Neuregulin 1-induced AKT and ERK phosphorylation in patients with Fragile X Syndrome (FXS) and intellectual disability associated with obstetric complications

Tamás Kovács, Boglárka Bánsági, Oguz Kelemen, Szabolcs Kéri

Research output: Article

4 Citations (Scopus)

Abstract

Animal models of fragile X syndrome (FXS) suggest the impairment of the intracellular AKT messenger system, which is activated by neuregulin 1 (NRG1), a key regulator of neurodevelopment. We investigated NRG1-induced activation of the AKT and extracellular signal-regulated kinase (ERK) systems by the measurement of the phosphorylated AKT/ERK to total AKT/ERK ratio in peripheral B lymphoblasts of patients with FXS, IQ-matched controls with intellectual disability (obstetric complications, preterm birth, perinatal hypoxia, and low birth weight), and typically developed healthy participants. Results revealed that patients with FXS displayed decreased AKT but normal ERK activation after the administration of NRG1. IQ-matched controls with intellectual disability displayed intact AKT/ERK activation. In conclusion, FXS, but not intellectual disability associated with obstetric complications, is associated with decreased NRG1-induced AKT phosphorylation.

Original languageEnglish
Pages (from-to)119-124
Number of pages6
JournalJournal of Molecular Neuroscience
Volume54
Issue number1
DOIs
Publication statusPublished - szept. 2014

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ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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