RNA-seq Analysis of the SCN1A-KO Model based on CRISPR/Cas9 Genome Editing Technology.
CRISPR/Cas9
Dravet syndrome
RNA-seq
SCN1A
epilepsy
genomics
Journal
Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074
Informations de publication
Date de publication:
01 02 2019
01 02 2019
Historique:
received:
20
06
2018
revised:
30
11
2018
accepted:
30
11
2018
pubmed:
12
12
2018
medline:
19
3
2019
entrez:
12
12
2018
Statut:
ppublish
Résumé
Dravet syndrome (DS) is a disease that is primarily caused by the inactivation of the SCN1A-encoded voltage-gated sodium channel alpha subunit (Nav1.1). In this study, we constructed an SCN1A gene knockout model using CRISPR/Cas9 genome editing technology to deprive the Nav1.1 function in vitro. With mRNA-seq analysis we found abundant gene changes after SCN1A knockout, which associated with various signaling pathways, such as cancer pathways, the PI3K-AKT signaling pathway, the MAPK signaling pathway, and pathways involved in HTLV-I infection. We also noticed changes in the spliceosome, decreased glycolytic capacity, disturbances in calcium signaling pathways, and changes in the potassium, sodium, chloride, and calcium plasma channels after SCN1A knockout. In this study, we have been the first time to discover these changes and summarize them here and hope it would provide some clue for the study of Nav1.1 in the nervous system.
Identifiants
pubmed: 30529264
pii: S0306-4522(18)30794-2
doi: 10.1016/j.neuroscience.2018.11.052
pii:
doi:
Substances chimiques
NAV1.1 Voltage-Gated Sodium Channel
0
RNA, Messenger
0
Scn1a protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-11Informations de copyright
Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.