%0 Journal Article %1 Nerb_2001_944 %A Nerbonne, J. M. %A Nichols, C. G. %A Schwarz, T. L. %A Escande, D. %D 2001 %J Circ. Res. %K 11717150 Action Animal, Animals, Channels, Conductivity, Disease Diseases, Electric Forecasting, Gov't, Heart Heart, Humans, Inwardly Knockout, Mice, Models, Non-U.S. P.H.S., Potassium Potentials, Rectifying, Research Support, Transgenic, U.S. Voltage-Gated, %N 11 %P 944--956 %T Genetic manipulation of cardiac K$^+$ channel function in mice: what have we learned, and where do we go from here? %U http://circres.ahajournals.org/cgi/content/full/89/11/944 %V 89 %X In the mammalian myocardium, potassium (K$^+$) channels control resting potentials, action potential waveforms, automaticity, and refractory periods and, in most cardiac cells, multiple types of K$^+$ channels that subserve these functions are expressed. Molecular cloning has revealed the presence of a large number of K$^+$ channel pore forming (alpha) and accessory (beta) subunits in the heart, and considerable progress has been made recently in defining the relationships between expressed K$^+$ channel subunits and functional cardiac K$^+$ channels. To date, more than 20 mouse models with altered K$^+$ channel expression/functioning have been generated using dominant-negative transgenic and targeted gene deletion approaches. In several instances, the genetic manipulation of K$^+$ channel subunit expression has revealed the role of specific K$^+$ channel subunit subfamilies or individual K$^+$ channel subunit genes in the generation of myocardial K$^+$ channels. In other cases, however, the phenotypic consequences have been unexpected. This review summarizes what has been learned from the in situ genetic manipulation of cardiac K$^+$ channel functioning in the mouse, discusses the limitations of the models developed to date, and explores the likely directions of future research.

@article{Nerb_2001_944, abstract = {In the mammalian myocardium, potassium ({K}$^{+}$) channels control resting potentials, action potential waveforms, automaticity, and refractory periods and, in most cardiac cells, multiple types of {K}$^{+}$ channels that subserve these functions are expressed. Molecular cloning has revealed the presence of a large number of {K}$^{+}$ channel pore forming (alpha) and accessory (beta) subunits in the heart, and considerable progress has been made recently in defining the relationships between expressed {K}$^{+}$ channel subunits and functional cardiac {K}$^{+}$ channels. To date, more than 20 mouse models with altered {K}$^{+}$ channel expression/functioning have been generated using dominant-negative transgenic and targeted gene deletion approaches. In several instances, the genetic manipulation of {K}$^{+}$ channel subunit expression has revealed the role of specific {K}$^{+}$ channel subunit subfamilies or individual {K}$^{+}$ channel subunit genes in the generation of myocardial {K}$^{+}$ channels. In other cases, however, the phenotypic consequences have been unexpected. This review summarizes what has been learned from the in situ genetic manipulation of cardiac {K}$^{+}$ channel functioning in the mouse, discusses the limitations of the models developed to date, and explores the likely directions of future research.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Nerbonne, J. M. and Nichols, C. G. and Schwarz, T. L. and Escande, D.}, biburl = {https://www.bibsonomy.org/bibtex/237b904bdb6c7dbc41319e329d6a548d6/hake}, description = {The whole bibliography file I use.}, file = {Nerb_2001_944.pdf:Nerb_2001_944.pdf:PDF}, interhash = {39f064658d7ad83db22122a745a6a660}, intrahash = {37b904bdb6c7dbc41319e329d6a548d6}, journal = {Circ. Res.}, key = 81, keywords = {11717150 Action Animal, Animals, Channels, Conductivity, Disease Diseases, Electric Forecasting, Gov't, Heart Heart, Humans, Inwardly Knockout, Mice, Models, Non-U.S. P.H.S., Potassium Potentials, Rectifying, Research Support, Transgenic, U.S. Voltage-Gated,}, month = Nov, number = 11, pages = {944--956}, pmid = {11717150}, timestamp = {2009-06-03T11:21:23.000+0200}, title = {Genetic manipulation of cardiac {K}$^{+}$ channel function in mice: what have we learned, and where do we go from here?}, url = {http://circres.ahajournals.org/cgi/content/full/89/11/944}, volume = 89, year = 2001 }