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Gene Review

Kcnj12  -  potassium channel, inwardly rectifying...

Rattus norvegicus

Synonyms: ATP-sensitive inward rectifier potassium channel 12, IRK-2, IRK2, Inward rectifier K(+) channel Kir2.2, Irk2, ...
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Disease relevance of Kcnj12

  • The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered [1].

High impact information on Kcnj12

  • After coexpression of nerve growth factor receptor with Kir2.1 channels in tsA-201 cells and Xenopus oocytes, the activity of Kir2.1 was rapidly suppressed by applied nerve growth factor (0.5 microgram/ml) by 31 +/- 10 and 21 +/- 15%, respectively [2].
  • Acute suppression of inwardly rectifying Kir2.1 channels by direct tyrosine kinase phosphorylation [2].
  • Acute inhibition was also evoked by epidermal growth factor and insulin via endogenous insulin receptors, indicating that Kir2.1 channels may serve as a general target for neurotrophic growth factors in the brain [2].
  • Site mutation of a tyrosine consensus residue for TK phosphorylation in the C-terminal domain of Kir2.1 generated channel properties indistinguishable from wild-type Kir2.1 channels [2].
  • Whereas Kir2.1 shows prominent plasma membrane localization, Kir2.4 channels accumulate within the Golgi complex [3].

Biological context of Kcnj12

  • The kinetics of this voltage dependence were further investigated using recombinant inward rectifier K+ channels (Kir2.1) expressed in the MEL cell line [4].

Anatomical context of Kcnj12

  • By constructing chimeras between Kir2.1 and Kir2.4 subunits, a stretch of 20 amino acids was identified in the Kir2.1 C-terminus that is both necessary and sufficient to promote anterograde transport of Kir channel subunits at the level of trafficking from the Golgi to the plasma membrane [3].
  • We conclude that Kir2.1 encodes for inward rectifier K+ channels in arterial smooth muscle [5].
  • Microglia, the brain's resident immune cells, express voltage-gated Kv1.3 channels, a Kir2.1-like inward rectifier, a swelling-activated Cl(-) current and several other channels [6].
  • Overexpression of Kir2.1 by adenoviral gene transfer, a subunit contributing to I(K1) channels, in atrial myocytes resulted in a large I(K1)-like background current [7].
  • 4. Kir2.1 was cloned from rat mesenteric vascular smooth muscle cells and expressed in Xenopus oocytes [5].

Associations of Kcnj12 with chemical compounds

  • Direct block of native and cloned (Kir2.1) inward rectifier K+ channels by chloroethylclonidine [4].
  • We used two preparations; two-electrode voltage-clamp of rat isolated flexor digitorum brevis muscle and whole-cell patch-clamp of cell lines transfected with Kir2.1 (IRK1) [4].
  • A combination of two antisense phosphorothioate oligonucleotides inhibited heterologously expressed Kir2.1 currents in Xenopus oocytes, either when coinjected with Kir2.1 cRNA or when applied in the incubation medium [8].

Other interactions of Kcnj12

  • Subsequent mutation of homologous residues in both the GIRK4 subunit and Kir2.1 (Gbetagamma-independent inward rectifier) also resulted in a decrease in channel function [9].
  • At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered [1].
  • However, there are no significant expression changes of Kir2.1, Kir3.1, Kir6.1, and Kir6.2 in diabetic rats [10].
  • A two-fold difference was detected between Kir2.1 mRNA and beta-actin mRNA in coronary arteries when compared with relative levels measured in mesenteric and basilar preparations [5].
  • We have raised affinity-purified polyclonal antibodies specific for the inward rectifying K+ channel (IRK1/Kir2.1) and the G protein-activated inward rectifying K+ channel (GIRK1/Kir3.1) examined their distributions in the rat brain immunohistochemically [11].

Analytical, diagnostic and therapeutic context of Kcnj12

  • In PCR analyses using isolated juxtaglomerular cells, the mRNA for Kir2.1 and Kir2.2 was detected [12].
  • RT-PCR revealed transcripts for Kir2.1 in the SMCs [13].
  • In the present experiments, we investigated the subcellular localizations of the strong inward rectifier 2.1 K+ (Kir2.1) channel and the Na+-K+-2Cl- (NKCC)1 cotransporter with Western blot analysis of different muscle fractions [14].


  1. Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina. Iandiev, I., Tenckhoff, S., Pannicke, T., Biedermann, B., Hollborn, M., Wiedemann, P., Reichenbach, A., Bringmann, A. Neurosci. Lett. (2006) [Pubmed]
  2. Acute suppression of inwardly rectifying Kir2.1 channels by direct tyrosine kinase phosphorylation. Wischmeyer, E., Döring, F., Karschin, A. J. Biol. Chem. (1998) [Pubmed]
  3. Selective Golgi export of Kir2.1 controls the stoichiometry of functional Kir2.x channel heteromers. Hofherr, A., Fakler, B., Klöcker, N. J. Cell. Sci. (2005) [Pubmed]
  4. Direct block of native and cloned (Kir2.1) inward rectifier K+ channels by chloroethylclonidine. Barrett-Jolley, R., Dart, C., Standen, N.B. Br. J. Pharmacol. (1999) [Pubmed]
  5. Kir2.1 encodes the inward rectifier potassium channel in rat arterial smooth muscle cells. Bradley, K.K., Jaggar, J.H., Bonev, A.D., Heppner, T.J., Flynn, E.R., Nelson, M.T., Horowitz, B. J. Physiol. (Lond.) (1999) [Pubmed]
  6. Integration of K+ and Cl- currents regulate steady-state and dynamic membrane potentials in cultured rat microglia. Newell, E.W., Schlichter, L.C. J. Physiol. (Lond.) (2005) [Pubmed]
  7. Voltage dependence of ATP-dependent K+ current in rat cardiac myocytes is affected by IK1 and IK(ACh). Wellner-Kienitz, M.C., Bender, K., Rinne, A., Pott, L. J. Physiol. (Lond.) (2004) [Pubmed]
  8. Inhibition of rat ventricular IK1 with antisense oligonucleotides targeted to Kir2.1 mRNA. Nakamura, T.Y., Artman, M., Rudy, B., Coetzee, W.A. Am. J. Physiol. (1998) [Pubmed]
  9. Mutation of critical GIRK subunit residues disrupts N- and C-termini association and channel function. Sarac, R., Hou, P., Hurley, K.M., Hriciste, D., Cohen, N.A., Nelson, D.J. J. Neurosci. (2005) [Pubmed]
  10. Altered mRNA expression of ATP-sensitive and inward rectifier potassium channel subunits in streptozotocin-induced diabetic rat heart and aorta. Ren, Y., Xu, X., Wang, X. J. Pharmacol. Sci. (2003) [Pubmed]
  11. Localization and developmental changes of the expression of two inward rectifying K(+)-channel proteins in the rat brain. Miyashita, T., Kubo, Y. Brain Res. (1997) [Pubmed]
  12. Electrophysiological and molecular characterization of the inward rectifier in juxtaglomerular cells from rat kidney. Leichtle, A., Rauch, U., Albinus, M., Benöhr, P., Kalbacher, H., Mack, A.F., Veh, R.W., Quast, U., Russ, U. J. Physiol. (Lond.) (2004) [Pubmed]
  13. Contribution of Na+-K+ pump and KIR currents to extracellular pH-dependent changes of contractility in rat superior mesenteric artery. Kim, M.Y., Liang, G.H., Kim, J.A., Park, S.H., Hah, J.S., Suh, S.H. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  14. Membrane proteins involved in potassium shifts during muscle activity and fatigue. Kristensen, M., Hansen, T., Juel, C. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2006) [Pubmed]
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