus
Author:
Funder
Korea Research Institute of Chemical Technology
Publisher
Springer Science and Business Media LLC
Link
https://link.springer.com/content/pdf/10.1007/s00403-024-03136-4.pdf
Reference5 articles.
1. Mao X, Sano Y, Park JM, Payne AS (2011) p38 MAPK activation is downstream of the loss of intercellular adhesion in pemphigus vulgaris. J Biol Chem 286:1283–1291
2. Lu HT, Yang DD, Wysk M, Gatti E, Mellman I, Davis RJ, Flavell RA (1999) Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice. Embo J 18:1845–1857
3. Heupel WM, Engerer P, Schmidt E, Waschke J (2009) Pemphigus vulgaris IgG cause loss of desmoglein-mediated adhesion and keratinocyte dissociation independent of epidermal growth factor receptor. Am J Pathol 174:475–485
4. Mao X, Payne AS (2008) Seeking approval: present and future therapies for pemphigus vulgaris. Curr Opin Investig Drugs 9:497–504
5. Mavropoulos A, Orfanidou T, Liaskos C, Smyk DS, Spyrou V, Sakkas LI et al (2013) p38 MAPK Signaling in Pemphigus: Implications for Skin Autoimmunity. Autoimmune Dis. 2013:728529
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