Abstract |
About a decade age, loss-of-function mutations in the filaggrin molecule were first implicated in the pathogenesis of ichthyosis vulgaris and, subsequently, of atopic dermatitis and other atopic diseases. Since then, intensive study of the role of filaggrin null mutations have led to other milestones in understanding the pathologic pathways in these diseases, including the initiation, maintenance, and promotion of the disease processes. The result has been new and emerging clinical and pharmacologic strategies for early identification of and intervention in atopic diseases. Semin Cutan Med Surg 35(supp5):S89-S91.
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Authors | Alan D Irvine Md, Lawrence F Eichenfield Md, Sheila F Friedlander Md, Eric L Simpson Md McR |
Journal | Seminars in cutaneous medicine and surgery
(Semin Cutan Med Surg)
Vol. 35
Issue 5 Suppl
Pg. S89-91
(Jun 2016)
ISSN: 1085-5629 [Print] United States |
PMID | 27525507
(Publication Type: Journal Article, Review)
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Copyright | 2016 published by Frontline Medical Communications. |
Chemical References |
- FLG protein, human
- Filaggrin Proteins
- Intermediate Filament Proteins
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Topics |
- Dermatitis, Atopic
(complications, drug therapy, genetics, immunology)
- Environment
- Filaggrin Proteins
- Food Hypersensitivity
(complications)
- Humans
- Intermediate Filament Proteins
(genetics)
- Mutation
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