Ectodysplasin signaling in development

被引:157
作者
Mikkola, ML [1 ]
Thesleff, I [1 ]
机构
[1] Univ Helsinki, Viikki Bioctr, Inst Biotechnol, Dev Biol Program, FIN-00014 Helsinki, Finland
关键词
Eda; Edar; Xedar; Edaradd; HED; TNF; Tabby; downless; ectodermal organogenesis; morphogenesis;
D O I
10.1016/S1359-6101(03)00020-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ectodysplasin (Eda), a signaling molecule belonging to the tumor necrosis factor family, is required for normal development of several ectodermally derived organs in humans and mice. Two closely related isoforms of ectodysplasin, Eda-A1 and Eda-A2, have been described which bind to and activate two different receptors, Edar and X-linked Eda-A2 receptor (Xedar), respectively. Mutations in Eda, Edar or other molecules of this signaling pathway cause ectodermal dysplasias characterized by defective development of teeth, hairs, and several exocrine glands such as sweat glands presumably due to impaired NF-kappaB response. Studies with mice either lacking the functional proteins of Edar pathway or overexpressing the ligand or receptor suggest that Eda-A1-Edar signaling has multiple roles in ectodermal organ development regulating their initiation, morphogenesis, and differentiation. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:211 / 224
页数:14
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