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This is the community wiki page for the gene kcnj2 please feel free to add any information that is relevant to this gene that is not already captured elsewhere in Xenbase

nomenclature changes

01/15/2015 Human name has changed for Entrez Gene: 3759. From potassium inwardly-rectifying channel, subfamily J, member 2 to potassium channel, inwardly rectifying subfamily J, member 2.

08.23.2019 Human name has changed for Entrez Gene: 3759. From potassium voltage-gated channel subfamily J member 2 to potassium inwardly rectifying channel subfamily J member 2

summary from Adams et al 2016. J Physiol 594.12 (2016) pp 3245–3270

Kir2.1 (NP000882.1), encoded in KCNJ2(NM000891.2), is the potassium, inwardly rectifying channel, subfamily J member 2a.

It is a 427 amino acid, two-pass, transmembrane protein, with both termini located in the cytoplasm. Kir2.1 homotetramers form a K+ channel that contributes to the potassium efflux that is critical for the repolarization of excitable cell membranes after an action potential, the so-called IK current. Kir2.1 is negatively regulated (at membrane potentials positive to its equilibrium potential) by binding of spermine, spermidine and Mg2+(Yang et al. 1995), and by phosphorylation of Tyr242.

It is positively regulated(at potentials negative to its equilibrium potential) by binding of phosphoinositol bisphosphate (PIP2); three PIP2 binding sites have been identified in the long C terminus of the protein, at amino acids 175–206,207–246 and 324–365 (Soom et al. 2001). Kir2.1 is critical for controlling the membrane voltage of cardiac myocytes; it is the effect of mutations on the QT interval and the U-wave that are thought to cause the cardiac arrhythmia.

This symptom is the source of the synonym LQT for long Q-T interval (Hedley et al. 2009). Importantly, however, Kir2.1 also contributes to the resting potential (Vmem) of undifferentiated embryonic cells, including those found in Xenopus embryos. Its effect on cellular functions go way beyond propagation of action potentials (Jongsma &Wilders, 2001).