Mutations in CNNM4 cause recessive cone-rod dystrophy with amelogenesis imperfecta.


Autoria(s): Polok B.; Escher P.; Ambresin A.; Chouery E.; Bolay S.; Meunier I.; Nan F.; Hamel C.; Munier F.L.; Thilo B.; Mégarbané A.; Schorderet D.F.
Data(s)

2009

Resumo

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.

Identificador

http://serval.unil.ch/?id=serval:BIB_34261EDA46B0

isbn:1537-6605[electronic]

pmid:19200527

doi:10.1016/j.ajhg.2009.01.006

isiid:000263799700015

http://my.unil.ch/serval/document/BIB_34261EDA46B0.pdf

http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_34261EDA46B01

Idioma(s)

en

Direitos

info:eu-repo/semantics/openAccess

Fonte

American journal of human genetics, vol. 84, no. 2, pp. 259-65

Palavras-Chave #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
Tipo

info:eu-repo/semantics/article

article