Protein Kinase B/Akt1 Phosphorylates Dysbindin-1A at Serine 10 to Regulate Neuronal Development.
Akt
dendrite arborization
dendritic spine
dysbindin-1
phosphorylation
Journal
Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074
Informations de publication
Date de publication:
10 05 2022
10 05 2022
Historique:
received:
20
05
2021
revised:
24
01
2022
accepted:
28
01
2022
pubmed:
7
2
2022
medline:
27
4
2022
entrez:
6
2
2022
Statut:
ppublish
Résumé
Schizophrenia is a neurodevelopmental disorder with dendrite and dendritic spine dysfunction. Dysbindin-1, a protein decreased in the brains of schizophrenia patients, is involved in the development of dendrites and spines. However, it is still unclear how the role of dysbindin-1 in neuronal development is regulated. Here, we showed protein kinase B/Akt1, a serine/threonine kinase implicated in schizophrenia, phosphorylated dysbindin-1A at serine 10 (S10). S10 phosphorylation of dysbindin-1A was increased during postnatal neuronal and synapse development stage, and was enriched in postsynaptic densities (PSDs). Furthermore, overexpressing wild type or S10 phospho-mimic mutant (S10D), but not S10 phospho-dead mutant (S10A) of dysbindin-1A rescued the dendrite and spine deficits in dysbindin-1A knockdown neurons. These results indicate S10 phosphorylation of dysbindin-1A by Akt1 is essential for neuronal development, providing a potential regulation mechanism for dysbindin-1A in neuronal development.
Identifiants
pubmed: 35124166
pii: S0306-4522(22)00046-X
doi: 10.1016/j.neuroscience.2022.01.025
pii:
doi:
Substances chimiques
DTNBP1 protein, human
0
Dysbindin
0
Dystrophin-Associated Proteins
0
Serine
452VLY9402
AKT1 protein, human
EC 2.7.11.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
66-78Informations de copyright
Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.