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Literature DB >> 24352077

A new light on an old disease: adhesion signaling in pemphigus vulgaris.

Arnaud Galichet¹, Luca Borradori², Eliane J Müller³.

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.

Entities: Gene

Mesh：

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Year: 2014 PMID： 24352077 DOI： 10.1038/jid.2013.439

Source DB: PubMed Journal: J Invest Dermatol ISSN： 0022-202X Impact factor: 8.551

18 in total

1. p38 MAPK activation is downstream of the loss of intercellular adhesion in pemphigus vulgaris.

Authors: Xuming Mao; Yasuyo Sano; Jin Mo Park; Aimee S Payne
Journal: J Biol Chem Date: 2010-11-15 Impact factor: 5.157

Review 2. Beyond steric hindrance: the role of adhesion signaling pathways in the pathogenesis of pemphigus.

Authors: Preety Sharma; Xuming Mao; Aimee S Payne
Journal: J Dermatol Sci Date: 2007-06-18 Impact factor: 4.563

Review 3. Outside-in signaling through integrins and cadherins: a central mechanism to control epidermal growth and differentiation?

Authors: Eliane J Müller; Lina Williamson; Carine Kolly; Maja M Suter
Journal: J Invest Dermatol Date: 2008-03 Impact factor: 8.551

4. Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering.

Authors: Volker Spindler; Vera Rötzer; Carina Dehner; Bettina Kempf; Martin Gliem; Mariya Radeva; Eva Hartlieb; Gregory S Harms; Enno Schmidt; Jens Waschke
Journal: J Clin Invest Date: 2013-01-09 Impact factor: 14.808

5. Desmosome signaling. Inhibition of p38MAPK prevents pemphigus vulgaris IgG-induced cytoskeleton reorganization.

Authors: Paula Berkowitz; Peiqi Hu; Zhi Liu; Luis A Diaz; Jan J Enghild; Michael P Chua; David S Rubenstein
Journal: J Biol Chem Date: 2005-04-19 Impact factor: 5.157

6. A pathophysiologic role for epidermal growth factor receptor in pemphigus acantholysis.

Authors: Meryem Bektas; Puneet S Jolly; Paula Berkowitz; Masayuki Amagai; David S Rubenstein
Journal: J Biol Chem Date: 2013-02-12 Impact factor: 5.157

7. Desmoglein versus non-desmoglein signaling in pemphigus acantholysis: characterization of novel signaling pathways downstream of pemphigus vulgaris antigens.

Authors: Alex I Chernyavsky; Juan Arredondo; Yasuo Kitajima; Miki Sato-Nagai; Sergei A Grando
Journal: J Biol Chem Date: 2007-03-07 Impact factor: 5.157

A new light on an old disease: adhesion signaling in pemphigus vulgaris.

1. p38 MAPK activation is downstream of the loss of intercellular adhesion in pemphigus vulgaris.

Review 2. Beyond steric hindrance: the role of adhesion signaling pathways in the pathogenesis of pemphigus.

Review 3. Outside-in signaling through integrins and cadherins: a central mechanism to control epidermal growth and differentiation?

4. Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering.

5. Desmosome signaling. Inhibition of p38MAPK prevents pemphigus vulgaris IgG-induced cytoskeleton reorganization.

6. A pathophysiologic role for epidermal growth factor receptor in pemphigus acantholysis.

7. Desmoglein versus non-desmoglein signaling in pemphigus acantholysis: characterization of novel signaling pathways downstream of pemphigus vulgaris antigens.

8. MAPKAP kinase 2 (MK2)-dependent and -independent models of blister formation in pemphigus vulgaris.

Review 9. Three functions of cadherins in cell adhesion.

10. Signaling dependent and independent mechanisms in pemphigus vulgaris blister formation.

Review 1. Pemphigus: a Comprehensive Review on Pathogenesis, Clinical Presentation and Novel Therapeutic Approaches.

Review 2. Immune response in pemphigus and beyond: progresses and emerging concepts.