Hypertrophy, increased ejection fraction, and reduced Na-K-ATPase activity in phospholemman-deficient mice.

@article{Jia2005HypertrophyIE,
  title={Hypertrophy, increased ejection fraction, and reduced Na-K-ATPase activity in phospholemman-deficient mice.},
  author={L G Jia and Claudia Donnet and Roberta C Bogaev and Rebecca J. Blatt and Cindy E. McKinney and Kathleen H Day and Stuart S. Berr and Larry R. Jones and J. Randall Moorman and Kathleen J Sweadner and Amy L. Tucker},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2005},
  volume={288 4},
  pages={H1982-8}
}
Phospholemman (FXYD1), a 72-amino acid transmembrane protein abundantly expressed in the heart and skeletal muscle, is a major substrate for phosphorylation in the cardiomyocyte sarcolemma. Biochemical, cellular, and electrophysiological studies have suggested a number of possible roles for this protein, including ion channel modulator, taurine-release channel, Na(+)/Ca(2+) exchanger modulator, and Na-K-ATPase-associated subunit. We have generated a phospholemman-deficient mouse. The adult null… CONTINUE READING

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