Ad blocker interference detected!
Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers
Wikia is not accessible if you’ve made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected.
Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
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.
- 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.
- ↑ Entrez Gene: KCNQ2 potassium voltage-gated channel, KQT-like subfamily, member 2.
- ↑ Amato G, JMC Lett 2011, 481, DOI:10.1021/ml200053x
- 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.