FEBS Letters
Volume 584, Issue 10 , Pages 1956-1965, 17 May 2010

Ryanodine receptor studies using genetically engineered mice

Edited by Adam Szewczyk

  • Alexander Kushnir

      Affiliations

    • Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, New York, NY, USA
    • ,
  • Matthew J. Betzenhauser

      Affiliations

    • Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, New York, NY, USA
    • ,
  • Andrew R. Marks

      Affiliations

    • Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, New York, NY, USA
    • Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA
    • Corresponding Author InformationCorresponding author. Russ Berrie Medical Science Pavilion, Room 520, 1150, St. Nicholas Ave, New York, NY 10032, USA. Fax: +1 212 851 5345.

Received 26 January 2010; received in revised form 24 February 2010; accepted 3 March 2010. published online 08 March 2010.

Abstract 

Ryanodine receptors (RyR) regulate intracellular Ca2+ release in many cell types and have been implicated in a number of inherited human diseases. Over the past 15years genetically engineered mouse models have been developed to elucidate the role that RyRs play in physiology and pathophysiology. To date these models have implicated RyRs in fundamental biological processes including excitation–contraction coupling and long term plasticity as well as diseases including malignant hyperthermia, cardiac arrhythmias, heart failure, and seizures. In this review we summarize the RyR mouse models and how they have enhanced our understanding of the RyR channels and their roles in cellular physiology and disease.

Keywords: Ryanodine receptor, Transgenic mice, Excitation–contraction coupling, Calstabin2

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PII: S0014-5793(10)00199-7

doi:10.1016/j.febslet.2010.03.005

FEBS Letters
Volume 584, Issue 10 , Pages 1956-1965, 17 May 2010

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