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Kcnj10  -  potassium channel, inwardly rectifying...

Rattus norvegicus

Synonyms: ATP-sensitive inward rectifier potassium channel 10, ATP-sensitive inward rectifier potassium channel KAB-2, BIR10, BIRK1, Brain-specific inwardly rectifying K(+) channel 1, ...
 
 
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Disease relevance of Kcnj10

  • The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered [1].
  • Except for Kir4.1, the subunits tested were all expressed on neurons in the inner nuclear and ganglion cell layers [2].
 

High impact information on Kcnj10

  • BIRK1 mRNA is extremely abundant and is enriched in specific brainstem nuclei, BIRK1 displays a consensus phosphate-binding loop, and expression in Xenopus oocytes has shown that its conductance is inhibited by ATP and adenosine 5'-[gamma-thio]triphosphate [3].
  • Expression and clustered distribution of an inwardly rectifying potassium channel, KAB-2/Kir4.1, on mammalian retinal Müller cell membrane: their regulation by insulin and laminin signals [4].
  • Glial cells from diabetic retinas displayed a decrease of K+ currents that was associated with an altered subcellular distribution of the K+ conductance and a loss of perivascular Kir4.1 protein [5].
  • In this study we have used Kir5.1-specific antibodies to reveal abundant expression of Kir5.1 in renal tubular epithelial cells, where Kir4.1 is also expressed [6].
  • Guanosine promotes the up-regulation of inward rectifier potassium current mediated by Kir4.1 in cultured rat cortical astrocytes [7].
 

Biological context of Kcnj10

  • Finally, we showed that inhibition of translational process, but not depression of transcription, prevents the Guo-induced up-regulation of Kir4.1, indicating that this nucleoside acts through de novo protein synthesis [7].
  • Müller cells of LPS-treated eyes displayed a downregulation of inward K(+) currents and upregulation of A-type K(+) currents that was associated with a decreased expression of Kir4.1 protein in retinal slices [8].
  • The early appearance of Kir4.1 mRNA in various brain regions suggests an involvement of the channel in cell proliferation, migration and differentiation in the rat CNS [9].
  • Expression of chimeric subunits between Kir4.1 and either Kir5.1 or Kir3.4 suggested that the transmembrane domains determine the specificity of subunit heteropolymerization, while the C-terminal domains contribute to alterations in activation kinetics and rectification [10].
  • Developmental expression of Kir4.1 in satellite cells paralleled development of the action potential in the auditory nerve [11].
 

Anatomical context of Kcnj10

 

Associations of Kcnj10 with chemical compounds

  • Colocalization of Kir5.1 with Kir4.1 indicated expression of Kir5.1/Kir4.1 heteromer in these nephron segments [12].
  • Moreover, BIR10 and BIR11, two strong rectifier subunits originally cloned from rat brain, exerted subunit-specific sensitivity to quinidine, being much higher for BIR11 [16].
  • Our results indicated that CAII and Kir4.1 are located in type III cells of the laryngeal taste buds, and supported the idea that the buds may be involved in the recognition of CO2 [17].
  • CAII-reactive cells were also reactive to Kir4.1, PGP 9.5 and serotonin [17].
 

Other interactions of Kcnj10

  • At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered [1].
  • Quantitative studies show a significant increase of Kir4.1 and AQP4 channel aggregates in astrocytes cultured in the presence of laminin when compared with those in the absence of laminin [14].
  • We have analyzed the transcriptional regulation of K(ATP) genes in rat kidney following transient renal ischemia.We observed that mRNA expression level was down-regulated for Kir1.1 and Kir4.1 potassium channels between 24 and 120 h after ischemia [18].
  • Laminin-induced aggregation of the inwardly rectifying potassium channel, Kir4.1, and the water-permeable channel, AQP4, via a dystroglycan-containing complex in astrocytes [14].
  • In the olfactory bulb, Kir4.1 immunoreactivity was detected in a scattered manner in about one-half of the glial fibrillary acidic protein-positive astrocytes [19].
 

Analytical, diagnostic and therapeutic context of Kcnj10

  • By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia-reperfusion on retinal expression of two inward-rectifying K+ (Kir) channels, Kir4.1 and Kir2 [1].
  • 3. The expression of Kir4.1 mRNA in RPE cells was confirmed by RT-PCR analysis and in situ hybridization [15].
  • Furthermore, using immunohistochemistry, we found that Kir4.1 was prominently expressed in RPE cells and localized specifically on the processes on their apical membrane [15].
  • Subcellular localization of the Kir4.1 channel to the plasma membrane of the intermediate cell was confirmed by immunoelectron microscopy [20].

References

  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. Expression patterns of inwardly rectifying potassium channel subunits in rat retina. Tian, M., Chen, L., Xie, J.X., Yang, X.L., Zhao, J.W. Neurosci. Lett. (2003) [Pubmed]
  3. Cloning and expression of two brain-specific inwardly rectifying potassium channels. Bredt, D.S., Wang, T.L., Cohen, N.A., Guggino, W.B., Snyder, S.H. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  4. Expression and clustered distribution of an inwardly rectifying potassium channel, KAB-2/Kir4.1, on mammalian retinal Müller cell membrane: their regulation by insulin and laminin signals. Ishii, M., Horio, Y., Tada, Y., Hibino, H., Inanobe, A., Ito, M., Yamada, M., Gotow, T., Uchiyama, Y., Kurachi, Y. J. Neurosci. (1997) [Pubmed]
  5. Diabetes alters osmotic swelling characteristics and membrane conductance of glial cells in rat retina. Pannicke, T., Iandiev, I., Wurm, A., Uckermann, O., vom Hagen, F., Reichenbach, A., Wiedemann, P., Hammes, H.P., Bringmann, A. Diabetes (2006) [Pubmed]
  6. pH dependence of the inwardly rectifying potassium channel, Kir5.1, and localization in renal tubular epithelia. Tucker, S.J., Imbrici, P., Salvatore, L., D'Adamo, M.C., Pessia, M. J. Biol. Chem. (2000) [Pubmed]
  7. Guanosine promotes the up-regulation of inward rectifier potassium current mediated by Kir4.1 in cultured rat cortical astrocytes. Benfenati, V., Caprini, M., Nobile, M., Rapisarda, C., Ferroni, S. J. Neurochem. (2006) [Pubmed]
  8. Ocular inflammation alters swelling and membrane characteristics of rat Müller glial cells. Pannicke, T., Uckermann, O., Iandiev, I., Wiedemann, P., Reichenbach, A., Bringmann, A. J. Neuroimmunol. (2005) [Pubmed]
  9. Prenatal expression of inwardly rectifying potassium channel mRNA (Kir4.1) in rat brain. Ma, W., Zhang, L., Xing, G., Hu, Z., Iwasa, K.H., Clay, J.R. Neuroreport (1998) [Pubmed]
  10. Inward rectifier potassium channels. Cloning, expression and structure-function studies. Lagrutta, A.A., Bond, C.T., Xia, X.M., Pessia, M., Tucker, S., Adelman, J.P. Japanese heart journal. (1996) [Pubmed]
  11. Expression of an inwardly rectifying K(+) channel, Kir4.1, in satellite cells of rat cochlear ganglia. Hibino, H., Horio, Y., Fujita, A., Inanobe, A., Doi, K., Gotow, T., Uchiyama, Y., Kubo, T., Kurachi, Y. Am. J. Physiol. (1999) [Pubmed]
  12. PDZ binding motif-dependent localization of K+ channel on the basolateral side in distal tubules. Tanemoto, M., Abe, T., Onogawa, T., Ito, S. Am. J. Physiol. Renal Physiol. (2004) [Pubmed]
  13. Glial heterogeneity in expression of the inwardly rectifying K(+) channel, Kir4.1, in adult rat CNS. Poopalasundaram, S., Knott, C., Shamotienko, O.G., Foran, P.G., Dolly, J.O., Ghiani, C.A., Gallo, V., Wilkin, G.P. Glia (2000) [Pubmed]
  14. Laminin-induced aggregation of the inwardly rectifying potassium channel, Kir4.1, and the water-permeable channel, AQP4, via a dystroglycan-containing complex in astrocytes. Guadagno, E., Moukhles, H. Glia (2004) [Pubmed]
  15. Expression and polarized distribution of an inwardly rectifying K+ channel, Kir4.1, in rat retinal pigment epithelium. Kusaka, S., Horio, Y., Fujita, A., Matsushita, K., Inanobe, A., Gotow, T., Uchiyama, Y., Tano, Y., Kurachi, Y. J. Physiol. (Lond.) (1999) [Pubmed]
  16. Subunit-specific inhibition of inward-rectifier K+ channels by quinidine. Doi, T., Fakler, B., Schultz, J.H., Ehmke, H., Brändle, U., Zenner, H.P., Süssbrich, H., Lang, F., Ruppersberg, J.P., Busch, A.E. FEBS Lett. (1995) [Pubmed]
  17. Taste buds and nerve fibers in the rat larynx: an ultrastructural and immunohistochemical study. Nishijima, K., Atoji, Y. Arch. Histol. Cytol. (2004) [Pubmed]
  18. Regulation of ATP-sensitive potassium channel mRNA expression in rat kidney following ischemic injury. Sgard, F., Faure, C., Drieu la Rochelle, C., Graham, D., O'Connor, S.E., Janiak, P., Besnard, F. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  19. An inwardly rectifying K(+) channel, Kir4.1, expressed in astrocytes surrounds synapses and blood vessels in brain. Higashi, K., Fujita, A., Inanobe, A., Tanemoto, M., Doi, K., Kubo, T., Kurachi, Y. Am. J. Physiol., Cell Physiol. (2001) [Pubmed]
  20. Immunological identification of an inward rectifier K+ channel (Kir4.1) in the intermediate cell (melanocyte) of the cochlear stria vascularis of gerbils and rats. Ando, M., Takeuchi, S. Cell Tissue Res. (1999) [Pubmed]
 
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