Mice lacking inward-rectifying potassium channel Kir6.1
AssigneesJCR Pharmaceuticals Co., Ltd., Susumu Seino
InventorsSusumu Seino, Takashi Miki, Haruaki Nakaya
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Abstract
Mice homozygous for the lack of inward-rectifying potassium channel Kir6.1 gene are disclosed. The mice causes a high incidence of sudden death associated with arrhythmia (atrioventricular block) caused by spontaneous cardiac ischemia, a condition similar to Prinzmetal angina (variant angina) in human, representing an animal model of Prinzmetal angina. Mice heterozygous for the lack of inward-rectifying potassium channel Kir6.1 gene are also disclosed, which are used as parent mice for reproduction of the homozygous mice.
Claims1
A transgenic mouse comprising a homozygous disruption in the endogenous Kir6.1 gene, wherein said transgenic mouse exhibits sudden cardiac death, atrioventricular blockage, spontaneous cardiac ischemia, or spontaneous cardiac spasms.
Dependencies are inferred from the claim text.