Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC.
Cav3.2 calcium channels
Dorsal horn
Dorsal root ganglia (DRG)
Epithelial Sodium Channel (ENaC)
Journal
Molecular brain
ISSN: 1756-6606
Titre abrégé: Mol Brain
Pays: England
ID NLM: 101468876
Informations de publication
Date de publication:
08 02 2019
08 02 2019
Historique:
received:
26
10
2018
accepted:
04
02
2019
entrez:
10
2
2019
pubmed:
10
2
2019
medline:
14
6
2019
Statut:
epublish
Résumé
This study describes the functional interaction between Cav3.2 calcium channels and the Epithelial Sodium Channel (ENaC). β-ENaC subunits showed overlapping expression with endogenous Cav3.2 calcium channels in the thalamus and hypothalamus as detected by immunostaining. Moreover, β- and γ-ENaC subunits could be co-immunoprecipitated with Cav3.2 calcium channels from brain lysates, dorsal horn and lumbar dorsal root ganglia. Mutation of a cluster of lysines present in the intracellular N-terminus region of β-ENaC (K4R/ K5R/ K9R/ K16R/ K23R) reduced interactions with Cav3.2 calcium channels. Αβγ-ENaC channels enhanced Cav3.2 calcium channel trafficking to the plasma membrane in tsA-201 cells. This effect was reciprocal such that Cav3.2 channel expression also enhanced β-ENaC trafficking to the cell surface. T-type current density was increased when fully assembled αβγ-ENaC channels were transiently expressed in CAD cells, a neuronal derived cell line. Altogether, these findings reveal ENaC as an interactor and potential regulator of Cav3.2 calcium channels expressed in neuronal tissues.
Identifiants
pubmed: 30736831
doi: 10.1186/s13041-019-0433-8
pii: 10.1186/s13041-019-0433-8
pmc: PMC6368719
doi:
Substances chimiques
Cacna1h protein, mouse
0
Calcium Channels, T-Type
0
Epithelial Sodium Channels
0
Protein Subunits
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
12Subventions
Organisme : CIHR
Pays : Canada
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