| Literature DB >> 8630502 |
P Edery1, T Attié, J Amiel, A Pelet, C Eng, R M Hofstra, H Martelli, C Bidaud, A Munnich, S Lyonnet.
Abstract
Hirschsprung disease (HSCR) and Waardenburg sundrome (WS) are congenital malformations regarded as neurocristopathies since both disorders involve neural crest-derived cells. The WS-HSCR association (Shah-Waardenburg syndrome) is a rare autosomal recessive condition that occasionally has been ascribed to mutations of the endothelin-receptor B (EDNRB) gene. WS-HSCR mimicks the megacolon and white coat-spotting observed in Ednrb mouse mutants. Since mouse mutants for the EDNRB ligand, endothelin-3 (EDN3), displayed a similar phenotype, the EDN3 gene was regarded as an alternative candidate gene in WS-HSCR. Here, we report a homozygous substitution/deletion mutation of the EDN3 gene in a WS-HSCR patient. EDN3 thus becomes the third known gene (after RET and EDNRB) predisposing to HSCR, supporting the view that the endothelin-signaling pathways play a major role in the development of neural crests.Entities:
Mesh:
Substances:
Year: 1996 PMID: 8630502 DOI: 10.1038/ng0496-442
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330