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First published online February 22, 2006
doi: 10.1242/10.1242/jcs.02888
Commentary |
1 Department of Dermatology, Emory University School of Medicine, Emory University, Atlanta, GA 30322, USA
2 Department of Cell Biology, Emory University School of Medicine, Emory University, Atlanta, GA 30322, USA
* Author for correspondence (e-mail: akowalc{at}emory.edu)
Accepted 12 January 2006
Human skin diseases have revealed fundamental mechanisms by which cytoskeletal proteins contribute to tissue architecture and function. In particular, the analysis of epidermal blistering disorders and the role of keratin gene mutations in these diseases has led to significant increases in our understanding of intermediate filament biology. The major cell-surface attachment site for intermediate filament networks is the desmosome, an adhesive intercellular junction prominent in the epidermis and the heart. During the past decade, substantial progress has been made in understanding the molecular basis of a variety of epidermal autoimmune diseases, skin fragility syndromes, and disorders that involve a combination of heart and skin defects caused by perturbations in desmosome structure and function. These human diseases reveal key roles for desmosomes in maintaining tissue integrity, but also suggest functions for desmosomal components in signal transduction pathways and epidermal organization.
Key words: Desmosome, Cadherin, Plakoglobin, Plakophilin, Pemphigus, Keratoderma, Cardiomyopathy
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