. Author manuscript; available in PMC: 2013 Mar 1.

Published in final edited form as: J Mol Cell Cardiol. 2012 Jan 3;52(3):596–607. doi: 10.1016/j.yjmcc.2011.12.012

Table 3.

Genetically modified mice in the study of the K_ATP channel.

Transgenesis
Subunit targeted	Type of modification	Cell type targeted	Functions modified/studied	References

Kir6.2	Pore mutant	Pancreatic	Pancreatic β-cell function	[108–109]
Kir6.1, Kir6.2	Pore mutant	Cardiac	Exercise stress, K_ATP activity	[59]
Kir6.2	ATP insensitive	Cardiac	Cardiovascular function	[110]
SUR1, SUR2A	Overexpression	Cardiac	Cardiovascular function	[111]
Kir6	Pore mutant	Endothelial	Hypertension, endothelial endothelin-1 release	[112]
Kir6	Pore mutant	Smooth muscle	Energetics	[113]

Gene targeting
Subunit targeted	Total number of exons	Exon(s) targeted	Functions modified/studied	References

Kir6.1	3	3^rd	Vascular	[114]
Kir6.2	1	1^st	Stress, ischemic preconditioning, insulin release	[115–117]
SUR1	39	1^st	Insulin release	[118]
SUR1	39	2^nd	Insulin release, cardiac ischemia, atrial K_ATP	[52, 119–120]
SUR2	41	12^th to 16^th	Vascular, cardiac ischemia	[65, 121–123]

Exons are numbered according to the cited references.