Solute carrier family 9A6 (SLC9A6) is also known as sodium-hydrogen antiporter 6 (NHE-6) or sodium/hydrogen exchanger 6. SLC9A6 is encoded by the SLC9A6 gene in humans, which is ubiquitously expressed in the brain, adrenal, and 23 other tissues. The SLC9A6 gene is conserved in Rhesus monkey, chicken, chimpanzee, dog, rat, zebrafish, fruit fly, mouse, mosquito, cow, C.elegans, and frog. It belongs to the solute carrier family 9, and functions as a Na+/H+ antiporter. SLC9A6 is documented to be involved in pH homeostasis, and signal transduction.
|Basic Information of SLC9A6|
|Protein Name||Sodium/hydrogen exchanger 6|
|Aliases||Na(+)/H(+) exchanger 6, KIAA0267, NHE6|
|Organism||Homo sapiens (Human)|
As a proton exchanger and transporter, SLC9A6 mediates the sodium-ion transport by exchanging intracellular hydrogen ions to external sodium ions and plays an important role in cell pH regulation and cell volume. As a member of SLC9A family, SLC9A6 is associated with Nef internalization into M2 macrophages. The relocalization of SLC9A6 from endosomes to plasma membrane is related to endosome hyperacidification. In addition, SLC9A6 is identified in the choroid plexus and it may be involved in pH modulation of the CSF. SLC9A6 expression is down-regulated in Caco-2 cells via the mechanisms of rotavirus-induced diarrhea. Moreover, SLC9A6 is associated with recycling endosomal function and neuronal degeneration and cell death. SLC9A6 is also functionally associated with Alzheimer disease via endosomal pH modulation and amyloid precursor protein. Furthermore, SLC9A6 plays a critical role in endosome hyperacidification and chemoresistance.
Fig.1 Model for endosomal pH regulation of Aβ production by NHE6. (Prasad, 2015)
This article indicates that SLC9A6 is identified in the choroid plexus for the first time, and it may be involved in pH modulation of the CSF.
This article shows that NHE6 plays a critical role in endosome hyperacidification and chemoresistance.
This article indicates that SLC9A6 expression is down-regulated in Caco-2 cells via the mechanisms of rotavirus-induced diarrhea.
This article shows that functional deficiency caused by the mutation in SLC9A6 is associated with recycling endosomal function and neuronal degeneration and cell death.
This article demonstrates that SLC9A6 is functionally associated with Alzheimer disease via endosomal pH modulation and amyloid precursor protein.
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