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KCNQ5  -  potassium channel, voltage gated KQT-like...

Homo sapiens

Synonyms: KQT-like 5, Kv7.5, Potassium channel subunit alpha KvLQT5, Potassium voltage-gated channel subfamily KQT member 5, Voltage-gated potassium channel subunit Kv7.5
 
 
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Disease relevance of KCNQ5

  • Mutation analysis made KCNQ5 unlikely as a candidate gene for benign neonatal convulsions in patients with a positive family history for neonatal or early infantile seizures, but without mutations in the KCNQ2 or KCNQ3 genes [1].
 

High impact information on KCNQ5

  • We found that CaM overexpression reduced NEM augmentation of KCNQ2, KCNQ4, and KCNQ5, and NEM pretreatment reduced Ca2+/CaM-mediated suppression of M current in sympathetic neurons by bradykinin [2].
  • KCNQ5 yields currents that activate slowly with depolarization and can form heteromeric channels with KCNQ3 [3].
  • We have isolated KCNQ5, a novel human member of the KCNQ potassium channel gene family that is differentially expressed in subregions of the brain and in skeletal muscle [4].
  • KCNQ5 currents were insensitive to the K(+) channel blocker tetraethylammonium but were strongly inhibited by the selective M-current blocker linopirdine [4].
  • A KCNQ5 splice variant found in skeletal muscle displays altered gating kinetics [3].
 

Biological context of KCNQ5

  • We have now identified another brain-expressed member of this ion channel subfamily, KCNQ5, which maps to chromosome 6q14 [1].
  • On the genomic level KCNQ5 is composed of 14 exons, which are coding for 897 amino acid residues [1].
 

Anatomical context of KCNQ5

  • The recently identified KCNQ5 gene is expressed in brain and skeletal muscle, and can co-assemble with KCNQ3, suggesting it may also play a role in the M-current heterogeneity [5].
  • When expressed in Xenopus oocytes, KCNQ5 generated voltage-dependent, slowly activating K(+)-selective currents that displayed a marked inward rectification at positive membrane voltages [4].
  • Localization of KCNQ5 in the normal and epileptic human temporal neocortex and hippocampal formation [6].
  • Intense KCNQ5 immunoreactivity was found to be widely distributed throughout the temporal neocortex and the hippocampal formation [6].
  • In these structures, both pyramidal and non-pyramidal neurons and a population of glial cells in the white matter expressed the KCNQ5 subunit [6].
 

Associations of KCNQ5 with chemical compounds

  • KCNQ5/Q3 channels were inhibited by linopirdine (IC(50) 7.7 microM) and barium (IC(50) 0.46 mM), at concentrations similar to those required to inhibit native M-currents [7].
  • KCNQ5/Q3 channels were activated by the novel anticonvulsant, retigabine (EC(50) 1.4 microM) by a mechanism that involved drug-induced, leftward shifts in the voltage-dependence of channel activation (-31.8 mV by 30 microM retigabine) [7].
  • Activation of KCNQ5 channels stably expressed in HEK293 cells by BMS-204352 [8].
 

Other interactions of KCNQ5

  • The widespread distribution of KCNQ5 subunits, its persistence in pharmacoresistant epilepsy, along with the significant role of the M-current in the control of neuronal excitability, makes this protein a possible target for the development of anticonvulsant drugs [6].
 

Analytical, diagnostic and therapeutic context of KCNQ5

References

  1. The new voltage gated potassium channel KCNQ5 and neonatal convulsions. Kananura, C., Biervert, C., Hechenberger, M., Engels, H., Steinlein, O.K. Neuroreport (2000) [Pubmed]
  2. Structural requirements for differential sensitivity of KCNQ K+ channels to modulation by Ca2+/calmodulin. Gamper, N., Li, Y., Shapiro, M.S. Mol. Biol. Cell (2005) [Pubmed]
  3. KCNQ5, a novel potassium channel broadly expressed in brain, mediates M-type currents. Schroeder, B.C., Hechenberger, M., Weinreich, F., Kubisch, C., Jentsch, T.J. J. Biol. Chem. (2000) [Pubmed]
  4. Molecular cloning and functional expression of KCNQ5, a potassium channel subunit that may contribute to neuronal M-current diversity. Lerche, C., Scherer, C.R., Seebohm, G., Derst, C., Wei, A.D., Busch, A.E., Steinmeyer, K. J. Biol. Chem. (2000) [Pubmed]
  5. KCNQ potassium channels: physiology, pathophysiology, and pharmacology. Robbins, J. Pharmacol. Ther. (2001) [Pubmed]
  6. Localization of KCNQ5 in the normal and epileptic human temporal neocortex and hippocampal formation. Yus-Nájera, E., Muñoz, A., Salvador, N., Jensen, B.S., Rasmussen, H.B., Defelipe, J., Villarroel, A. Neuroscience (2003) [Pubmed]
  7. Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells. Wickenden, A.D., Zou, A., Wagoner, P.K., Jegla, T. Br. J. Pharmacol. (2001) [Pubmed]
  8. Activation of KCNQ5 channels stably expressed in HEK293 cells by BMS-204352. Dupuis, D.S., Schrøder, R.L., Jespersen, T., Christensen, J.K., Christophersen, P., Jensen, B.S., Olesen, S.P. Eur. J. Pharmacol. (2002) [Pubmed]
 
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