Anti-KCNN2 (K Ca2.2, SK2) Antibody (#APC-028) was used for demonstration of channel expression in mouse, cat, rat and human heart (western blot) and in mouse ventricle and atria or human atrial myocytes (immunocytochemistry) 5. Anti-KCNMA1 (K Ca1.1) (1097-1196) Antibody (#APC-021) was used for demonstration (western blot) of the expression of the channel in mouse heart (presumably in mitochondria) 4. Physiol.Īnti-KCNK3 (TASK-1) Antibody (#APC-024) was used for demonstration (western blot and immunocytochemistry) of the expression of the channel in rat atria and ventricles (Figure 1.) 3. Jones of the University of Hull, UK and the Am. Bar, 15 µm.Īdapted from reference #3, with the kind permission of Dr. Colocalization of KCNK3 and WGA is indicated in yellow (+/WGA). Immunofluorescence images from single ventricular (A ) and atrial (B) myocytes were stained with Anti-KCNK3 (TASK-1) Antibody (#APC-024) (+), eliminated by competitive inhibition with the antigenic peptide (-), and costained with wheat germ agglutinin (WGA). Immunocytochemical Detection of KCNK3 Channels in Rat Myocytes.Įxpression of KCNK3 (TASK-1) protein in rat myocytes. The use of specific antibodies serves as a tool to demonstrate the expression of ion channels in the heart, in different species and under diverse conditions. The concerted activity of many different types of K + channels (of which some 80 human genes are known to encode members of the four main families in this protein group), determines the precise timing and efficiency of cardiac repolarization 1,2. Repolarization of the cardiomyocyte action potential is achieved by the delayed activation of potassium channels facilitating K + efflux. As in many other cellular processes, this transient Ca 2+ elevation is initiated and maintained by depolarization of the cell membrane potential and is terminated by its repolarization back to resting values (in the form of an action potential waveform). Heart beats result from nearly regular changes in intracellular Ca 2+ in heart muscle cells (cardiomyocytes), with elevated Ca 2+ causing muscle contraction. Below we review the use of Alomone Labs’ K + channels antibodies and toxins in such aspects of cardiac research. The repertoire of K + channels in these cells is plastic and is changing under different physiological and pathological conditions. However, cardiomyocytes express several different K + channels, all contributing to the electrical control of the cardiac muscle contraction-relaxation cycle. This voltage dependent cardiac K + channel is called hERG (K V 11.1) and both mutations in the gene encoding this channel (KCNH2) and drugs that block the channel might cause arrhythmia and death. The contribution and importance of K + channels to the normal activity of the heart is best exemplified by disturbances in the activity of one K + channel, causing cardiac arrhythmia. Subscribe – Newsletters and Email Updates.
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