Introduction of KCNJ15
KCNJ15 (also known as Kir4.2, or Kir1.3) is a member of Kir4 subfamily, which belongs to the family of inward-rectifier potassium channels (Kir, IRK), a specific subset of potassium channels. Isolation, mapping, and sequencing of trapped exons have revealed that gene KCNJ15 is localized on the sub-band q22.2 of chromosome 21, mainly in the down syndrome chromosome region 1 (DCR1). There are three transcript variants encoding the same protein of this gene. It is predominantly expressed in kidney and lung during childhood development, while in adults, the distribution is abundant in several tissues including kidney and brain. Possessing a pore domain and flanking transmembrane segments (TMSs), KCNJ15 is homologous to that of voltage-gated ion channels, and it may exist in the membrane as homo- or heterooligomers and each monomer possesses between 1 and 4 TMSs.
|Basic Information of KCNJ15|
|Protein Name||ATP-sensitive inward rectifier potassium channel 15|
|Organism||Homo sapiens (Human)|
Function of KCNJ15 Membrane Protein
As its name implies, KCNJ15 can transport potassium (K+), with a greater tendency to allow K+ to flow into a cell rather than out of a cell. The alteration of ion currents in cellular inner and outer contributes to the generation of action potential in various excitable cells, the maintenance of resting membrane potential in either excitable and non-excitable cells, and homeostasis of intracellular environmental. It has been well documented that mutation of an extracellular lysine residue can increase K+ current up to 6-fold, while intracellular acidification will decrease the K+ current. KCNJ15 was found to interact with the Ca(2+)-sensing receptor (CsR) in human kidney. Expression of KCNJ15 mRNA in islets is higher in patients with type 2 diabetes, so it has been recognized as a type 2 diabetes-associated risk gene. Overexpression of KCNJ15 can suppress insulin secretion in rat insulinoma (INS1) cells. Moreover, KCNJ15 is closely associated with the acid secretion in the lung and in gastric mucosa, where it is expressed at a higher level and can be translocated to the apical membrane on histamine stimulation. Knocking down KCNJ15 will abolish histamine-stimulated acid secretion. Additionally, coupling with polyamines, KCNJ15 plays a critical role in sensing weak extracellular electric fields in galvanotaxis.
Fig.1 The localization of KCNJ15.
Application of KCNJ15 Membrane Protein in Literature
In this review, the authors provide evidence that KCNJ15 plays a critical role in histamine-stimulated gastric acid secretion. Furthermore, using a short hairpin RNA adenoviral construct to knock down KCNJ15 expression will abolish stimulated acid secretion in rabbit primary parietal cells.
This article demonstrates that downregulation of KCNJ15 will lead to increased insulin secretion in vitro and in vivo and the regulation involves KCNJ15 and Ca(2+)-sensing receptor (CsR).
The authors use an RNAi library targeting ion transporters in human cells to perform a large-scale screen and they verify that knockdown of the KCNJ15 gene specifically abolishes galvanotaxis, without affecting basal motility and directional migration in a monolayer scratch assay. Coupling with polyamines, KCNJ15/Kir4.2 plays roles in sensing weak electric fields.
This article reveals that KCNJ15 is stored in vesicles distinct from the H(+)-K(+)-ATPase-enriched tubulovesicles in nonsecreting parietal cells. Once stimulated in gastric parietal cells, KCNJ15 and H(+)-K(+)-ATPase can translocate to the apical membrane for active acid secretion.
This article firstly finds the presence of gene KCNJ15 encoding a potassium K(+) channel, and identifies it as a member of inward-rectifier potassium channels family. Moreover, the authors show that KCNJ15 is localized on chromosome 21 in the down syndrome chromosome region 1 (DCR1).
KCNJ15 Preparation Options
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