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Antibodies against keratinocyte antigens other than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions.

Nguyen VT, Ndoye A, Shultz LD, Pittelkow MR, Grando SA.

J Clin Invest. 2000 Dec;106(12):1467-79.


Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris.

Mahoney MG, Wang Z, Rothenberger K, Koch PJ, Amagai M, Stanley JR.

J Clin Invest. 1999 Feb;103(4):461-8.


Pemphigus vulgaris: recent advances in our understanding of its pathogenesis.

Femiano F.

Minerva Stomatol. 2007 Apr;56(4):215-23. Review. English, Italian.


Induction of pemphigus phenotype by a mouse monoclonal antibody against the amino-terminal adhesive interface of desmoglein 3.

Tsunoda K, Ota T, Aoki M, Yamada T, Nagai T, Nakagawa T, Koyasu S, Nishikawa T, Amagai M.

J Immunol. 2003 Feb 15;170(4):2170-8.


Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) gene in mice causes loss of keratinocyte cell adhesion with a phenotype similar to pemphigus vulgaris.

Koch PJ, Mahoney MG, Ishikawa H, Pulkkinen L, Uitto J, Shultz L, Murphy GF, Whitaker-Menezes D, Stanley JR.

J Cell Biol. 1997 Jun 2;137(5):1091-102.


Conformational epitope mapping of antibodies against desmoglein 3 in experimental murine pemphigus vulgaris.

Anzai H, Fujii Y, Nishifuji K, Aoki-Ota M, Ota T, Amagai M, Nishikawa T.

J Dermatol Sci. 2004 Aug;35(2):133-42.


Ultrastructural changes in mice actively producing antibodies to desmoglein 3 parallel those in patients with pemphigus vulgaris.

Shimizu A, Ishiko A, Ota T, Tsunoda K, Koyasu S, Amagai M, Nishikawa T.

Arch Dermatol Res. 2002 Oct;294(7):318-23. Epub 2002 Sep 5.


The extent of desmoglein 3 depletion in pemphigus vulgaris is dependent on Ca(2+)-induced differentiation: a role in suprabasal epidermal skin splitting?

Spindler V, Endlich A, Hartlieb E, Vielmuth F, Schmidt E, Waschke J.

Am J Pathol. 2011 Oct;179(4):1905-16. doi: 10.1016/j.ajpath.2011.06.043. Epub 2011 Aug 22.


Peptides Targeting the Desmoglein 3 Adhesive Interface Prevent Autoantibody-induced Acantholysis in Pemphigus.

Heupel WM, Müller T, Efthymiadis A, Schmidt E, Drenckhahn D, Waschke J.

J Biol Chem. 2009 Mar 27;284(13):8589-95. doi: 10.1074/jbc.M808813200. Epub 2009 Jan 21.


Low pathogenicity of anti-desmoglein 3 immunoglobulin G autoantibodies contributes to the atypical clinical phenotypes in pemphigus.

Saleh MA, Hashimoto R, Kase Y, Amagai M, Yamagami J.

J Dermatol. 2015 Jul;42(7):685-9. doi: 10.1111/1346-8138.12888. Epub 2015 Apr 24.


IgG-induced clustering of desmogleins 1 and 3 in skin of patients with pemphigus fits with the desmoglein nonassembly depletion hypothesis.

Oktarina DA, van der Wier G, Diercks GF, Jonkman MF, Pas HH.

Br J Dermatol. 2011 Sep;165(3):552-62. doi: 10.1111/j.1365-2133.2011.10463.x.


IgG binds to desmoglein 3 in desmosomes and causes a desmosomal split without keratin retraction in a pemphigus mouse model.

Shimizu A, Ishiko A, Ota T, Tsunoda K, Amagai M, Nishikawa T.

J Invest Dermatol. 2004 May;122(5):1145-53.


Synergistic pathogenic effects of combined mouse monoclonal anti-desmoglein 3 IgG antibodies on pemphigus vulgaris blister formation.

Kawasaki H, Tsunoda K, Hata T, Ishii K, Yamada T, Amagai M.

J Invest Dermatol. 2006 Dec;126(12):2621-30. Epub 2006 Jul 13.


IgG autoantibodies directed against desmoglein 3 cause dissociation of keratinocytes in canine pemphigus vulgaris and paraneoplastic pemphigus.

Nishifuji K, Olivry T, Ishii K, Iwasaki T, Amagai M.

Vet Immunol Immunopathol. 2007 Jun 15;117(3-4):209-21. Epub 2007 Feb 16.


Pathogenic autoantibody production requires loss of tolerance against desmoglein 3 in both T and B cells in experimental pemphigus vulgaris.

Tsunoda K, Ota T, Suzuki H, Ohyama M, Nagai T, Nishikawa T, Amagai M, Koyasu S.

Eur J Immunol. 2002 Mar;32(3):627-33.


Relevance of differential immunogenicity of human and mouse recombinant desmoglein-3 for the induction of acantholytic autoantibodies in mice.

Kaithamana S, Fan JL, Memar O, Li K, Uitto J, Seetharamaiah GS, Prabhakar BS.

Clin Exp Immunol. 2003 Apr;132(1):16-23.

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