KvLQT3: Difference between revisions
Jump to navigation
Jump to search
m (Bot: HTTP→HTTPS (v470)) |
m (Adding 0 arxiv eprint(s), 3 bibcode(s) and 0 doi(s). Did it miss something? Report bugs, errors, and suggestions at User talk:Bibcode Bot) |
||
| Line 7: | Line 7: | ||
{{PBB_Summary | {{PBB_Summary | ||
| section_title = | | section_title = | ||
| summary_text = 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).<ref name="entrez"/> | | summary_text = 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).<ref name="entrez"/> | ||
}} | }} | ||
| Line 25: | Line 25: | ||
*{{cite journal |vauthors=Charlier C, Singh NA, Ryan SG, etal |title=A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family. |journal=Nat. Genet. |volume=18 |issue= 1 |pages= 53–5 |year= 1998 |pmid= 9425900 |doi= 10.1038/ng0198-53 }} | *{{cite journal |vauthors=Charlier C, Singh NA, Ryan SG, etal |title=A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family. |journal=Nat. Genet. |volume=18 |issue= 1 |pages= 53–5 |year= 1998 |pmid= 9425900 |doi= 10.1038/ng0198-53 }} | ||
*{{cite journal |vauthors=Yang WP, Levesque PC, Little WA, etal |title=Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy. |journal=J. Biol. Chem. |volume=273 |issue= 31 |pages= 19419–23 |year= 1998 |pmid= 9677360 |doi=10.1074/jbc.273.31.19419 }} | *{{cite journal |vauthors=Yang WP, Levesque PC, Little WA, etal |title=Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy. |journal=J. Biol. Chem. |volume=273 |issue= 31 |pages= 19419–23 |year= 1998 |pmid= 9677360 |doi=10.1074/jbc.273.31.19419 }} | ||
*{{cite journal |vauthors=Wang HS, Pan Z, Shi W, etal |title=KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel. |journal=Science |volume=282 |issue= 5395 |pages= 1890–3 |year= 1998 |pmid= 9836639 |doi=10.1126/science.282.5395.1890 }} | *{{cite journal |vauthors=Wang HS, Pan Z, Shi W, etal |title=KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel. |journal=Science |volume=282 |issue= 5395 |pages= 1890–3 |year= 1998 |pmid= 9836639 |doi=10.1126/science.282.5395.1890 |bibcode=1998Sci...282.1890W }} | ||
*{{cite journal |vauthors=Schroeder BC, Kubisch C, Stein V, Jentsch TJ |title=Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. |journal=Nature |volume=396 |issue= 6712 |pages= 687–90 |year= 1999 |pmid= 9872318 |doi= 10.1038/25367 }} | *{{cite journal |vauthors=Schroeder BC, Kubisch C, Stein V, Jentsch TJ |title=Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. |journal=Nature |volume=396 |issue= 6712 |pages= 687–90 |year= 1999 |pmid= 9872318 |doi= 10.1038/25367 |bibcode=1998Natur.396..687S }} | ||
*{{cite journal |vauthors=Kubisch C, Schroeder BC, Friedrich T, etal |title=KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness. |journal=Cell |volume=96 |issue= 3 |pages= 437–46 |year= 1999 |pmid= 10025409 |doi=10.1016/S0092-8674(00)80556-5 }} | *{{cite journal |vauthors=Kubisch C, Schroeder BC, Friedrich T, etal |title=KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness. |journal=Cell |volume=96 |issue= 3 |pages= 437–46 |year= 1999 |pmid= 10025409 |doi=10.1016/S0092-8674(00)80556-5 }} | ||
*{{cite journal |vauthors=Selyanko AA, Hadley JK, Wood IC, etal |title=Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell. |journal=J. Neurosci. |volume=19 |issue= 18 |pages= 7742–56 |year= 1999 |pmid= 10479678 |doi= }} | *{{cite journal |vauthors=Selyanko AA, Hadley JK, Wood IC, etal |title=Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell. |journal=J. Neurosci. |volume=19 |issue= 18 |pages= 7742–56 |year= 1999 |pmid= 10479678 |doi= }} | ||
| Line 32: | Line 32: | ||
*{{cite journal |vauthors=Rundfeldt C, Netzer R |title=The novel anticonvulsant retigabine activates M-currents in Chinese hamster ovary-cells tranfected with human KCNQ2/3 subunits. |journal=Neurosci. Lett. |volume=282 |issue= 1-2 |pages= 73–6 |year= 2000 |pmid= 10713399 |doi=10.1016/S0304-3940(00)00866-1 }} | *{{cite journal |vauthors=Rundfeldt C, Netzer R |title=The novel anticonvulsant retigabine activates M-currents in Chinese hamster ovary-cells tranfected with human KCNQ2/3 subunits. |journal=Neurosci. Lett. |volume=282 |issue= 1-2 |pages= 73–6 |year= 2000 |pmid= 10713399 |doi=10.1016/S0304-3940(00)00866-1 }} | ||
*{{cite journal |vauthors=Selyanko AA, Hadley JK, Wood IC, etal |title=Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors. |journal=J. Physiol. |volume=522 Pt 3 |issue= 3|pages= 349–55 |year= 2000 |pmid= 10713961 |doi=10.1111/j.1469-7793.2000.t01-2-00349.x | pmc=2269765 }} | *{{cite journal |vauthors=Selyanko AA, Hadley JK, Wood IC, etal |title=Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors. |journal=J. Physiol. |volume=522 Pt 3 |issue= 3|pages= 349–55 |year= 2000 |pmid= 10713961 |doi=10.1111/j.1469-7793.2000.t01-2-00349.x | pmc=2269765 }} | ||
*{{cite journal |vauthors=Cooper EC, Aldape KD, Abosch A, etal |title=Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=97 |issue= 9 |pages= 4914–9 |year= 2000 |pmid= 10781098 |doi= 10.1073/pnas.090092797 | pmc=18332 }} | *{{cite journal |vauthors=Cooper EC, Aldape KD, Abosch A, etal |title=Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=97 |issue= 9 |pages= 4914–9 |year= 2000 |pmid= 10781098 |doi= 10.1073/pnas.090092797 | pmc=18332 |bibcode=2000PNAS...97.4914C }} | ||
*{{cite journal |vauthors=Schwake M, Pusch M, Kharkovets T, Jentsch TJ |title=Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsy. |journal=J. Biol. Chem. |volume=275 |issue= 18 |pages= 13343–8 |year= 2000 |pmid= 10788442 |doi=10.1074/jbc.275.18.13343 }} | *{{cite journal |vauthors=Schwake M, Pusch M, Kharkovets T, Jentsch TJ |title=Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsy. |journal=J. Biol. Chem. |volume=275 |issue= 18 |pages= 13343–8 |year= 2000 |pmid= 10788442 |doi=10.1074/jbc.275.18.13343 }} | ||
*{{cite journal |vauthors=Hirose S, Zenri F, Akiyoshi H, etal |title=A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions. |journal=Ann. Neurol. |volume=47 |issue= 6 |pages= 822–6 |year= 2000 |pmid= 10852552 |doi=10.1002/1531-8249(200006)47:6<822::AID-ANA19>3.0.CO;2-X }} | *{{cite journal |vauthors=Hirose S, Zenri F, Akiyoshi H, etal |title=A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions. |journal=Ann. Neurol. |volume=47 |issue= 6 |pages= 822–6 |year= 2000 |pmid= 10852552 |doi=10.1002/1531-8249(200006)47:6<822::AID-ANA19>3.0.CO;2-X }} | ||
Revision as of 18:30, 24 June 2018
| VALUE_ERROR (nil) | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Aliases | |||||||
| External IDs | GeneCards: [1] | ||||||
| Orthologs | |||||||
| Species | Human | Mouse | |||||
| Entrez |
|
| |||||
| Ensembl |
|
| |||||
| UniProt |
|
| |||||
| RefSeq (mRNA) |
|
| |||||
| RefSeq (protein) |
|
| |||||
| Location (UCSC) | n/a | n/a | |||||
| PubMed search | n/a | n/a | |||||
| Wikidata | |||||||
| |||||||
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".
- ↑ 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. United States. 120 (2): 353–64. doi:10.1016/S0306-4522(03)00321-X. ISSN 0306-4522. PMID 12890507.
Further reading
- 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. doi:10.1124/pr.57.4.10. PMID 16382104.
- Ryan SG, Wiznitzer M, Hollman C, et al. (1991). "Benign familial neonatal convulsions: evidence for clinical and genetic heterogeneity". Ann. Neurol. 29 (5): 469–73. doi:10.1002/ana.410290504. PMID 1859177.
- Lewis TB, Leach RJ, Ward K, et al. (1993). "Genetic heterogeneity in benign familial neonatal convulsions: identification of a new locus on chromosome 8q". Am. J. Hum. Genet. 53 (3): 670–5. PMC 1682419. PMID 8102508.
- Charlier C, Singh NA, Ryan SG, et al. (1998). "A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family". Nat. Genet. 18 (1): 53–5. doi:10.1038/ng0198-53. PMID 9425900.
- 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. doi:10.1074/jbc.273.31.19419. PMID 9677360.
- 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. Bibcode:1998Sci...282.1890W. doi:10.1126/science.282.5395.1890. PMID 9836639.
- 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. Bibcode:1998Natur.396..687S. doi:10.1038/25367. PMID 9872318.
- Kubisch C, Schroeder BC, Friedrich T, et al. (1999). "KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness". Cell. 96 (3): 437–46. doi:10.1016/S0092-8674(00)80556-5. PMID 10025409.
- 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. PMID 10479678.
- 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. PMID 10684873.
- 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. doi:10.1016/S0304-3940(00)00866-1. PMID 10713399.
- 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. 522 Pt 3 (3): 349–55. doi:10.1111/j.1469-7793.2000.t01-2-00349.x. PMC 2269765. PMID 10713961.
- 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. Bibcode:2000PNAS...97.4914C. doi:10.1073/pnas.090092797. PMC 18332. PMID 10781098.
- 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. doi:10.1074/jbc.275.18.13343. PMID 10788442.
- Hirose S, Zenri F, Akiyoshi H, et al. (2000). "A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions". Ann. Neurol. 47 (6): 822–6. doi:10.1002/1531-8249(200006)47:6<822::AID-ANA19>3.0.CO;2-X. PMID 10852552.
- 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. PMID 10908292.
- 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. PMID 10953053.
- 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. doi:10.1016/S0014-5793(00)01918-9. PMID 11034315.
- Wickenden AD, Zou A, Wagoner PK, Jegla T (2001). "Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells". Br. J. Pharmacol. 132 (2): 381–4. doi:10.1038/sj.bjp.0703861. PMC 1572592. PMID 11159685.
- Yus-Najera E, Santana-Castro I, Villarroel A (2002). "The identification and characterization of a noncontinuous calmodulin-binding site in noninactivating voltage-dependent KCNQ potassium channels". J. Biol. Chem. 277 (32): 28545–53. 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.
| Stub icon | This membrane protein–related article is a stub. You can help Wikipedia by expanding it. |
