Solute carrier family 9A2 (SLC9A2) is also known as sodium-hydrogen antiporter 2 (NHE-2) or sodium/hydrogen exchanger 2. It is encoded by the SLC9A2 gene in humans. It’s biased expressed in stomach, colon and 10 other tissues. It belongs to the solute carrier family 9, and functions as a Na+/H+ antiporter. SLC9A2 is localized to the apical membrane and associated with apical absorption of sodium.
|Basic Information of SLC9A2|
|Protein Name||Sodium/hydrogen exchanger 2|
|Organism||Homo sapiens (Human)|
SLC9A2 is also known as sodium/hydrogen exchanger 2 (NHE2) or sodium-hydrogen antiporter 2, which belongs to proton exchangers and transporters. Sodium-hydrogen exchanger (NHE) protein family 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. SLC9A2 is localized to the apical membrane and associated with apical absorption of sodium. As a member of SLC9A family, SLC9A2 might be affected by clinical exposure to NSAIDs just like other family members and this will lead to transport modulation and barrier function. While there are different activities between the isoforms, SLC9A2 activation can increase the migratory velocity of RGM1 cells, but SLC9A1 activation can inhibit migratory velocity; SLC9A2 is necessary for mouse gastric epithelial restitution, while SLC9A1 is not essential. SLC9A2 can mediate butyrate-dependent sodium absorption in dextran sulfate sodium-induced colitis. It’s also regulated at the post-translational level, and regulated by different binding proteins.
Fig.1 Topology of SLC9A family. (Hendus-Altenburger, 2014)
This article indicates that SLC9A2 plays an opposite activity compared with SLC9A1. SLC9A1 can increase the migratory velocity of RGM1 cells, while SLC9A2 inhibits this activity.
This article demonstrates that SLC9A2 can mediate butyrate-dependent sodium absorption in DSS induced colitis. This finding provides insight that SLC9A2 can be as a therapeutic target.
This article shows that NHE isoforms including NHE2 might be affected by clinical exposure to NSAIDs, and this will lead to transport modulation and barrier function.
This article demonstrates that NHE2 expression can be upregulated by PKCδ dependent activation of ERK1/2 in the intestinal epithelial cell line.
This article demonstrates that SLC9A2 is necessary for mouse gastric epithelial restitution, while SLC9A1 is not necessary.
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