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Gene Review

Kcnj2  -  potassium inwardly-rectifying channel,...

Mus musculus

Synonyms: IRK-1, IRK1, Inward rectifier K(+) channel Kir2.1, Inward rectifier potassium channel 2, Irk1, ...
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Disease relevance of Kcnj2

  • 2. The physiological consequences of the loss of these genes were studied in newborn animals because mice lacking Kir2.1 have a cleft palate and die shortly after birth [1].
  • 4. In electrocardiograms of Kir2.1 (-/-) neonates, neither ectopic beats nor re-entry arrhythmias were observed [1].
  • Kv1.3 and Kir2.1 expression was impaired in brain during cancer cachexia [2].
  • 2. A model of the Kir2.1 channel, built by homology with the structure of the Streptomyces lividans K+ channel KcsA, suggested the existence of an intersubunit hydrogen bond between Ser165 and Thr141 in the channel pore-forming P-region that helps stabilise the structure of this region [3].
  • 1. We used an adenovirus vector encoding Kir2.1 fused to GFP under the control of an ecdysone promoter [4].

Psychiatry related information on Kcnj2


High impact information on Kcnj2

  • A complementary DNA encoding an inward rectifier K+ channel (IRK1) was isolated from a mouse macrophage cell line by expression cloning [6].
  • Overexpression of the inward rectifying potassium channel, Kir2.1, diminishes the excitability of sensory neurons and more severely disrupts the formation of an olfactory map [7].
  • Complementary DNAs encoding two types of inwardly rectifying K+ channels, GIRK1 and IRK1, have been cloned from rat atrium and mouse macrophage, respectively [8].
  • Targeted disruption of Kir2.1 and Kir2.2 genes reveals the essential role of the inwardly rectifying K(+) current in K(+)-mediated vasodilation [9].
  • Kir currents were observed in cerebral artery myocytes isolated from control neonatal animals but were absent in myocytes from Kir2.1(-/-) animals [9].

Biological context of Kcnj2


Anatomical context of Kcnj2

  • The level of inwardly rectifying K+ channel 1 (IRK1) mRNA decreased upon denervation and increased during muscle differentiation in mouse skeletal muscle [12].
  • Confocal microscopy analysis of cells transfected with the fusion construct green fluorescent protein-IRK1 shows that the channel is mainly localized at the plasma membrane [14].
  • To address these issues, macroscopic currents were recorded from inside-out giant patches from Xenopus oocytes and from single-channel currents from COS7 cells expressing wild-type and mutant Kir2.1 channels, during exposure to polyamines of varying length and charge [15].
  • 2. Kir2.1 (-/-) ventricular myocytes lack detectable I(K1) in whole-cell recordings in 4 mM external K(+) [1].
  • MB-IRK3 mRNA expressed specifically in the forebrain, which clearly differed from MB-IRK1 and RB-IRK2 mRNAs [16].

Associations of Kcnj2 with chemical compounds

  • However, neither ionomycin nor TPA appreciably altered the rate of IRK1 gene transcription [12].
  • Using a molecular model of Kir2.1 channels, three candidate negatively charged residues were identified near the extracellular mouth of the pore and mutated to cysteine (E125C, D152C, and E153C) [17].
  • We recently characterized two distinct mechanisms by which the polyamine spermine blocks Kir2.1 channels: (1) by reduction of negative surface charges in the cytoplasmic pore, thereby reducing single-channel conductance, and (2) by direct open channel transmembrane pore block [15].
  • The role of a single aspartate residue in ionic selectivity and block of a murine inward rectifier K+ channel Kir2.1 [18].
  • This potential pharmacological benefit motivated us to further characterize the energetic, kinetic, and molecular properties of IRK1 inhibition by piperazine [13].

Regulatory relationships of Kcnj2

  • However, LPS treatment induced Kv1.3 and downregulated Kir2.1 expression, and TNF-alpha administration mimicked these results [2].
  • To increase IK1 density, a pore-forming subunit of the Kir2.1 (green fluorescent protein-tagged) channel was expressed in the heart under control of the alpha-myosin heavy chain promoter [19].

Other interactions of Kcnj2


Analytical, diagnostic and therapeutic context of Kcnj2


  1. The consequences of disrupting cardiac inwardly rectifying K(+) current (I(K1)) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes. Zaritsky, J.J., Redell, J.B., Tempel, B.L., Schwarz, T.L. J. Physiol. (Lond.) (2001) [Pubmed]
  2. The systemic inflammatory response is involved in the regulation of K(+) channel expression in brain via TNF-alpha-dependent and -independent pathways. Vicente, R., Coma, M., Busquets, S., Moore-Carrasco, R., López-Soriano, F.J., Argilés, J.M., Felipe, A. FEBS Lett. (2004) [Pubmed]
  3. Residues beyond the selectivity filter of the K+ channel kir2.1 regulate permeation and block by external Rb+ and Cs+. Thompson, G.A., Leyland, M.L., Ashmole, I., Sutcliffe, M.J., Stanfield, P.R. J. Physiol. (Lond.) (2000) [Pubmed]
  4. Functional expression of exogenous proteins in mammalian sensory hair cells infected with adenoviral vectors. Holt, J.R., Johns, D.C., Wang, S., Chen, Z.Y., Dunn, R.J., Marban, E., Corey, D.P. J. Neurophysiol. (1999) [Pubmed]
  5. Knockout blow for channel identity crisis : vasodilation to potassium is mediated via Kir2.1. Sobey, C.G., Faraci, F.M. Circ. Res. (2000) [Pubmed]
  6. Primary structure and functional expression of a mouse inward rectifier potassium channel. Kubo, Y., Baldwin, T.J., Jan, Y.N., Jan, L.Y. Nature (1993) [Pubmed]
  7. Spontaneous neural activity is required for the establishment and maintenance of the olfactory sensory map. Yu, C.R., Power, J., Barnea, G., O'Donnell, S., Brown, H.E., Osborne, J., Axel, R., Gogos, J.A. Neuron (2004) [Pubmed]
  8. A region of the muscarinic-gated atrial K+ channel critical for activation by G protein beta gamma subunits. Takao, K., Yoshii, M., Kanda, A., Kokubun, S., Nukada, T. Neuron (1994) [Pubmed]
  9. Targeted disruption of Kir2.1 and Kir2.2 genes reveals the essential role of the inwardly rectifying K(+) current in K(+)-mediated vasodilation. Zaritsky, J.J., Eckman, D.M., Wellman, G.C., Nelson, M.T., Schwarz, T.L. Circ. Res. (2000) [Pubmed]
  10. Multiple promoter elements interact to control the transcription of the potassium channel gene, KCNJ2. Redell, J.B., Tempel, B.L. J. Biol. Chem. (1998) [Pubmed]
  11. Molecular cloning and functional expression of cDNA encoding a second class of inward rectifier potassium channels in the mouse brain. Takahashi, N., Morishige, K., Jahangir, A., Yamada, M., Findlay, I., Koyama, H., Kurachi, Y. J. Biol. Chem. (1994) [Pubmed]
  12. Opposite effect of intracellular Ca2+ and protein kinase C on the expression of inwardly rectifying K+ channel 1 in mouse skeletal muscle. Shin, K.S., Park, J.Y., Kwon, H., Chung, C.H., Kang, M.S. J. Biol. Chem. (1997) [Pubmed]
  13. Characterization of inward-rectifier K+ channel inhibition by antiarrhythmic piperazine. Xu, Y., Lu, Z. Biochemistry (2004) [Pubmed]
  14. Modulation of the inward rectifier potassium channel IRK1 by the Ras signaling pathway. Giovannardi, S., Forlani, G., Balestrini, M., Bossi, E., Tonini, R., Sturani, E., Peres, A., Zippel, R. J. Biol. Chem. (2002) [Pubmed]
  15. Inward rectification by polyamines in mouse Kir2.1 channels: synergy between blocking components. Xie, L.H., John, S.A., Weiss, J.N. J. Physiol. (Lond.) (2003) [Pubmed]
  16. Molecular cloning and functional expression of a novel brain-specific inward rectifier potassium channel. Morishige, K., Takahashi, N., Jahangir, A., Yamada, M., Koyama, H., Zanelli, J.S., Kurachi, Y. FEBS Lett. (1994) [Pubmed]
  17. Conduction through the inward rectifier potassium channel, Kir2.1, is increased by negatively charged extracellular residues. D'Avanzo, N., Cho, H.C., Tolokh, I., Pekhletski, R., Tolokh, I., Gray, C., Goldman, S., Backx, P.H. J. Gen. Physiol. (2005) [Pubmed]
  18. The role of a single aspartate residue in ionic selectivity and block of a murine inward rectifier K+ channel Kir2.1. Abrams, C.J., Davies, N.W., Shelton, P.A., Stanfield, P.R. J. Physiol. (Lond.) (1996) [Pubmed]
  19. Transgenic upregulation of IK1 in the mouse heart leads to multiple abnormalities of cardiac excitability. Li, J., McLerie, M., Lopatin, A.N. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  20. AMPA receptor-mediated modulation of inward rectifier K+ channels in astrocytes of mouse hippocampus. Schröder, W., Seifert, G., Hüttmann, K., Hinterkeuser, S., Steinhäuser, C. Mol. Cell. Neurosci. (2002) [Pubmed]
  21. Cloning provides evidence for a family of inward rectifier and G-protein coupled K+ channels in the brain. Lesage, F., Duprat, F., Fink, M., Guillemare, E., Coppola, T., Lazdunski, M., Hugnot, J.P. FEBS Lett. (1994) [Pubmed]
  22. Differential voltage-dependent K+ channel responses during proliferation and activation in macrophages. Vicente, R., Escalada, A., Coma, M., Fuster, G., Sánchez-Tilló, E., López-Iglesias, C., Soler, C., Solsona, C., Celada, A., Felipe, A. J. Biol. Chem. (2003) [Pubmed]
  23. Mutations in the putative pore-forming segment favor short-lived wild-type Kir2.1 pore conformations. Schwalbe, R.A., Wingo, C.S., Xia, S.L. Biochemistry (2002) [Pubmed]
  24. Molecular cloning, functional expression and localization of an inward rectifier potassium channel in the mouse brain. Morishige, K., Takahashi, N., Findlay, I., Koyama, H., Zanelli, J.S., Peterson, C., Jenkins, N.A., Copeland, N.G., Mori, N., Kurachi, Y. FEBS Lett. (1993) [Pubmed]
  25. Upregulation of Kv1.3 K(+) channels in microglia deactivated by TGF-beta. Schilling, T., Quandt, F.N., Cherny, V.V., Zhou, W., Heinemann, U., Decoursey, T.E., Eder, C. Am. J. Physiol., Cell Physiol. (2000) [Pubmed]
  26. Molecular cloning, functional expression and localization of a novel inward rectifier potassium channel in the rat brain. Koyama, H., Morishige, K., Takahashi, N., Zanelli, J.S., Fass, D.N., Kurachi, Y. FEBS Lett. (1994) [Pubmed]
  27. A single aspartate residue is involved in both intrinsic gating and blockage by Mg2+ of the inward rectifier, IRK1. Stanfield, P.R., Davies, N.W., Shelton, P.A., Sutcliffe, M.J., Khan, I.A., Brammar, W.J., Conley, E.C. J. Physiol. (Lond.) (1994) [Pubmed]
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