Biology:KvLQT3
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Short description: Protein-coding gene in the species Homo sapiens
 Generic protein structure example |
Kv7.3 (KvLQT3) is a potassium channel protein coded for by the gene KCNQ3.[1]
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 one of two related proteins encoded by the KCNQ2 and KCNQ5 genes, 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 2 (BFNC2), also known as epilepsy, benign neonatal type 2 (EBN2).[1]
Interactions
KvLQT3 has been shown to interact with KCNQ5.[2]
References
- ↑ 1.0 1.1 "Entrez Gene: KCNQ3 potassium voltage-gated channel, KQT-like subfamily, member 3". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3786.
- ↑ Yus-Nájera, E; Muñoz A; Salvador N; Jensen B S; Rasmussen H B; Defelipe J; Villarroel A (2003). "Localization of KCNQ5 in the normal and epileptic human temporal neocortex and hippocampal formation". Neuroscience 120 (2): 353–64. doi:10.1016/S0306-4522(03)00321-X. ISSN 0306-4522. PMID 12890507.
Further reading
- "International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels.". Pharmacol. Rev. 57 (4): 473–508. 2006. doi:10.1124/pr.57.4.10. PMID 16382104.
- "Benign familial neonatal convulsions: evidence for clinical and genetic heterogeneity.". Ann. Neurol. 29 (5): 469–73. 1991. doi:10.1002/ana.410290504. PMID 1859177.
- "Genetic heterogeneity in benign familial neonatal convulsions: identification of a new locus on chromosome 8q.". Am. J. Hum. Genet. 53 (3): 670–5. 1993. PMID 8102508.
- "A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family.". Nat. Genet. 18 (1): 53–5. 1998. doi:10.1038/ng0198-53. PMID 9425900.
- "Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy.". J. Biol. Chem. 273 (31): 19419–23. 1998. doi:10.1074/jbc.273.31.19419. PMID 9677360.
- "KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel.". Science 282 (5395): 1890–3. 1998. doi:10.1126/science.282.5395.1890. PMID 9836639. Bibcode: 1998Sci...282.1890W.
- "Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy.". Nature 396 (6712): 687–90. 1999. doi:10.1038/25367. PMID 9872318. Bibcode: 1998Natur.396..687S.
- "KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness.". Cell 96 (3): 437–46. 1999. doi:10.1016/S0092-8674(00)80556-5. PMID 10025409.
- "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. 1999. doi:10.1523/JNEUROSCI.19-18-07742.1999. PMID 10479678. PMC 6782456. http://discovery.ucl.ac.uk/22399/4/Brown_Two%20Types%20of%20K%E2%81%BA%20Channel%20Subunit%2C%20Erg1%20and%20KCNQ23%2C%20Contribute%20to%20the%20M-Like%20Current%20in%20a%20Mammalian%20Neuronal%20Cell_VoR.pdf.
- "Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current.". J. Neurosci. 20 (5): 1710–21. 2000. doi:10.1523/JNEUROSCI.20-05-01710.2000. PMID 10684873.
- "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. 2000. doi:10.1016/S0304-3940(00)00866-1. PMID 10713399.
- "Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors.". J. Physiol. 522 Pt 3 (3): 349–55. 2000. doi:10.1111/j.1469-7793.2000.t01-2-00349.x. PMID 10713961.
- "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. 2000. doi:10.1073/pnas.090092797. PMID 10781098. Bibcode: 2000PNAS...97.4914C.
- "Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsy.". J. Biol. Chem. 275 (18): 13343–8. 2000. doi:10.1074/jbc.275.18.13343. PMID 10788442.
- "A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions.". Ann. Neurol. 47 (6): 822–6. 2000. doi:10.1002/1531-8249(200006)47:6<822::AID-ANA19>3.0.CO;2-X. PMID 10852552.
- "Modulation of KCNQ2/3 potassium channels by the novel anticonvulsant retigabine.". Mol. Pharmacol. 58 (2): 253–62. 2000. doi:10.1124/mol.58.2.253. PMID 10908292.
- "Retigabine, a novel anti-convulsant, enhances activation of KCNQ2/Q3 potassium channels.". Mol. Pharmacol. 58 (3): 591–600. 2000. doi:10.1124/mol.58.3.591. PMID 10953053.
- "M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit.". FEBS Lett. 480 (2–3): 137–41. 2000. doi:10.1016/S0014-5793(00)01918-9. PMID 11034315.
- "Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells.". Br. J. Pharmacol. 132 (2): 381–4. 2001. doi:10.1038/sj.bjp.0703861. PMID 11159685.
- "The identification and characterization of a noncontinuous calmodulin-binding site in noninactivating voltage-dependent KCNQ potassium channels.". J. Biol. Chem. 277 (32): 28545–53. 2002. doi:10.1074/jbc.M204130200. PMID 12032157.
External links
- KCNQ3+Potassium+Channel at the US National Library of Medicine Medical Subject Headings (MeSH)
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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