Enables calcium:monoatomic cation antiporter activity involved in regulation of postsynaptic cytosolic calcium ion concentration and calcium:sodium antiporter activity. Involved in cellular response to cAMP; metal ion transport; and telencephalon development. Acts upstream of or within intracellular calcium ion homeostasis. Located in several cellular components, including dendritic spine; neuronal cell body; and sarcolemma. Is active in postsynaptic membrane. Biomarker of brain ischemia and status epilepticus. Orthologous to human SLC8A3 (solute carrier family 8 member A3); PARTICIPATES IN calcium transport pathway; calcium/calcium-mediated signaling pathway; INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; 2,3,7,8-Tetrachlorodibenzofuran; acrylamide.
na(+)/Ca(2+)-exchange protein 3; Ncx3; sodium/calcium exchanger 3; solute carrier family 8 (sodium/calcium exchanger), member 3; solute carrier family 8 member 3
[sodium arsenate co-treated with sodium arsenite co-treated with monomethylarsonic acid co-treated with Cacodylic Acid] results in increased expression of SLC8A3 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SLC8A3 mRNA
2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate inhibits the reaction [Kainic Acid results in increased cleavage of SLC8A3 protein]
[sodium arsenate co-treated with sodium arsenite co-treated with monomethylarsonic acid co-treated with Cacodylic Acid] results in increased expression of SLC8A3 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SLC8A3 mRNA
[sodium arsenate co-treated with sodium arsenite co-treated with monomethylarsonic acid co-treated with Cacodylic Acid] results in increased expression of SLC8A3 mRNA
[sodium arsenate co-treated with sodium arsenite co-treated with monomethylarsonic acid co-treated with Cacodylic Acid] results in increased expression of SLC8A3 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SLC8A3 mRNA
Na+/Ca2+ exchanger subtype (NCX1, NCX2, NCX3) protein expression in the rat hippocampus following 3 min and 8 min durations of global cerebral ischemia.
Permanent focal brain ischemia induces isoform-dependent changes in the pattern of Na+/Ca2+ exchanger gene expression in the ischemic core, periinfarct area, and intact brain regions.
High level over-expression of different NCX isoforms in HEK293 cell lines and primary neuronal cultures is protective following oxygen glucose deprivation.
BHK cells transfected with NCX3 are more resistant to hypoxia followed by reoxygenation than those transfected with NCX1 and NCX2: Possible relationship with mitochondrial membrane potential.
High levels of synaptosomal Na(+)-Ca(2+) exchangers (NCX1, NCX2, NCX3) co-localized with amyloid-beta in human cerebral cortex affected by Alzheimer's disease.