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76行目: |
76行目: |
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| {| class="wikitable" | | {| class="wikitable" |
| |+Potassium channel classes, function, and pharmacology.<ref name=Rang60>{{cite book | author=Rang, HP | title = Pharmacology | publisher = Churchill Livingstone | location = Edinburgh | year = 2003 | isbn = 0-443-07145-4 | oclc = | doi = | page = 60 }}</ref> | | |+カリウムチャネルのクラス、機能、薬理学<ref name="pmid16382103"/><ref name="pmid16382104"/><ref name="16382105"/><ref name="pmid16382106"/> |
| | |
| |- | | |- |
| |'''Class''' | | |'''Class''' |
| ! Subclasses | | ! IUPHAR Name |
| !Function | | !Human Gene Name |
| !Blockers | | !Other Name |
| !Activators | | !補助サブユニット |
| | !分子機能 |
| | !生理的意義 |
| | !阻害薬(IC<sub>50</sub>) |
| | !活性化薬(EC<sub>50</sub>) |
| |- | | |- |
| | [[Calcium-activated potassium channel|Calcium-activated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]] | | |rowspan=5 | [[Calcium-activated potassium channel|Calcium-activated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]] |
| | | | | |
| * [[BK channel]]
| | K<sub>Ca</sub>1.1 |
| * [[SK channel]]
| |
| | | | | |
| * inhibition following stimuli increasing intracellular calcium
| | KCNMA1 |
| | | | | |
| * [[charybdotoxin]], [[iberiotoxin]]
| | Slo, Slo1, BK |
| * [[apamin]]
| | | |
| | | |
| | 脱分極によって活性化、細胞内Ca<sup>2+</sup>濃度上昇による活性化 |
| | | |
| | 書く |
| | | |
| | charybdotoxin(2.9 nM), iberiotoxin(1.7 nM), TEA(0.14 mM) |
| | | |
| | |- |
| | | |
| | K<sub>Ca</sub>2.1-2.3 |
| | | |
| | KCNN1-3 |
| | | |
| | SK<sub>Ca</sub>1-3 |
| | | |
| | calmodulin |
| | | |
| | 細胞内Ca<sup>2+</sup>濃度上昇による活性化 |
| | | |
| | 書く |
| | | |
| | UCL1684(1 nM for K<sub>Ca</sub>2.1; 250 pM for K<sub>Ca</sub>2.2), apamin(8 nM for K<sub>Ca</sub>2.1; 60-200 pM for K<sub>Ca</sub>2.2; 10 nM for K<sub>Ca</sub>2.3), tamapin(42 nM for K<sub>Ca</sub>2.1; 24 pM for K<sub>Ca</sub>2.2) |
| | | |
| | EBIO(630 µM), NS309(30 nM) |
| | |- |
| | | |
| | K<sub>Ca</sub>3.1 |
| | | |
| | KCNT1 |
| | | |
| | IK<sub>Ca</sub>1 |
| | | |
| | calmodulin |
| | | |
| | 細胞内Ca<sup>2+</sup>濃度上昇による活性化 |
| | | |
| | 書く |
| | | |
| | charybdotoxin(5 nM), iberiotoxin(1.7 nM), TEA(24 mM), ketoconazol(30 µM), econazole(12 µM) |
| | | |
| | EBIO, NS309(10 nM) |
| | |- |
| | | |
| | K<sub>Ca</sub>4.1, 4.2 |
| | | |
| | KCNT2 |
| | | |
| | Slack, Slo2.2; Slick, Slo2.1 |
| | | |
| | | |
| | 細胞内Na<sup>+</sup>濃度上昇による活性化 |
| | | |
| | 書く |
| | | |
| | TEA, quinidine |
| | | |
| | |- |
| | | |
| | K<sub>Ca</sub>5.1 |
| | | |
| | KCNU1 |
| | | |
| | Slo3 |
| | | |
| | | |
| | 細胞内Ca<sup>2+</sup>濃度上昇による活性化 |
| | | |
| | 書く |
| | | |
| | TEA |
| | | |
| | |rowspan=8 | [[Inward-rectifier potassium ion channel|Inwardly rectifying]] <br /> 2[[transmembrane helix|T]] & 1[[pore-forming loop|P]] |
| | | |
| | K<sub>ir</sub>2.1-2.4 |
| | | |
| | KCNJ2,12,4,14 |
| | | |
| | IRK |
| | | |
| | | |
| | 常時活性 |
| | | |
| | 静止膜電位形成への関与、心臓におけるIK1電流(Kir2.1/Kir2.2) |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内Mg<sup>2+</sup>, 細胞内polyamines |
| | | |
| | |- |
| | | |
| | K<sub>ir</sub>3.1-3.4 |
| | | |
| | KCNJ3,6,9,5 |
| | | |
| | GIRK |
| | | |
| | | |
| | Gbgによる活性化、代謝型受容体依存的な膜興奮性抑制 |
| | | |
| | 神経細胞における遅延性の抑制性シナプス後電位の形成(Kir3.1/Kir3.2)、心臓における徐脈の分子機構(Kir3.1/Kir3.4) |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, terpiapin |
| | | |
| | Gbg、細胞内Na<sup>+</sup>、PIP<sub>2</sub>、GPCR活性化薬(三量体G蛋白質シグナルを介して) |
| | |- |
| | | |
| | K<sub>ir</sub>4.1-4.2 |
| | | |
| | KCNJ10,15 |
| | | |
| | KAB-2, BIR(K)10 |
| | | |
| | | |
| | 常時活性 |
| | | |
| | 脳内におけるグリア細胞によるカリウムバッファリング機構、内耳や腎臓におけるカリウム恒常性 |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内Mg<sup>2+</sup>, 細胞内polyamines |
| | | |
| | |- |
| | | |
| | K<sub>ir</sub>5.1 |
| | | |
| | KCNJ16 |
| | | |
| | BIR9 |
| | | |
| | | |
| | 常時活性 |
| | | |
| | pHセンシング機構 |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, 細胞内H<sup>+</sup> |
| | | |
| | |- |
| | | |
| | K<sub>ir</sub>6.1 |
| | | |
| | KCNJ8 |
| | | |
| | uKATP-1 |
| | | |
| | SUR2B(血管平滑筋) |
| | | |
| | 細胞内ヌクレオチドによる活性化 |
| | | |
| | 血管平滑筋の緊張度調節 |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, スルホニル尿素剤(SURに結合することによる) |
| | | |
| | カリウムチャネル開口薬(diazoxide, pinacidil, nicorandilなど、SURに結合することによる) |
| | |- |
| | | |
| | K<sub>ir</sub>6.2 |
| | | |
| | KCNJ11 |
| | | |
| | BIR |
| | | |
| | SUR1(膵臓b細胞), SUR2A(心筋細胞), SUR2B(血管平滑筋) |
| | | |
| | 細胞内ATPによる抑制 |
| | | |
| | 膵臓b細胞からのインスリン分泌、脳内における酸素・グルコースセンサー機能、心臓、脳における虚血に対する細胞保護作用 |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>, スルホニル尿素剤(SURに結合することによる) |
| | | |
| | カリウムチャネル開口薬(diazoxide, pinacidil, nicorandilなど、SURに結合することによる) |
| | |- |
| | | |
| | K<sub>ir</sub>7.1 |
| | | |
| | KCNJ13 |
| | | |
| | | |
| | | |
| | 常時活性 |
| | | |
| | | |
| | Ba<sup>2+</sup>, Cs<sup>+</sup>(他のKirファミリーに比べて感受性は低い) |
| | | |
| | |- |
| | |rowspan=18 | [[Tandem pore domain potassium channel|Tandem pore domain]] <br /> 4[[transmembrane helix|T]] & 2[[pore-forming loop|P]] |
| | | |
| | K<sub>2P</sub>1.1 |
| | | |
| | KCNK1 |
| | | |
| | TWIK-1 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>2.1 |
| | | |
| | KCNK2 |
| | | |
| | TREK-1 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | アラキドン酸(10 mM)、揮発性吸入麻酔薬(halothane, isofluorane)など |
| | |- |
| | | |
| | K<sub>2P</sub>3.1 |
| | | |
| | KCNK3 |
| | | |
| | TASK-1 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | 細胞外酸性化(pH7.3) |
| | | |
| | 揮発性吸入麻酔薬(halothane, isofluorane)など |
| | |- |
| | | |
| | K<sub>2P</sub>4.1 |
| | | |
| | KCNK4 |
| | | |
| | TRAAK |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>5.1 |
| | | |
| | KCNK5 |
| | | |
| | TASK-2 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | 細胞外酸性化(pH6.5) |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>6.1 |
| | | |
| | KCNK6 |
| | | |
| | TWIK-2 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>7.1 |
| | | |
| | KCNK7 |
| | | |
| | (KCNK8) |
| | | |
| | | |
| | 常時活性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>8.1 |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>9.1 |
| | | |
| | KCNK9 |
| | | |
| | TASK-3 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | 細胞外酸性化(pH6.5)、ruthenium red (700 nM) |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>10.1 |
| | | |
| | KCNK10 |
| | | |
| | TREK-2 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>11.1 |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>12.1 |
| | | |
| | KCNK12 |
| | | |
| | THIK-2 |
| | | |
| | | |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>13.1 |
| | | |
| | KCNK13 |
| | | |
| | THIK-1 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | アラキドン酸(0.98 mM) |
| | |- |
| | | |
| | K<sub>2P</sub>14.1 |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>15.1 |
| | | |
| | KCNK15 |
| | | |
| | TASK-5 |
| | | |
| | | |
| | 機能的なチャネル発現の報告なし |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>16.1 |
| | | |
| | KCNK16 |
| | | |
| | TALK-1 |
| | | |
| | | |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>17.1 |
| | | |
| | KCNK17 |
| | | |
| | TASK-4 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | | |
| | K<sub>2P</sub>18.1 |
| | | |
| | KCNK18 |
| | | |
| | TRESK-1/TRESK-2 |
| | | |
| | | |
| | 常時活性、GHK整流性 |
| | | |
| | 静止膜電位形成への関与 |
| | | |
| | | |
| | |- |
| | |rowspan=19 | [[Voltage-gated potassium channel|Voltage-gated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]] |
| | | |
| | Kv1.1-1.3 |
| | | |
| | KCNA1-3 |
| | | |
| | |rowspan=6 |Shaker-related |
| | | |
| | Kvb |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 神経細胞、骨格筋細胞における興奮性の制御(遅延性整流性カリウム電流 Kv1.2) |
| | | |
| | 4-Aminopyridine(< mM), TEA(0.3 mM)(Kv1.1) |
| | | |
| | |- |
| | | |
| | Kv1.4 |
| | | |
| | KCNA4 |
| | | |
| | Kvb |
| | | |
| | 脱分極によって活性化、早い不活性化(A-type) |
| | | |
| | A-type電流、神経細胞における脱分極後過分極AHP |
| | | |
| | 4-Aminopyridine(13 µM), TEA(>100 mM) |
| | | |
| | |- |
| | | |
| | Kv1.5 |
| | | |
| | KCNA5 |
| | | |
| | Kvb |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 心臓におけるIKur |
| | | |
| | quinidine(0.6 µM), propafenone(4.4 µM), 4-Aminopyridine(270 µM), TEA(330 mM) |
| | | |
| | |- |
| | | |
| | Kv1.6 |
| | | |
| | KCNA6 |
| | | |
| | Kvb |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 神経細胞における膜電位の制御 |
| | | |
| | a-dendrotoxin(20 nM), 4-Aminopyridine(1.5 mM), TEA(7 mM) |
| | | |
| | |- |
| | | |
| | Kv1.7 |
| | | |
| | KCNA7 |
| | | |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 心臓におけるIKur |
| | | |
| | flecainide(8 µM), quinidine(15 µM), verapamil(16 µM), amiodarone(35 µM), 4-Aminopyridine(150 µM), TEA(150 mM) |
| | | | | |
| * 1-EBIO
| |
| * NS309
| |
| * CyPPA
| |
| |- | | |- |
| |rowspan=3 | [[Inward-rectifier potassium ion channel|Inwardly rectifying]] <br /> 2[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
| |
| | | | | |
| * [[ROMK]] (K<sub>ir</sub>1.1)
| | Kv1.8 |
| | | |
| | KCNA10 |
| | | |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 腎近位尿細管における膜電位の制御 |
| | | |
| | Ba<sup>2+</sup>(5 mM), charybdotoxin(100 nM), 4-Aminopyridine(1.5 mM), TEA(50 mM) |
| | | |
| | |- |
| | | |
| | Kv2.1, 2.2 |
| | | |
| | KCNB1,2 |
| | | |
| | Shab-related |
| | | |
| | Kv5,6,8,9, KChaP |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | | | |
| * recycling and secretion of potassium in [[nephron]]s
| | 神経細胞、骨格筋細胞における興奮性の制御 |
| | | | | |
| * Nonselective: Ba<sup>2+</sup>, Cs<sup>+</sup>
| | Hanatoxin(42 nM)(Kv2.1), 細胞内TEA, 細胞外TEA(2.6 mM)(Kv2.2), 4-Aminopyridine(18 mM for Kv2.1; 1.5 mM for Kv2.2) |
| | | | | |
| * none
| |
| |- | | |- |
| | | | | |
| * [[G protein-coupled inwardly-rectifying potassium channel|GPCR regulated]] (K<sub>ir</sub>3.x)
| | Kv3.1, 3.2 |
| | | |
| | KCNC1,2 |
| | | |
| | |rowspan=2 |Shaw-related |
| | | | | |
| * mediate the inhibitory effect of many [[GPCR]]s
| |
| | | | | |
| * [[GPCR]] antagonists
| | 脱分極によって活性化、遅延性整流性 |
| * [[ifenprodil]]<ref name="pmid16123769"><pubmed>16123769</pubmed></ref>
| | | |
| | 神経細胞の高頻度発火、fast spiking |
| | | |
| | 4-Aminopyridine(29 µM for Kv3.1; 0.1 mM for Kv3.2), TEA(0.2 mM for Kv3.1; 0.1 mM for Kv3.2) |
| | | | | |
| * [[GPCR]] agonists
| |
| |- | | |- |
| | | | | |
| * [[ATP-sensitive K+ channels|ATP-sensitive]] (K<sub>ir</sub>6.x)
| | Kv3.3, 3.4 |
| | | | | |
| * close when [[adenosine triphosphate|ATP]] is high to promote [[insulin]] secretion
| | KCNC3,4 |
| | | | | |
| * [[glibenclamide]]
| |
| * [[tolbutamide]]
| |
| | | | | |
| * [[diazoxide]]
| | 脱分極によって活性化、早い不活性化(A-type) |
| * [[pinacidil]]
| | | |
| | 書く |
| | | |
| | 4-Aminopyridine(1.2 mM for Kv3.3), TEA(0.14 mM for Kv3.3; 0.3 mM for Kv3.4) |
| | | |
| |- | | |- |
| | [[Tandem pore domain potassium channel|Tandem pore domain]] <br /> 4[[transmembrane helix|T]] & 2[[pore-forming loop|P]]
| |
| | | | | |
| * TWIK ([[KCNK1|TWIK-1]], [[KCNK6|TWIK-2]], [[KCNK7]])<ref name="pmid20393194">{{cite journal | author = Enyedi P, Czirják G | title = Molecular background of leak K<sup>+</sup> currents: two-pore domain potassium channels | journal = Physiological Reviews | volume = 90 | issue = 2 | pages = 559–605 | year = 2010 | pmid = 20393194 | doi = 10.1152/physrev.00029.2009 }}</ref><ref name="pmid17652773">{{cite journal | author = Lotshaw DP | title = Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels | journal = Cell Biochemistry and Biophysics | volume = 47 | issue = 2 | pages = 209–56 | year = 2007 | pmid = 17652773 | doi = 10.1007/s12013-007-0007-8 }}</ref>
| | Kv4.1-4.3 |
| * TREK ([[KCNK2|TREK-1]], [[KCNK10|TREK-2]], [[KCNK4|TRAAK]]<ref name="pmid9628867">{{cite journal | author = Fink M, Lesage F, Duprat F, Heurteaux C, Reyes R, Fosset M, Lazdunski M | title = A neuronal two P domain K+ channel stimulated by arachidonic acid and polyunsaturated fatty acids | journal = The EMBO Journal | volume = 17 | issue = 12 | pages = 3297–308 | year = 1998 | pmid = 9628867 | pmc = 1170668 | doi = 10.1093/emboj/17.12.3297 }}</ref>)<ref name="pmid20393194"/><ref name="pmid17652773"/>
| | | |
| * TASK ([[KCNK3|TASK-1]], [[KCNK9|TASK-3]], [[KCNK15|TASK-5]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
| | KCND1-3 |
| * TALK ([[KCNK5|TASK-2]],<ref name="pmid11256078">{{cite journal | author = Goldstein SA, Bockenhauer D, O'Kelly I, Zilberberg N | title = Potassium leak channels and the KCNK family of two-P-domain subunits | journal = Nature Reviews Neuroscience | volume = 2 | issue = 3 | pages = 175–84 | year = 2001 | pmid = 11256078 | doi = 10.1038/35058574 }}</ref> [[KCNK16|TALK-1]], [[KCNK17|TALK-2]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
| | | |
| * THIK ([[KCNK13|THIK-1]], [[KCNK12|THIK-2]])<ref name="pmid20393194"/><ref name="pmid17652773"/>
| | Shal-related |
| * [[KCNK18|TRESK]]<ref name="pmid20393194"/><ref name="pmid17652773"/><ref name="pmid12754259">{{cite journal | author = Sano Y, Inamura K, Miyake A, Mochizuki S, Kitada C, Yokoi H, Nozawa K, Okada H, Matsushime H, Furuichi K | title = A novel two-pore domain K+ channel, TRESK, is localized in the spinal cord | journal = The Journal of Biological Chemistry | volume = 278 | issue = 30 | pages = 27406–12 | year = 2003 | pmid = 12754259 | doi = 10.1074/jbc.M206810200 }}</ref><ref name="pmid14981085">{{cite journal | author = Czirják G, Tóth ZE, Enyedi P | title = The two-pore domain K+ channel, TRESK, is activated by the cytoplasmic calcium signal through calcineurin | journal = The Journal of Biological Chemistry | volume = 279 | issue = 18 | pages = 18550–8 | year = 2004 | pmid = 14981085 | doi = 10.1074/jbc.M312229200 }}</ref>
| | | |
| | KChiP1, KChiPs, DPPX, DPP10(Kv4.2) |
| | | | | |
| * Contribute to [[resting potential]]
| | 脱分極によって活性化、早い不活性化(A-type) |
| | | | | |
| * [[bupivacaine]]<ref name="pmid10201682">{{cite journal | doi = 10.1097/00000542-199904000-00024 | author = Kindler CH, Yost CS, Gray AT | title = Local anesthetic inhibition of baseline potassium channels with two pore domains in tandem | journal = Anesthesiology | volume = 90 | issue = 4 | pages = 1092–102 | year = 1999 | pmid = 10201682 }}</ref><ref name="pmid11249964">{{cite journal | author = Meadows HJ, Randall AD | title = Functional characterisation of human TASK-3, an acid-sensitive two-pore domain potassium channel | journal = Neuropharmacology | volume = 40 | issue = 4 | pages = 551–9 | year = 2001 | pmid = 11249964 | doi = 10.1016/S0028-3908(00)00189-1 }}</ref><ref name="pmid12660311">{{cite journal | author = Kindler CH, Paul M, Zou H, Liu C, Winegar BD, Gray AT, Yost CS | title = Amide local anesthetics potently inhibit the human tandem pore domain background K+ channel TASK-2 (KCNK5) | journal = Journal of Pharmacology and Experimental Therapeutics | volume = 306 | issue = 1 | pages = 84–92 | year = 2003 | pmid = 12660311 | doi = 10.1124/jpet.103.049809 }}</ref><ref name="pmid12760993">{{cite journal | author = Punke MA, Licher T, Pongs O, Friederich P | title = Inhibition of human TREK-1 channels by bupivacaine | journal = Anesthesia & Analgesia | volume = 96 | issue = 6 | pages = 1665–73 | year = 2003 | pmid = 12760993 | doi = 10.1213/01.ANE.0000062524.90936.1F }}</ref>
| | 心臓におけるIto(Kv4.2/Kv4.3/KChiP2)、神経細胞の細胞体におけるISA |
| * [[quinidine]]<ref name="pmid11249964"/><ref name="pmid8605869">{{cite journal | author = Lesage F, Guillemare E, Fink M, Duprat F, Lazdunski M, Romey G, Barhanin J | title = TWIK-1, a ubiquitous human weakly inward rectifying K+ channel with a novel structure | journal = The EMBO Journal | volume = 15 | issue = 5 | pages = 1004–11 | year = 1996 | pmid = 8605869 | pmc = 449995 }}</ref><ref name="pmid9312005">{{cite journal | author = Duprat F, Lesage F, Fink M, Reyes R, Heurteaux C, Lazdunski M | title = TASK, a human background K+ channel to sense external pH variations near physiological pH | journal = The EMBO Journal | volume = 16 | issue = 17 | pages = 5464–71 | year = 1997 | pmid = 9312005 | pmc = 1170177 | doi = 10.1093/emboj/16.17.5464 }}</ref><ref name="pmid9812978">{{cite journal | author = Reyes R, Duprat F, Lesage F, Fink M, Salinas M, Farman N, Lazdunski M | title = Cloning and expression of a novel pH-sensitive two pore domain K+ channel from human kidney | journal = The Journal of Biological Chemistry | volume = 273 | issue = 47 | pages = 30863–9 | year = 1998 | pmid = 9812978 | doi = 10.1074/jbc.273.47.30863 }}</ref><ref name="pmid10784345">{{cite journal | author = Meadows HJ, Benham CD, Cairns W, Gloger I, Jennings C, Medhurst AD, Murdock P, Chapman CG | title = Cloning, localisation and functional expression of the human orthologue of the TREK-1 potassium channel | journal = Pflügers Archiv : European Journal of Physiology | volume = 439 | issue = 6 | pages = 714–22 | year = 2000 | pmid = 10784345 | doi = 10.1007/s004240050997 }}</ref>
| | | |
| | 4-Aminopyridine(9 mM for Kv4.1; 5 mM for Kv4.2), TEA(>10 mM for Kv4.1) |
| | | | | |
| * [[halothane]]<ref name="pmid11249964"/><ref name="pmid10321245">{{cite journal | author = Patel AJ, Honoré E, Lesage F, Fink M, Romey G, Lazdunski M| title = Inhalational anesthetics activate two-pore-domain background K+ channels | journal = Nature Neuroscience | volume = 2 | issue = 5 | pages = 422–6 | year = 1999 | pmid = 10321245 | doi = 10.1038/8084 }}</ref><ref name="pmid10839924">{{cite journal | doi = 10.1097/00000542-200006000-00032 | author = Gray AT, Zhao BB, Kindler CH, Winegar BD, Mazurek MJ, Xu J, Chavez RA, Forsayeth JR, Yost CS | title = Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5 | journal = Anesthesiology | volume = 92 | issue = 6 | pages = 1722–30 | year = 2000 | pmid = 10839924 }}</ref>
| |
| |- | | |- |
| | [[Voltage-gated potassium channel|Voltage-gated]] <br /> 6[[transmembrane helix|T]] & 1[[pore-forming loop|P]]
| |
| | | | | |
| * [[hERG]] (K<sub>v</sub>11.1)
| | Kv5.1 |
| * [[KvLQT1]] (K<sub>v</sub>7.1)
| | | |
| | KCNF1 |
| | | |
| | modifier |
| | | |
| | | |
| | Kv2 familyのmodifier |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | Kv6.1-6.4 |
| | | |
| | KCNG1-4 |
| | | |
| | modifiers |
| | | |
| | | |
| | Kv2 familyのmodifiers |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | Kv7.1 |
| | | |
| | KCNQ1 |
| | | |
| | KVLQT, KQT |
| | | |
| | KCNE1-3 |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 活動電位の再分極、心臓におけるIKs電流(Kv7.1(KCNQ1)/KCNE1)、LQT1の原因遺伝子 |
| | | |
| | Chlomanol 298B(1 µM)(Kv7.1) |
| | | |
| | |- |
| | | |
| | Kv7.2-7.5 |
| | | |
| | KCNQ2-5 |
| | | |
| | | |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | 神経細胞におけるM電流(Kv7.2/7.3, Kv7.5)、内耳機能(Kv7.4) |
| | | |
| | | |
| | Retigabine(10 µM for Kv7.2; 0.6 µM for Kv7.3; 1 µM for Kv7.4; 1.4 µM for Kv7.3/Kv7.5) |
| | |- |
| | | |
| | Kv8.1-8.2 |
| | | |
| | KCNV1-2 |
| | | |
| | modifiers |
| | | |
| | | |
| | Kv2 familyのmodifiers |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | Kv9.1-9.3 |
| | | |
| | KCNS1-3 |
| | | |
| | modifiers |
| | | |
| | | |
| | Kv2 familyのmodifiers |
| | | |
| | | |
| | | |
| | |- |
| | | |
| | Kv10.1, 10.2 |
| | | |
| | KCNH1, 5 |
| | | |
| | eag |
| | | |
| | | |
| | 脱分極によって活性化、遅延性整流性 |
| | | |
| | | |
| | quinidine(1.4 µM for Kv10.4) |
| | | |
| | |- |
| | | |
| | Kv11.1-11.3 |
| | | |
| | KCNH2,6,7 |
| | | |
| | erg |
| | | |
| | minK, KCNE2(Kv11.1) |
| | | |
| | 脱分極によって活性化、早い不活性化機構(C-type)による内向き整流性 |
| | | |
| | 活動電位の再分極、心臓におけるIKr電流、LQT2の原因遺伝子、薬物誘発性不整脈の分子機構(Kv11.1) |
| | | |
| | astemizol(1 nM for Kv11.1), dofetilide(15-35 nM for Kv11.1), sertindole(3 nM for Kv11.1; 43 nM for Kv11.3) |
| | | |
| | |- |
| | | |
| | Kv12.1-12.3 |
| | | |
| | KCNH8,3,4 |
| | | |
| | elk |
| | | |
| | | |
| | | | | |
| * [[action potential]] [[repolarization]]
| |
| * limits frequency of action potentials (disturbances cause [[Cardiac dysrhythmia|dysrhythmia]])
| |
| | | | | |
| * [[tetraethylammonium]]
| |
| * [[4-Aminopyridine|4-aminopyridine]]
| |
| * [[dendrotoxin]]s (some types)
| |
| | | | | |
| * [[retigabine]] (K<sub>v</sub>7)<ref name=Rogawski>{{cite journal |author=Rogawski MA, Bazil CW |title=New Molecular Targets for Antiepileptic Drugs: α2δ, SV2A, and Kv7/KCNQ/M Potassium Channels |journal=Curr Neurol Neurosci Rep |volume=8 |issue=4 |pages=345–52 |year=2008 |month=July |pmid=18590620 |pmc=2587091 |doi=10.1007/s11910-008-0053-7}}</ref>
| |
| |- | | |- |
| |} | | |} |