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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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Vol. 5; no. 21; pp. 2477 - 2483
Main Authors: Cui, Chang-Yi, Schlessinger, David
Format: Journal Article
Language:English
Published: United States Taylor & Francis 01.11.2006
Subjects:
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
Online Access:Get full text
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Summary: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.
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ISSN:1538-4101
1551-4005
1551-4005
DOI:10.4161/cc.5.21.3403