The Ectodysplasin and NFκB signalling pathways in odontogenesis
The Ectodysplasin and NFκB signalling pathways in odontogenesis
复制标题
DOI:
10.1016/j.archoralbio.2004.11.019
复制
发表时间:
2005-02-01
影响因子:
3
通讯作者:
Sharpe, PT
中科院分区:
文献类型:
--
作者:
Courtney, JM;Blackburn, J;Sharpe, PT
Hypohidrotic ectodermal dysplasia (HED) is a congenital disorder affecting organs of ectodermal origin including teeth, hair and sweat glands. Defects in Ectodysplasin (tabby), Edar (downless) and Edar associated death domain (Edaradd) (crinkled) cause HED in both humans and mice. Ectodysplasin is a tumour necrosis factor (TNF) superfamily member whose downstream signalling is transduced by the inhibitor Of kappa B kinase (IKK) complex and inhibitors of kappa B (I kappa B) to activate the transcription factor NF kappa B. NF kappa B signalling is involved in a wide range of cellular processes and at each stage the different family members must be tightly regulated for each function. Recent data have demonstrated the importance of this signalling pathway in odontogenesis, particularly in the formation of cusps. Here we review recent advances in our understanding of Ectodysplasin/NF kappa B signalling in tooth development and in particular the central rote of the IKK complex. (c) 2005 Elsevier Ltd. All rights reserved.