New evidence that biallelic loss of function in EEF1B2 gene leads to intellectual disability.


Journal

Clinical genetics
ISSN: 1399-0004
Titre abrégé: Clin Genet
Pays: Denmark
ID NLM: 0253664

Informations de publication

Date de publication:
04 2020
Historique:
received: 02 11 2019
revised: 01 12 2019
accepted: 06 12 2019
pubmed: 18 12 2019
medline: 4 6 2021
entrez: 18 12 2019
Statut: ppublish

Résumé

The guanine exchange factor subunit eEF1Bα encoded by the EEF1B2 gene belongs to the eukaryotic elongation translational machinery. Pathogen variants in genes of the translational machinery have been associated with several neurodevelopmental disorders. However, only one family of three siblings with intellectual disability (ID) has been reported so far with a homozygous variant in EEF1B2. Here, we report a second family with a novel homozygous loss of function (LoF) variant p.(Ser128*), carried by two siblings with moderate ID and seizures. Our findings confirm the role of EEF1B2 variants in the pathogenesis of autosomal-recessive ID, expand the variant spectrum and precisely describe the clinical consequences of the LoF of EEF1B2.

Identifiants

pubmed: 31845318
doi: 10.1111/cge.13688
doi:

Substances chimiques

Guanine Nucleotide Exchange Factors 0
Peptide Elongation Factor 1 0
eEF1B-beta protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

639-643

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Références

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McLachlan F, Sires AM, Abbott CM. The role of translation elongation factor eEF1 subunits in neurodevelopmental disorders. Hum Mutat. 2019;40(2):131-141. https://doi.org/10.1002/humu.23677.
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Auteurs

Lise Larcher (L)

APHP, Département de Génétique, Centre de Référence Déficiences Intellectuelles de Causes Rares, Groupe Hospitalier Pitié Salpêtrière et GHUEP Hôpital Trousseau, Sorbonne Université, GRC "Déficience Intellectuelle et Autisme,", Paris, France.

Julien Buratti (J)

APHP, Département de Génétique, Centre de Référence Déficiences Intellectuelles de Causes Rares, Groupe Hospitalier Pitié Salpêtrière et GHUEP Hôpital Trousseau, Sorbonne Université, GRC "Déficience Intellectuelle et Autisme,", Paris, France.

Bénédicte Héron-Longe (B)

APHP, Service de Neuropédiatrie, Hôpital Trousseau, Paris, France.

Brigitte Benzacken (B)

APHP, Département d'Histologie, Embryologie et Cytogénétique, Hôpital Jean Verdier, Bondy, France.
Université Paris 13, Sorbonne Paris Cité, UFR SMBH, Bobigny, France.
Neurodiderot, UMR 1141, INSERM, Université de Paris, Paris, France.

Eva Pipiras (E)

APHP, Département d'Histologie, Embryologie et Cytogénétique, Hôpital Jean Verdier, Bondy, France.
Université Paris 13, Sorbonne Paris Cité, UFR SMBH, Bobigny, France.
Neurodiderot, UMR 1141, INSERM, Université de Paris, Paris, France.

Boris Keren (B)

APHP, Département de Génétique, Centre de Référence Déficiences Intellectuelles de Causes Rares, Groupe Hospitalier Pitié Salpêtrière et GHUEP Hôpital Trousseau, Sorbonne Université, GRC "Déficience Intellectuelle et Autisme,", Paris, France.

Andrée Delahaye-Duriez (A)

APHP, Département d'Histologie, Embryologie et Cytogénétique, Hôpital Jean Verdier, Bondy, France.
Université Paris 13, Sorbonne Paris Cité, UFR SMBH, Bobigny, France.
Neurodiderot, UMR 1141, INSERM, Université de Paris, Paris, France.
Division of Brain Sciences, Imperial College Faculty of Medicine, London, UK.

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