Abstract: Disclosed are methods of terminating acute episodes of cardiac arrhythmia, such as atrial fibrillation or ventricular fibrillation, in a mammal, such as a human, by administering to that mammal an amount of domperidone, or a pharmaceutically acceptable salt, derivative or metabolite thereof, effective to terminate an acute episode of cardiac arrhythmia and/or restore normal sinus rhythm or heart rate. Also disclosed are methods of maintaining normal sinus rhythm or heart rate in a mammal, such as a human, and preventing a recurrence of an episode of cardiac arrhythmia in a mammal, by administering an amount of domperidone, or a pharmaceutically acceptable salt, derivative or metabolite thereof, effective to maintain normal sinus rhythm or heart rate in a mammal that has experienced at least one prior episode of cardiac arrhythmia. Pharmaceutical compositions for use in these methods are also disclosed.

Abstract: Disclosed are high throughput assay systems and methods for identifying agents that alter the level of expression of proteins in mammalian cells, particularly integral membrane proteins.

Abstract: Disclosed are methods of preventing or treating cardiac arrhythmia comprising administering to a mammal in need thereof, such as a human, an effective amount of vanoxerine (GBR 12909) or a pharmaceutically acceptable salt, derivative or metabolite thereof.

Abstract: Disclosed are high throughput assay systems and methods for identifying agents that alter the level of surface expression of integral membrane proteins, such as cardiac ion channels, in mammalian cells. Also disclosed are therapeutic methods of using agents identified using such methods.

Abstract: The present invention provides polynucleotides that encode a protein, designated herein as K+ Channel Associated Protein or “KChAP”. It has been determined that expressing polynucleotides that encode KChAP in host cells, along with polynucleotides that encode the Kv? channel subunit Kv 2.1, the Kv? channel subunit Kv 2.2, the Kv? channel subunit Kv 1.3, or the Kv? channel subunit Kv 4.3, increases the number of Kv2.1, Kv 2.2, Kv1.3 or Kv4.3 channels, respectively, in the plasma membrane of such cells. The present invention also relates to a method of making cells that have increased numbers of Kv channels on the plasma membranes thereof and to a method of using such cells as model systems for studying the effect of pharmacological agents on Kv channels, particularly on Kv2.1, Kv 2.2, Kv 1.3, and Kv 4.3 channels. The present invention also relates to the protein KChAP.

Abstract: Methods of inducing apoptosis in hyperproliferative cells, particularly cancer cells are provided. Such method involves increasing the levels of a potassium channel modulatory protein in the cell. Examples of such proteins are native KChAP protein, a biologically active variant of native KChAP protein, or a biologically active KChAP-related protein (collectively referred to hereinafter as “KChAP protein”). In one embodiment, the cells are contacted with the KChAP protein under conditions permitting uptake of the protein by the cells. In another embodiment, the cells are contacted with (i) a nucleic acid encoding the KChAP protein, and (ii) a promoter active in the cancer cell, wherein the promoter is operably linked to the region encoding the KChAP protein, under conditions permitting the uptake of the nucleic acid by the cancer cell.

Abstract: Disclosed are methods of preventing or treating cardiac arrhythmia comprising administering to a mammal in need thereof, such as a human, an effective amount of vanoxerine (GBR 12909) or a pharmaceutically acceptable salt, derivative or metabolite thereof.

Abstract: Disclosed are methods of preventing or treating cardiac arrhythmia comprising administering to a mammal in need thereof, such as a human, an effective amount of vanoxerine (GBR 12909) or a pharmaceutically acceptable salt, derivative or metabolite thereof.

Abstract: Disclosed are methods of preventing or treating cardiac arrhythmia comprising administering to a mammal in need thereof, such as a human, an effective amount of vanoxerine (GBR 12909) or a pharmaceutically acceptable salt, derivative or metabolite thereof.

Abstract: Methods of inducing apoptosis in hyperproliferative cells, particularly cancer cells are provided. Such method involves increasing the levels of a potassium channel modulatory protein in the cell. Examples of such proteins are native KChAP protein, a biologically active variant of native KChAP protein, or a biologically active KChAP-related protein (collectively referred to hereinafter as “KChAP protein”). In one embodiment, the cells are contacted with the KChAP protein under conditions permitting uptake of the protein by the cells. In another embodiment, the cells are contacted with (i) a nucleic acid encoding the KChAP protein, and (ii) a promoter active in the cancer cell, wherein the promoter is operably linked to the region encoding the KChAP protein, under conditions permitting the uptake of the nucleic acid by the cancer cell.

Abstract: The present invention provides polynucleotides that encode a protein, designated herein as K+ Channel Associated Protein or “KChAP”. It has been determined that expressing polynucleotides that encode KChAP in host cells, along with polynucleotides that encode the Kv&agr; channel subunit Kv 2.1, the Kv&agr; channel subunit Kv 2.2, the Kv&agr; channel subunit Kv 1.3, or the Kv&agr; channel subunit Kv 4.3, increases the number of Kv2.1, Kv 2.2, Kv1.3 or Kv4.3 channels, respectively, in the plasma membrane of such cells. The present invention also relates to a method of making cells that have increased numbers of Kv channels on the plasma membranes thereof and to a method of using such cells as model systems for studying the effect of pharmacological agents on Kv channels, particularly on Kv2.1, Kv 2.2, Kv 1.3, and Kv 4.3 channels. The present invention also relates to the protein KChAP.

Abstract: The present invention provides polynucleotides that encode a protein, designated herein as K+ Channel Associated Protein or “KChAP”. It has been determined that expressing polynucleotides that encode KChAP in host cells, along with polynucleotides that encode the Kv&agr; channel subunit Kv 2.1, the Kv&agr; channel subunit Kv 2.2, the Kv&agr; channel subunit Kv 1.3, or the Kv&agr; channel subunit Kv 4.3, increases the number of Kv2.1, Kv 2.2, Kv1.3 or Kv4.3 channels, respectively, in the plasma membrane of such cells. The present invention also relates to a method of making cells that have increased numbers of Kv channels on the plasma membranes thereof and to a method of using such cells as model systems for studying the effect of pharmacological agents on Kv channels, particularly on Kv2.1, Kv 2.2, Kv 1.3, and Kv 4.3 channels. The present invention also relates to the protein KChAP.

Abstract: The present invention provides polynucleotides that encode a protein, designated herein as K+ Channel Associated Protein or “KChAP”. It has been determined that expressing polynucleotides that encode KChAP in host cells, along with polynucleotides that encode the Kv&agr; channel subunit Kv 2.1, the Kv&agr; channel subunit Kv 2.2, the Kv&agr; channel subunit Kv 1.3, or the Kv&agr; channel subunit Kv 4.3, increases the number of Kv2.1, Kv 2.2, Kv1.3 or Kv4.3 channels, respectively, in the plasma membrane of such cells. The present invention also relates to a method of making cells that have increased numbers of Kv channels on the plasma membranes thereof and to a method of using such cells as model systems for studying the effect of pharmacological agents on Kv channels, particularly on Kv2.1, Kv 2.2, Kv 1.3, and Kv 4.3 channels. The present invention also relates to the protein KChAP.

Abstract: The present invention provides a novel treatment for cardiac arrhythmias, by administering S-adenosyl methionine decarboxylase inhibitors, preferably 5'-({(Z)-4-amino-2-butenyl}methylamino)-5'-deoxyadenosine. It has been discovered that 5'-({(Z)-4-amino-2-butenyl}methylamino)-5'-deoxyadenosine, increases the P--R interval, increases outward current through inward rectifier K.sup.+ channels and increases the hyperpolarization, of cardiac cells, thereby reducing cardiac excitability. Specifically, the method involves providing an S-adenosyl methionine decarboxylase inhibitor; combining the S-adenosyl methionine decarboxylase inhibitor with a pharmaceutically acceptable carrier to provide a pharmaceutical composition; administering an effective amount of the pharmaceutical composition to a patient suffering from a cardiac arrhythmia, wether such arrhythmias are induced by disease or cardiotoxicity.

Abstract: An electrical sensing and stimulation electrode small enough to record intracellular activity within a single living cell. The electrode incorporates a cylindrical chamber with a finely tapered end section. The chamber is evacuated to hold the cell at its tip. Contained within the chamber are piping, circuitry, and controls to provide selected life support environment, stimulation, and continuous sensing of the iternal ionic composition of the captured cell.