Introduction of SLC4A10
SLC4A10, encoded by SLC4A10 gene, also known as NCBE, is a member of the sodium-coupled bicarbonate transporters (NCBTs) family that is involved in solute transport and pH homeostasis. SLC4A10 protein was originally thought to be an atrium-driven chloride-bicarbonate exchanger, but now there is evidence that its sodium/bicarbonate co-transport activity is not related to any chloride ion reverse transport under physiological conditions. SLC4A10 is especially expressed in the brain and adrenal.
|Basic Information of SLC4A10|
|Protein Name||Sodium-driven chloride bicarbonate exchanger|
|Organism||Homo sapiens (Human)|
Function of SLC4A10 Membrane Protein
SLC4A10 is electrogenic sodium/bicarbonate cotransporter in exchange for intracellular chloride. It is expressed in principal and inhibitory neurons as well as in choroid plexus epithelial cells of the brain. The functional studies reveal that it plays an important role in the regulation of intracellular pH of neurons, the secretion of bicarbonate ions across the choroid plexus, and the pH of the brain extracellular fluid. Besides, SLC4A10 is also associated with the regulation of neuroticism and involved in the secretion of cerebrospinal fluid. The loss function of SLC4A10 in mice significantly decreases brain ventricle volume and protects from fatal epileptic seizures. And SLC4A10 gene knockout in mice displays the reduced neuronal excitability. Heterozygous deletions of SLC4A10 in man show the association with idiopathic epilepsy and other neurological symptoms. Hence, SLC4A10 is a potential drug target for the therapy of epilepsy or elevated intracranial pressure.
Fig.1 Synaptic expression of SLC4A10 in the cortex. (Sinning, 2015)
Application of SLC4A10 Membrane Protein in Literature
The article reveals that the regulation of human cognition and epilepsy may be associated with sodium bicarbonate transporter SLC4A10.
The study indicates that the genetic variants and function of NFAT5 and SLC4A10 in the CNS may influence the regulation of systemic water balance.
In the study, authors rename NCBE as the second electroneutral Na/HCO(3) cotransporter with Cl(-) self-exchange activity.
The experimental data suggest that Slc4a10 inhibits neuronal excitability and thus sets forth the pathophysiology of SLC4A10 associated pathologies.
The research implicates that the abundance of the tight junction protein claudin-2 is significantly decreased in the slc4a10 knockout mice, which may critically influence paracellular transport in this epithelium.
SLC4A10 Preparation Options
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