PubMed · 2385287
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J Dart. 1990-08-16. EB research grants.. https://doi.org/10.1038/346604d0
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In recent years, the genes responsible for many hereditary skin diseases have been discovered. These genes encode different proteins that participate in the terminal differentiation of the epidermis, so their alteration or absence causes a keratinization disorder and/or an increase in skin fragility. Thanks to genetic analyses, we have been able to understand the physiopathology of numerous genodermatoses and we have become closer to diagnosing many others. In the not-too-distant future, biomolecular techniques may foreseeably help us prevent and treat these processes, which include skin diseases as serious as epidermolysis bullosa or epidermolytic hyperkeratosis. In this article, we will study the most recent biomolecular findings referring to keratinization and epidermal disorders, mentioning the altered genes and/ or the defective proteins that cause them.