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Kv7.2 (KvLQT2) is a potassium channel protein coded for by the gene KCNQ2.

It is associated with benign familial neonatal epilepsy.

The M channel is a slowly activating and deactivating potassium channel that plays a critical role in the regulation of neuronal excitability. The M channel is formed by the association of the protein encoded by this gene and a related protein encoded by the KCNQ3 gene, both integral membrane proteins. M channel currents are inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. Defects in this gene are a cause of benign familial neonatal convulsions type 1 (BFNC), also known as epilepsy, benign neonatal type 1 (EBN1). At least five transcript variants encoding five different isoforms have been found for this gene.[1]

LigandsEdit

  • ICA-069673: channel opener at KNCQ2/Q3, 20-fold selective over KCNQ3/Q5, no measurable activity against a panel of cardiac ion channels (hERG, Nav1.5, L type channels, and KCNQ1) and no activity on GABAA gated channels at 10 μM. A range of related benzamides exhibited activity, of which compound number 40 is shown here.[2]
File:ICA-069673.png
File:Amato's potassium-channel opener number 40 (2011).png

ReferencesEdit

Further readingEdit


  • Gutman GA, Chandy KG, Grissmer S, et al. (2006). International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels.. Pharmacol. Rev. 57 (4): 473–508.
  • Yokoyama M, Nishi Y, Yoshii J, et al. (1997). Identification and cloning of neuroblastoma-specific and nerve tissue-specific genes through compiled expression profiles.. DNA Res. 3 (5): 311–20.
  • Singh NA, Charlier C, Stauffer D, et al. (1998). A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns.. Nat. Genet. 18 (1): 25–9.
  • Biervert C, Schroeder BC, Kubisch C, et al. (1998). A potassium channel mutation in neonatal human epilepsy.. Science 279 (5349): 403–6.
  • Yang WP, Levesque PC, Little WA, et al. (1998). Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy.. J. Biol. Chem. 273 (31): 19419–23.
  • Tinel N, Lauritzen I, Chouabe C, et al. (1998). The KCNQ2 potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with KCNQ3.. FEBS Lett. 438 (3): 171–6.
  • Wang HS, Pan Z, Shi W, et al. (1998). KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel.. Science 282 (5395): 1890–3.
  • Schroeder BC, Kubisch C, Stein V, Jentsch TJ (1999). Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy.. Nature 396 (6712): 687–90.
  • Biervert C, Steinlein OK (1999). Structural and mutational analysis of KCNQ2, the major gene locus for benign familial neonatal convulsions.. Hum. Genet. 104 (3): 234–40.
  • Selyanko AA, Hadley JK, Wood IC, et al. (1999). Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell.. J. Neurosci. 19 (18): 7742–56.
  • Shapiro MS, Roche JP, Kaftan EJ, et al. (2000). Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current.. J. Neurosci. 20 (5): 1710–21.
  • Rundfeldt C, Netzer R (2000). The novel anticonvulsant retigabine activates M-currents in Chinese hamster ovary-cells tranfected with human KCNQ2/3 subunits.. Neurosci. Lett. 282 (1-2): 73–6.
  • Selyanko AA, Hadley JK, Wood IC, et al. (2000). Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors.. J. Physiol. (Lond.) 522 Pt 3: 349–55.
  • Cooper EC, Aldape KD, Abosch A, et al. (2000). Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy.. Proc. Natl. Acad. Sci. U.S.A. 97 (9): 4914–9.
  • Schwake M, Pusch M, Kharkovets T, Jentsch TJ (2000). Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsy.. J. Biol. Chem. 275 (18): 13343–8.
  • Main MJ, Cryan JE, Dupere JR, et al. (2000). Modulation of KCNQ2/3 potassium channels by the novel anticonvulsant retigabine.. Mol. Pharmacol. 58 (2): 253–62.
  • Wickenden AD, Yu W, Zou A, et al. (2000). Retigabine, a novel anti-convulsant, enhances activation of KCNQ2/Q3 potassium channels.. Mol. Pharmacol. 58 (3): 591–600.
  • Tinel N, Diochot S, Lauritzen I, et al. (2000). M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit.. FEBS Lett. 480 (2-3): 137–41.
  • Smith JS, Iannotti CA, Dargis P, et al. (2001). Differential expression of kcnq2 splice variants: implications to m current function during neuronal development.. J. Neurosci. 21 (4): 1096–103.
  • Miraglia del Giudice E, Coppola G, Scuccimarra G, et al. (2001). Benign familial neonatal convulsions (BFNC) resulting from mutation of the KCNQ2 voltage sensor.. Eur. J. Hum. Genet. 8 (12): 994–7.




External linksEdit

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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