Consequences of cardiac myocyte-specific ablation of KATP channels in transgenic mice expressing dominant negative Kir6 subunits.

@article{Tong2006ConsequencesOC,
  title={Consequences of cardiac myocyte-specific ablation of KATP channels in transgenic mice expressing dominant negative Kir6 subunits.},
  author={Xiaoyong Tong and Lisa M. Porter and Gongxin Liu and Piyali Dhar-Chowdhury and Shekhar Srivastava and David J. Pountney and Hidetada Yoshida and Michael Artman and Glenn I. Fishman and Cindy Yu and Rishabh K. Iyer and Gregory E. Morley and David E. Gutstein and William A Coetzee},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2006},
  volume={291 2},
  pages={
          H543-51
        }
}
Cardiac ATP-sensitive K+ (K(ATP)) channels are formed by Kir6.2 and SUR2A subunits. We produced transgenic mice that express dominant negative Kir6.x pore-forming subunits (Kir6.1-AAA or Kir6.2-AAA) in cardiac myocytes by driving their expression with the alpha-myosin heavy chain promoter. Weight gain and development after birth of these mice were similar to nontransgenic mice, but an increased mortality was noted after the age of 4-5 mo. Transgenic mice lacked cardiac K(ATP) channel activity… CONTINUE READING

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