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

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 t...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Kovács Tamás
Bánsági Boglárka
Kelemen Oguz
Kéri Szabolcs
Dokumentumtípus: Cikk
Megjelent: 2014
Sorozat:JOURNAL OF MOLECULAR NEUROSCIENCE 54 No. 1
doi:10.1007/s12031-014-0257-z

mtmt:2782623
Online Access:http://publicatio.bibl.u-szeged.hu/11362
Leíró adatok
Tartalmi kivonat: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.
Terjedelem/Fizikai jellemzők:119-124
ISSN:0895-8696