B. Attali, K. Chandy, M. Giese, S. Grissmer, G. Gutman, L. Jan, M. Lazdunski, D. Mckinnon, J. Nerbonne, L. Pardo, Gail A. Robertson, B. Rudy, M. Sanguinetti, W. Stühmer, J. Trimmer, Xiaoliang Wang
{"title":"GtoPdb v.2023.1中的电压门控钾通道(Kv)","authors":"B. Attali, K. Chandy, M. Giese, S. Grissmer, G. Gutman, L. Jan, M. Lazdunski, D. Mckinnon, J. Nerbonne, L. Pardo, Gail A. Robertson, B. Rudy, M. Sanguinetti, W. Stühmer, J. Trimmer, Xiaoliang Wang","doi":"10.2218/gtopdb/f81/2023.1","DOIUrl":null,"url":null,"abstract":"The 6TM family of K channels comprises the voltage-gated KV subfamilies, the EAG subfamily (which includes hERG channels), the Ca2+-activated Slo subfamily (actually with 7TM, termed BK) and the Ca2+-activated SK subfamily. These channels possess a pore-forming α subunit that comprise tetramers of identical subunits (homomeric) or of different subunits (heteromeric). Heteromeric channels can only be formed within subfamilies (e.g. Kv1.1 with Kv1.2; Kv7.2 with Kv7.3). The pharmacology largely reflects the subunit composition of the functional channel.Kv7 channelsKv7.1-Kv7.5 (KCNQ1-5) K+ channels are voltage-gated K+ channels with major roles in neurons, muscle cells and epithelia where they underlie physiologically important K+ currents, such as the neuronal M-current and the cardiac IKs. Genetic deficiencies in all five KCNQ genes result in human excitability disorders, including epilepsy, autism spectrum disorders, cardiac arrhythmias and deafness. Thanks to the recent knowledge of the structure and function of human KCNQ-encoded proteins, these channels are increasingly used as drug targets for treating diseases [326, 2, 767].","PeriodicalId":14617,"journal":{"name":"IUPHAR/BPS Guide to Pharmacology CITE","volume":"21 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Voltage-gated potassium channels (Kv) in GtoPdb v.2023.1\",\"authors\":\"B. Attali, K. Chandy, M. Giese, S. Grissmer, G. Gutman, L. Jan, M. Lazdunski, D. Mckinnon, J. Nerbonne, L. Pardo, Gail A. Robertson, B. Rudy, M. Sanguinetti, W. Stühmer, J. Trimmer, Xiaoliang Wang\",\"doi\":\"10.2218/gtopdb/f81/2023.1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The 6TM family of K channels comprises the voltage-gated KV subfamilies, the EAG subfamily (which includes hERG channels), the Ca2+-activated Slo subfamily (actually with 7TM, termed BK) and the Ca2+-activated SK subfamily. These channels possess a pore-forming α subunit that comprise tetramers of identical subunits (homomeric) or of different subunits (heteromeric). Heteromeric channels can only be formed within subfamilies (e.g. Kv1.1 with Kv1.2; Kv7.2 with Kv7.3). The pharmacology largely reflects the subunit composition of the functional channel.Kv7 channelsKv7.1-Kv7.5 (KCNQ1-5) K+ channels are voltage-gated K+ channels with major roles in neurons, muscle cells and epithelia where they underlie physiologically important K+ currents, such as the neuronal M-current and the cardiac IKs. Genetic deficiencies in all five KCNQ genes result in human excitability disorders, including epilepsy, autism spectrum disorders, cardiac arrhythmias and deafness. Thanks to the recent knowledge of the structure and function of human KCNQ-encoded proteins, these channels are increasingly used as drug targets for treating diseases [326, 2, 767].\",\"PeriodicalId\":14617,\"journal\":{\"name\":\"IUPHAR/BPS Guide to Pharmacology CITE\",\"volume\":\"21 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-04-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"IUPHAR/BPS Guide to Pharmacology CITE\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2218/gtopdb/f81/2023.1\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"IUPHAR/BPS Guide to Pharmacology CITE","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2218/gtopdb/f81/2023.1","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Voltage-gated potassium channels (Kv) in GtoPdb v.2023.1
The 6TM family of K channels comprises the voltage-gated KV subfamilies, the EAG subfamily (which includes hERG channels), the Ca2+-activated Slo subfamily (actually with 7TM, termed BK) and the Ca2+-activated SK subfamily. These channels possess a pore-forming α subunit that comprise tetramers of identical subunits (homomeric) or of different subunits (heteromeric). Heteromeric channels can only be formed within subfamilies (e.g. Kv1.1 with Kv1.2; Kv7.2 with Kv7.3). The pharmacology largely reflects the subunit composition of the functional channel.Kv7 channelsKv7.1-Kv7.5 (KCNQ1-5) K+ channels are voltage-gated K+ channels with major roles in neurons, muscle cells and epithelia where they underlie physiologically important K+ currents, such as the neuronal M-current and the cardiac IKs. Genetic deficiencies in all five KCNQ genes result in human excitability disorders, including epilepsy, autism spectrum disorders, cardiac arrhythmias and deafness. Thanks to the recent knowledge of the structure and function of human KCNQ-encoded proteins, these channels are increasingly used as drug targets for treating diseases [326, 2, 767].