The Kir2.1 inward-rectifier potassium channel is a lipid-gated ion channel encoded by the KCNJ2 gene.[5][6][7][8]
KCNJ2 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | KCNJ2, ATFB9, HHBIRK1, HHIRK1, IRK1, KIR2.1, LQT7, SQT3, potassium voltage-gated channel subfamily J member 2, potassium inwardly rectifying channel subfamily J member 2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 600681 MGI: 104744 HomoloGene: 20249 GeneCards: KCNJ2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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A defect in this gene is associated with Andersen-Tawil syndrome.[9]
A mutation in the KCNJ2 gene has also been shown to cause short QT syndrome.[10]
In neurogenetics, Kir2.1 is used in Drosophila research to inhibit neurons, as overexpression of this channel will hyperpolarize cells.
In optogenetics, a trafficking sequence from Kir2.1 has been added to halorhodopsin to improve its membrane localization. The resulting protein eNpHR3.0 is used in optogenetic research to inhibit neurons with light.[11]
Expression of Kir2.1 gene in human HEK293 cells induce a transient outward current, creating a steady membrane potential close to the reversal potential of potassium.[12]
Kir2.1 has been shown to interact with: