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The Ectodysplasin and NFkappaB signalling pathways in odontogenesis


Courtney, J and Blackburn, J and Sharpe, PT, The Ectodysplasin and NFkappaB signalling pathways in odontogenesis, Archives of Oral Biology: A Multidisciplinary Journal in Oral Research, 50, (2) pp. 159-63. ISSN 0003-9969 (2005) [Refereed Article]

DOI: doi:10.1016/j.archoralbio.2004.11.019


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 kappaB kinase (IKK) complex and inhibitors of kappaB (IkappaB) to activate the transcription factor NFkappaB. NFkappaB 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/NFkappaB signalling in tooth development and in particular the central role of the IKK complex.

Item Details

Item Type:Refereed Article
Research Division:Biological Sciences
Research Group:Biochemistry and cell biology
Research Field:Cell development, proliferation and death
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Courtney, J (Dr Jo-Maree Courtney)
ID Code:87613
Year Published:2005
Web of Science® Times Cited:45
Deposited By:Medicine
Deposited On:2013-11-27
Last Modified:2013-11-27

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