EDA Signaling and Skin Appendage Development

The same morphogenetic signals are often involved in the development of different organs. For developing skin appendages, a model for tissue-specific regulation of signaling is provided by the EDA pathway, which accesses the otherwise ubiquitous NF-κB transcription factors. EDA signaling is mediated...

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Vydané v:	Cell cycle (Georgetown, Tex.) Ročník 5; číslo 21; s. 2477 - 2483
Hlavní autori:	Cui, Chang-Yi, Schlessinger, David
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Taylor & Francis 01.11.2006
Predmet:	Amino Acid Sequence Animals Binding Biology Bioscience Calcium Cancer Cell Cycle Ectodermal Dysplasia - genetics Ectodysplasins - chemistry Ectodysplasins - genetics Ectodysplasins - physiology Gene Expression Regulation, Developmental Humans Landes Ligands Mice Mice, Knockout Mice, Transgenic Models, Biological Molecular Sequence Data Organogenesis Proteins Sequence Homology, Amino Acid Signal Transduction Skin - embryology Skin - metabolism
ISSN:	1538-4101, 1551-4005, 1551-4005
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Shrnutí:	The same morphogenetic signals are often involved in the development of different organs. For developing skin appendages, a model for tissue-specific regulation of signaling is provided by the EDA pathway, which accesses the otherwise ubiquitous NF-κB transcription factors. EDA signaling is mediated by ectodysplasin, EDAR and EDARADD, which form a new TNF ligand-receptor-adaptor family that is restricted to skin appendages in vertebrates from fish to human. The critical function of the pathway was demonstrated in the hereditary genetic disorder Anhidrotic Ectodermal Dysplasia (EDA), which is characterized by defective formation of hair follicles, sweat glands and teeth. The pathway does not appear to initiate the development of the appendages, but is regulated by and regulates the course of further morphogenesis. In mice, transgenic and knockout strains have increasingly revealed features of the mechanism, and suggest possible non-invasive interventions to alleviate EDA deficiency, especially in sweat glands and eyes.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23
ISSN:	1538-4101 1551-4005 1551-4005
DOI:	10.4161/cc.5.21.3403