Mutations in CNNM4 cause recessive cone-rod dystrophy with amelogenesis imperfecta.
Détails
Télécharger: BIB_34261EDA46B0.P001.pdf (1322.61 [Ko])
Etat: Public
Version: Final published version
Etat: Public
Version: Final published version
ID Serval
serval:BIB_34261EDA46B0
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Mutations in CNNM4 cause recessive cone-rod dystrophy with amelogenesis imperfecta.
Périodique
American journal of human genetics
ISSN
1537-6605[electronic]
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
84
Numéro
2
Pages
259-65
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
Cone-rod dystrophies are inherited dystrophies of the retina characterized by the accumulation of deposits mainly localized to the cone-rich macular region of the eye. Dystrophy can be limited to the retina or be part of a syndrome. Unlike nonsyndromic cone-rod dystrophies, syndromic cone-rod dystrophies are genetically heterogeneous with mutations in genes encoding structural, cell-adhesion, and transporter proteins. Using a genome-wide single-nucleotide polymorphism (SNP) haplotype analysis to fine map the locus and a gene-candidate approach, we identified homozygous mutations in the ancient conserved domain protein 4 gene (CNNM4) that either generate a truncated protein or occur in highly conserved regions of the protein. Given that CNNM4 is implicated in metal ion transport, cone-rod dystrophy and amelogenesis imperfecta may originate from abnormal ion homeostasis.
Mots-clé
Amelogenesis Imperfecta/genetics, Cation Transport Proteins/genetics, Female, Gene Duplication, Genes, Recessive, Humans, Male, Mutation, Pedigree, Polymorphism, Single Nucleotide, Retinal Cone Photoreceptor Cells/pathology, Retinal Rod Photoreceptor Cells/pathology, Retinitis Pigmentosa/genetics, Sequence Deletion
Pubmed
Web of science
Open Access
Oui
Création de la notice
30/09/2009 16:17
Dernière modification de la notice
20/08/2019 13:20