Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC

dc.contributor.authorGarcia-Caballero, Agustin
dc.contributor.authorGandini, Maria A
dc.contributor.authorHuang, Shuo
dc.contributor.authorChen, Lina
dc.contributor.authorSouza, Ivana A
dc.contributor.authorDang, Yan L
dc.contributor.authorStutts, M. J
dc.contributor.authorZamponi, Gerald W
dc.date.accessioned2019-02-10T01:03:55Z
dc.date.available2019-02-10T01:03:55Z
dc.date.issued2019-02-08
dc.date.updated2019-02-10T01:03:55Z
dc.description.abstractAbstract 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.
dc.identifier.citationMolecular Brain. 2019 Feb 08;12(1):12
dc.identifier.doihttps://doi.org/10.1186/s13041-019-0433-8
dc.identifier.urihttp://hdl.handle.net/1880/109896
dc.identifier.urihttps://doi.org/10.11575/PRISM/45982
dc.language.rfc3066en
dc.rights.holderThe Author(s).
dc.titleCav3.2 calcium channel interactions with the epithelial sodium channel ENaC
dc.typeJournal Article
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