KCNJ15

Official Full Name

potassium inwardly rectifying channel subfamily J member 15

Organism

Homo sapiens

GeneID

3772

Background

Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein has a greater tendency to allow potassium to flow into a cell rather than out of a cell. Eight transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Feb 2013]

Synonyms

IRKK; KIR1.3; KIR4.2;

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Detailed Information

Recent Research

Inward rectifier potassium (Kir) channels serve important functional and modulatory roles in a wide variety of cells. Potassium inwardly-rectifying channel, subfamily J, member 15 (KCNJ15) encodes potassium channel inward rectifiers (Kir) 4.2, which plays a role in maintaining the resting membrane potential of potassium ions close to equilibrium. The activity of KCNJ15 is directly regulated by the external potassium concentration. It is reported that KCNJ15 is frequently expressed in the brain, lung, pancreas, and whole blood. KCNJ15 is implicated as an essential factor for the secretion of insulin, brain development, and acid secretion in the lung. KCNJ15 is also expressed in the kidney. In lung epithelial cells, KCNJ15 supplies K⁺ to the proton pump on the apical membrane. Several studies showed that the KCNJ15 mRNA is the most highly expressed among all K⁺ channels in the gastric mucosa and that this channel showed a stimulation-associated translocation onto apical membrane indicative of a role for stimulated acid secretion.

In humans, KCNJ15 is closely related to type II diabetes. It has been reported that the synonymous single nucleotide polymorphism of KCNJ15 increases the risk of type II diabetes in Japanese, and the risk allele (T) is associated with increased levels of KCNJ15 mRNA in the peripheral blood of healthy volunteers. Clinical observations reveal that subjects with type II diabetes carrying the risk allele are more likely to require insulin, indicating that insulin secretion is low.

One report has revealed the mechanism of K⁺o-dependent regulation of Kir4.2. The K⁺o -dependent regulation is specific to the homomeric form of the channel and is abolished when Kir4.2 is co-expressed with Kir5.1. Different with Kir1.1, there is no coupling between the sensitivity to intracellular pH and K⁺o-dependent regulation of Kir4.2. Furthermore, the rate of activation is slower than the rate of inactivation (~30 min vs~2 min) and there is an inverse relationship between the rate of activation and the extracellular potassium concentration ([K⁺]o). Using biotinylation, it has been shown that K⁺o-dependent regulation does not involve a change in the surface expression of the channel, hence K⁺o affects the properties of the channel at the cell surface.

References:

Yuan J, et al. Potassium channel KCNJ15 is required for histamine-stimulated gastric acid secretion. American Journal of Physiology Cell Physiology, 2015, 309(4):C264.
Nakajima K I, et al. Concerted action of KCNJ15/Kir4.2 and intracellular polyamines in sensing physiological electric fields for galvanotaxis. Channels, 2016, 10(4):3.

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