SLC9B2 (sodium/hydrogen exchanger 9B2) is also known as NHA2 or NHEDC2. It is encoded by the SLC9B2 gene in humans and belongs to solute carrier family 9, subfamily B. SLC9B2 is broadly expressed in brain, liver and 21 other tissues. It functions as a sodium/hydrogen antiporter and converts the proton motive force into sodium gradients. Also, SLC9B2 is involved in signal transduction and drug efflux.
|Basic Information of SLC9B2|
|Protein Name||Sodium/hydrogen exchanger 9B2|
|Organism||Homo sapiens (Human)|
SLC9B2 is also known as NHA2 which belongs to proton exchangers and transporters. It was identified broadly expressed in the brain, liver, and some other tissues. SLC9B2 is shown to convert the proton motive force into sodium gradients, which is associated with energy-requiring processes. Also, it is involved in environmental signal transduction and drug efflux. Its family - SLC9B proteins (including SLC9B2 and SLC9B2) belong to the members of the sodium/lithium hydrogen antiporter family, and they play the functions as solute exchangers within cellular membranes of mammalian tissues. SLC9B2 is involved in the metabolism of the skeletal system, and it can be as a biomarker for bone homeostasis indicator of Arabians. In addition, SCL9B2 plays the electrogenic transporting role dependent on a lysine residue in the transmembrane domain. Moreover, SLC9B2 is necessary for survival, and show different transporting functions compared with SLC9B1. Furthermore, SLC9B2 deficiency can enhance aging and obesity-induced glucose intolerance in mice.
Fig.1 SLC9B2 acts as a Na+/H+ exchanger. (Chintapalli, 2015)
This article indicates that SLC9B2 is involved in the metabolism of the skeletal system, and it can be as a biomarker for bone homeostasis indicator of Arabians.
This article shows the identity between SLC9B1 and SLC9B2 and indicates that SLC9B1 originates from SLC9B2.
This article demonstrates that a lysine residue in the transmembrane domain is necessary for electrogenic transport in sodium/hydrogen antiporter - SCL9B2.
This article shows that SLC9B2 and SLC9B2 are necessary for survival, and shows different transporting functions.
This article shows that SLC9B2 deficiency enhances aging and obesity-induced glucose intolerance in mice, also it indicates the relationship between SLC9B2 expression and insulin secretion capacity in islets.
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