KvLQT2: Difference between revisions

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It is associated with [[benign familial neonatal epilepsy]].
It is associated with [[benign familial neonatal epilepsy]].


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
== Function ==
{{PBB_Summary
 
| section_title =
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.<ref name="entrez">{{cite web | title = Entrez Gene: KCNQ2 potassium voltage-gated channel, KQT-like subfamily, member 2| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3785| access-date = }}</ref>
| 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 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.<ref name="entrez">{{cite web | title = Entrez Gene: KCNQ2 potassium voltage-gated channel, KQT-like subfamily, member 2| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3785| accessdate = }}</ref>
}}


==Ligands==
==Ligands==
Line 14: Line 12:
[[File:Amato's potassium-channel opener number 40 (2011).png|200px|thumb|Compound #40 (Amato 2011)]]</div>
[[File:Amato's potassium-channel opener number 40 (2011).png|200px|thumb|Compound #40 (Amato 2011)]]</div>
* ICA-069673: channel opener at KCNQ2/[[KCNQ3|Q3]], 20-fold selective over KCNQ3/[[KCNQ5|Q5]], no measurable activity against a panel of cardiac ion channels ([[hERG]], [[Nav1.5]], L type channels, and [[KCNQ1]]) and no activity on [[GABA A receptor|GABA<sub>A</sub> gated channels]] at 10 μM. A range of related benzamides exhibited activity, of which compound number 40 is shown here.<ref>Amato G, JMC Lett 2011, 481, {{doi|10.1021/ml200053x}}</ref>
* ICA-069673: channel opener at KCNQ2/[[KCNQ3|Q3]], 20-fold selective over KCNQ3/[[KCNQ5|Q5]], no measurable activity against a panel of cardiac ion channels ([[hERG]], [[Nav1.5]], L type channels, and [[KCNQ1]]) and no activity on [[GABA A receptor|GABA<sub>A</sub> gated channels]] at 10 μM. A range of related benzamides exhibited activity, of which compound number 40 is shown here.<ref>Amato G, JMC Lett 2011, 481, {{doi|10.1021/ml200053x}}</ref>
* ML252: channel inhibitor, IC<sub>50</sub> = 70nM.<ref name="pmid22793372">{{cite journal |vauthors=Cheung YY, Yu H, Xu K, etal |title=Discovery of a series of 2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)acetamides as novel molecular switches that modulate modes of K(v)7.2 (KCNQ2) channel pharmacology: identification of (S)-2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)butanamide (ML252) as a potent, brain penetrant K(v)7.2 channel inhibitor |journal=J. Med. Chem. |volume=55 |issue=15 |pages=6975–9 |year=2012 |pmid=22793372 |pmc=3530927 |doi=10.1021/jm300700v |url=}}</ref>
* ML252: channel inhibitor, IC<sub>50</sub> = 70nM.<ref name="pmid22793372">{{cite journal | vauthors = Cheung YY, Yu H, Xu K, Zou B, Wu M, McManus OB, Li M, Lindsley CW, Hopkins CR | title = Discovery of a series of 2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)acetamides as novel molecular switches that modulate modes of K(v)7.2 (KCNQ2) channel pharmacology: identification of (S)-2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)butanamide (ML252) as a potent, brain penetrant K(v)7.2 channel inhibitor | journal = Journal of Medicinal Chemistry | volume = 55 | issue = 15 | pages = 6975–9 | date = August 2012 | pmid = 22793372 | pmc = 3530927 | doi = 10.1021/jm300700v }}</ref>


==References==
== References ==
{{reflist}}
{{reflist}}
<ref>http://www.KCNQ2cure.org</ref>


==Further reading==
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
* {{cite journal | vauthors = Gutman GA, Chandy KG, Grissmer S, Lazdunski M, McKinnon D, Pardo LA, Robertson GA, Rudy B, Sanguinetti MC, Stühmer W, Wang X | title = International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels | journal = Pharmacological Reviews | volume = 57 | issue = 4 | pages = 473–508 | date = December 2005 | pmid = 16382104 | doi = 10.1124/pr.57.4.10 }}
| citations =
* {{cite journal | vauthors = Yokoyama M, Nishi Y, Yoshii J, Okubo K, Matsubara K | title = Identification and cloning of neuroblastoma-specific and nerve tissue-specific genes through compiled expression profiles | journal = DNA Research | volume = 3 | issue = 5 | pages = 311–20 | date = October 1996 | pmid = 9039501 | doi = 10.1093/dnares/3.5.311 }}
*{{cite journal   |vauthors=Gutman GA, Chandy KG, Grissmer S, etal |title=International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels. |journal=Pharmacol. Rev. |volume=57 |issue= 4 |pages= 473–508 |year= 2006 |pmid= 16382104 |doi= 10.1124/pr.57.4.10 }}
* {{cite journal | vauthors = Singh NA, Charlier C, Stauffer D, DuPont BR, Leach RJ, Melis R, Ronen GM, Bjerre I, Quattlebaum T, Murphy JV, McHarg ML, Gagnon D, Rosales TO, Peiffer A, Anderson VE, Leppert M | title = A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns | journal = Nature Genetics | volume = 18 | issue = 1 | pages = 25–9 | date = January 1998 | pmid = 9425895 | doi = 10.1038/ng0198-25 }}
*{{cite journal   |vauthors=Yokoyama M, Nishi Y, Yoshii J, etal |title=Identification and cloning of neuroblastoma-specific and nerve tissue-specific genes through compiled expression profiles. |journal=DNA Res. |volume=3 |issue= 5 |pages= 311–20 |year= 1997 |pmid= 9039501 |doi=10.1093/dnares/3.5.311 }}
* {{cite journal | vauthors = Biervert C, Schroeder BC, Kubisch C, Berkovic SF, Propping P, Jentsch TJ, Steinlein OK | title = A potassium channel mutation in neonatal human epilepsy | journal = Science | volume = 279 | issue = 5349 | pages = 403–6 | date = January 1998 | pmid = 9430594 | doi = 10.1126/science.279.5349.403 }}
*{{cite journal   |vauthors=Singh NA, Charlier C, Stauffer D, etal |title=A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns. |journal=Nat. Genet. |volume=18 |issue= 1 |pages= 25–9 |year= 1998 |pmid= 9425895 |doi= 10.1038/ng0198-25 }}
* {{cite journal | vauthors = Yang WP, Levesque PC, Little WA, Conder ML, Ramakrishnan P, Neubauer MG, Blanar MA | title = Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy | journal = The Journal of Biological Chemistry | volume = 273 | issue = 31 | pages = 19419–23 | date = July 1998 | pmid = 9677360 | doi = 10.1074/jbc.273.31.19419 }}
*{{cite journal   |vauthors=Biervert C, Schroeder BC, Kubisch C, etal |title=A potassium channel mutation in neonatal human epilepsy. |journal=Science |volume=279 |issue= 5349 |pages= 403–6 |year= 1998 |pmid= 9430594 |doi=10.1126/science.279.5349.403 }}
* {{cite journal | vauthors = Tinel N, Lauritzen I, Chouabe C, Lazdunski M, Borsotto M | title = The KCNQ2 potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with KCNQ3 | journal = FEBS Letters | volume = 438 | issue = 3 | pages = 171–6 | date = November 1998 | pmid = 9827540 | doi = 10.1016/S0014-5793(98)01296-4 }}
*{{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, Brown BS, Wymore RS, Cohen IS, Dixon JE, McKinnon D | title = KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel | journal = Science | volume = 282 | issue = 5395 | pages = 1890–3 | date = December 1998 | pmid = 9836639 | doi = 10.1126/science.282.5395.1890 }}
*{{cite journal   |vauthors=Tinel N, Lauritzen I, Chouabe C, etal |title=The KCNQ2 potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with KCNQ3. |journal=FEBS Lett. |volume=438 |issue= 3 |pages= 171–6 |year= 1998 |pmid= 9827540 |doi=10.1016/S0014-5793(98)01296-4 }}
* {{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 | date = December 1998 | pmid = 9872318 | doi = 10.1038/25367 }}
*{{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 = Biervert C, Steinlein OK | title = Structural and mutational analysis of KCNQ2, the major gene locus for benign familial neonatal convulsions | journal = Human Genetics | volume = 104 | issue = 3 | pages = 234–40 | date = March 1999 | pmid = 10323247 | doi = 10.1007/PL00008713 }}
*{{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 = Selyanko AA, Hadley JK, Wood IC, Abogadie FC, Delmas P, Buckley NJ, London B, Brown DA | title = Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell | journal = The Journal of Neuroscience | volume = 19 | issue = 18 | pages = 7742–56 | date = September 1999 | pmid = 10479678 | doi =  }}
*{{cite journal |vauthors=Biervert C, Steinlein OK |title=Structural and mutational analysis of KCNQ2, the major gene locus for benign familial neonatal convulsions. |journal=Hum. Genet. |volume=104 |issue= 3 |pages= 234–40 |year= 1999 |pmid= 10323247 |doi=10.1007/PL00008713 }}
* {{cite journal | vauthors = Shapiro MS, Roche JP, Kaftan EJ, Cruzblanca H, Mackie K, Hille B | title = Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current | journal = The Journal of Neuroscience | volume = 20 | issue = 5 | pages = 1710–21 | date = March 2000 | pmid = 10684873 | 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=  }}
* {{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 = Neuroscience Letters | volume = 282 | issue = 1-2 | pages = 73–6 | date = March 2000 | pmid = 10713399 | doi = 10.1016/S0304-3940(00)00866-1 }}
*{{cite journal   |vauthors=Shapiro MS, Roche JP, Kaftan EJ, etal |title=Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current. |journal=J. Neurosci. |volume=20 |issue= 5 |pages= 1710–21 |year= 2000 |pmid= 10684873 |doi=  }}
* {{cite journal | vauthors = Selyanko AA, Hadley JK, Wood IC, Abogadie FC, Jentsch TJ, Brown DA | title = Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors | journal = The Journal of Physiology | volume = 522 Pt 3 | issue = 3 | pages = 349–55 | date = February 2000 | pmid = 10713961 | pmc = 2269765 | doi = 10.1111/j.1469-7793.2000.t01-2-00349.x }}
*{{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 = Cooper EC, Aldape KD, Abosch A, Barbaro NM, Berger MS, Peacock WS, Jan YN, Jan LY | title = Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 97 | issue = 9 | pages = 4914–9 | date = April 2000 | pmid = 10781098 | pmc = 18332 | doi = 10.1073/pnas.090092797 }}
*{{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 |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 = 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 = The Journal of Biological Chemistry | volume = 275 | issue = 18 | pages = 13343–8 | date = May 2000 | pmid = 10788442 | doi = 10.1074/jbc.275.18.13343 }}
*{{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 = Main MJ, Cryan JE, Dupere JR, Cox B, Clare JJ, Burbidge SA | title = Modulation of KCNQ2/3 potassium channels by the novel anticonvulsant retigabine | journal = Molecular Pharmacology | volume = 58 | issue = 2 | pages = 253–62 | date = August 2000 | pmid = 10908292 | doi =  }}
*{{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 = Wickenden AD, Yu W, Zou A, Jegla T, Wagoner PK | title = Retigabine, a novel anti-convulsant, enhances activation of KCNQ2/Q3 potassium channels | journal = Molecular Pharmacology | volume = 58 | issue = 3 | pages = 591–600 | date = September 2000 | pmid = 10953053 | doi =  }}
*{{cite journal   |vauthors=Main MJ, Cryan JE, Dupere JR, etal |title=Modulation of KCNQ2/3 potassium channels by the novel anticonvulsant retigabine. |journal=Mol. Pharmacol. |volume=58 |issue= 2 |pages= 253–62 |year= 2000 |pmid= 10908292 |doi=  }}
* {{cite journal | vauthors = Tinel N, Diochot S, Lauritzen I, Barhanin J, Lazdunski M, Borsotto M | title = M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit | journal = FEBS Letters | volume = 480 | issue = 2-3 | pages = 137–41 | date = September 2000 | pmid = 11034315 | doi = 10.1016/S0014-5793(00)01918-9 }}
*{{cite journal   |vauthors=Wickenden AD, Yu W, Zou A, etal |title=Retigabine, a novel anti-convulsant, enhances activation of KCNQ2/Q3 potassium channels. |journal=Mol. Pharmacol. |volume=58 |issue= 3 |pages= 591–600 |year= 2000 |pmid= 10953053 |doi=  }}
* {{cite journal | vauthors = Smith JS, Iannotti CA, Dargis P, Christian EP, Aiyar J | title = Differential expression of kcnq2 splice variants: implications to m current function during neuronal development | journal = The Journal of Neuroscience | volume = 21 | issue = 4 | pages = 1096–103 | date = February 2001 | pmid = 11160379 | doi =  }}
*{{cite journal   |vauthors=Tinel N, Diochot S, Lauritzen I, etal |title=M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit. |journal=FEBS Lett. |volume=480 |issue= 2-3 |pages= 137–41 |year= 2000 |pmid= 11034315 |doi=10.1016/S0014-5793(00)01918-9 }}
* {{cite journal | vauthors = Miraglia del Giudice E, Coppola G, Scuccimarra G, Cirillo G, Bellini G, Pascotto A | title = Benign familial neonatal convulsions (BFNC) resulting from mutation of the KCNQ2 voltage sensor | journal = European Journal of Human Genetics | volume = 8 | issue = 12 | pages = 994–7 | date = December 2000 | pmid = 11175290 | doi = 10.1038/sj.ejhg.5200570 }}
*{{cite journal   |vauthors=Smith JS, Iannotti CA, Dargis P, etal |title=Differential expression of kcnq2 splice variants: implications to m current function during neuronal development. |journal=J. Neurosci. |volume=21 |issue= 4 |pages= 1096–103 |year= 2001 |pmid= 11160379 |doi=  }}
*{{cite journal   |vauthors=Miraglia del Giudice E, Coppola G, Scuccimarra G, etal |title=Benign familial neonatal convulsions (BFNC) resulting from mutation of the KCNQ2 voltage sensor. |journal=Eur. J. Hum. Genet. |volume=8 |issue= 12 |pages= 994–7 |year= 2001 |pmid= 11175290 |doi= 10.1038/sj.ejhg.5200570 }}
}}
{{refend}}
{{refend}}


==External links==
== External links ==
* {{MeshName|KCNQ2+Potassium+Channel}}
* {{MeshName|KCNQ2+Potassium+Channel}}


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{{Ion channels|g3}}
{{Ion channels|g3}}


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[[Category:Ion channels]]
[[Category:Ion channels]]
[[Category:Proteins]]
[[Category:Proteins]]


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Latest revision as of 07:12, 10 January 2019

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

n/a

n/a

Ensembl

n/a

n/a

UniProt

n/a

n/a

RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

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

It is associated with benign familial neonatal epilepsy.

Function

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]

Ligands

File:ICA-069673.png
ICA-069673
File:Amato's potassium-channel opener number 40 (2011).png
Compound #40 (Amato 2011)
  • ICA-069673: channel opener at KCNQ2/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]
  • ML252: channel inhibitor, IC50 = 70nM.[3]

References

  1. ↑ "Entrez Gene: KCNQ2 potassium voltage-gated channel, KQT-like subfamily, member 2".
  2. ↑ Amato G, JMC Lett 2011, 481, doi:10.1021/ml200053x
  3. ↑ Cheung YY, Yu H, Xu K, Zou B, Wu M, McManus OB, Li M, Lindsley CW, Hopkins CR (August 2012). "Discovery of a series of 2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)acetamides as novel molecular switches that modulate modes of K(v)7.2 (KCNQ2) channel pharmacology: identification of (S)-2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)butanamide (ML252) as a potent, brain penetrant K(v)7.2 channel inhibitor". Journal of Medicinal Chemistry. 55 (15): 6975–9. doi:10.1021/jm300700v. PMC 3530927. PMID 22793372.

Further reading

  • Gutman GA, Chandy KG, Grissmer S, Lazdunski M, McKinnon D, Pardo LA, Robertson GA, Rudy B, Sanguinetti MC, Stühmer W, Wang X (December 2005). "International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels". Pharmacological Reviews. 57 (4): 473–508. doi:10.1124/pr.57.4.10. PMID 16382104.
  • Yokoyama M, Nishi Y, Yoshii J, Okubo K, Matsubara K (October 1996). "Identification and cloning of neuroblastoma-specific and nerve tissue-specific genes through compiled expression profiles". DNA Research. 3 (5): 311–20. doi:10.1093/dnares/3.5.311. PMID 9039501.
  • Singh NA, Charlier C, Stauffer D, DuPont BR, Leach RJ, Melis R, Ronen GM, Bjerre I, Quattlebaum T, Murphy JV, McHarg ML, Gagnon D, Rosales TO, Peiffer A, Anderson VE, Leppert M (January 1998). "A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns". Nature Genetics. 18 (1): 25–9. doi:10.1038/ng0198-25. PMID 9425895.
  • Biervert C, Schroeder BC, Kubisch C, Berkovic SF, Propping P, Jentsch TJ, Steinlein OK (January 1998). "A potassium channel mutation in neonatal human epilepsy". Science. 279 (5349): 403–6. doi:10.1126/science.279.5349.403. PMID 9430594.
  • Yang WP, Levesque PC, Little WA, Conder ML, Ramakrishnan P, Neubauer MG, Blanar MA (July 1998). "Functional expression of two KvLQT1-related potassium channels responsible for an inherited idiopathic epilepsy". The Journal of Biological Chemistry. 273 (31): 19419–23. doi:10.1074/jbc.273.31.19419. PMID 9677360.
  • Tinel N, Lauritzen I, Chouabe C, Lazdunski M, Borsotto M (November 1998). "The KCNQ2 potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with KCNQ3". FEBS Letters. 438 (3): 171–6. doi:10.1016/S0014-5793(98)01296-4. PMID 9827540.
  • Wang HS, Pan Z, Shi W, Brown BS, Wymore RS, Cohen IS, Dixon JE, McKinnon D (December 1998). "KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel". Science. 282 (5395): 1890–3. doi:10.1126/science.282.5395.1890. PMID 9836639.
  • Schroeder BC, Kubisch C, Stein V, Jentsch TJ (December 1998). "Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy". Nature. 396 (6712): 687–90. doi:10.1038/25367. PMID 9872318.
  • Biervert C, Steinlein OK (March 1999). "Structural and mutational analysis of KCNQ2, the major gene locus for benign familial neonatal convulsions". Human Genetics. 104 (3): 234–40. doi:10.1007/PL00008713. PMID 10323247.
  • Selyanko AA, Hadley JK, Wood IC, Abogadie FC, Delmas P, Buckley NJ, London B, Brown DA (September 1999). "Two types of K(+) channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell". The Journal of Neuroscience. 19 (18): 7742–56. PMID 10479678.
  • Shapiro MS, Roche JP, Kaftan EJ, Cruzblanca H, Mackie K, Hille B (March 2000). "Reconstitution of muscarinic modulation of the KCNQ2/KCNQ3 K(+) channels that underlie the neuronal M current". The Journal of Neuroscience. 20 (5): 1710–21. PMID 10684873.
  • Rundfeldt C, Netzer R (March 2000). "The novel anticonvulsant retigabine activates M-currents in Chinese hamster ovary-cells tranfected with human KCNQ2/3 subunits". Neuroscience Letters. 282 (1–2): 73–6. doi:10.1016/S0304-3940(00)00866-1. PMID 10713399.
  • Selyanko AA, Hadley JK, Wood IC, Abogadie FC, Jentsch TJ, Brown DA (February 2000). "Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors". The Journal of Physiology. 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, Barbaro NM, Berger MS, Peacock WS, Jan YN, Jan LY (April 2000). "Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy". Proceedings of the National Academy of Sciences of the United States of America. 97 (9): 4914–9. doi:10.1073/pnas.090092797. PMC 18332. PMID 10781098.
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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