Literature DB >> 24399846

NECAP1 loss of function leads to a severe infantile epileptic encephalopathy.

Anas M Alazami1, Hadia Hijazi, Amal Y Kentab, Fowzan S Alkuraya.   

Abstract

BACKGROUND: Epileptic encephalopathy is a broad clinical category that is highly heterogeneous genetically.
OBJECTIVE: To describe a multiplex extended consanguineous family that defines a molecularly novel subtype of early infantile epileptic encephalopathy.
METHODS: Autozygosity mapping and exome sequencing for the identification of the causal mutation. This was followed by expression analysis of the candidate gene.
RESULTS: In an extended multigenerational family with six affected individuals, a single novel disease locus was identified on chromosome 12p13.31-p13.2. Within that locus, the only deleterious novel exomic variant was a homozygous truncating mutation in NECAP1, encoding a clathrin-accessory protein. The mutation was confirmed to trigger nonsense-mediated decay. Consistent with previous reports, we show that NECAP1 is highly enriched in the central nervous system.
CONCLUSIONS: NECAP1 is known to regulate clathrin-mediated endocytosis in synapses. The mutation we report here links for the first time this trafficking pathway in early infantile epileptic encephalopathy.

Entities:  

Keywords:  Clathrin; Encephalopathy; Neuron; Synapse; Vesicle

Mesh:

Substances:

Year:  2014        PMID: 24399846     DOI: 10.1136/jmedgenet-2013-102030

Source DB:  PubMed          Journal:  J Med Genet        ISSN: 0022-2593            Impact factor:   6.318


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