Drug Modulation of Transductor Function of Na+,K+-ATPase

@article{Lopatina2008DrugMO,
  title={Drug Modulation of Transductor Function of Na+,K+-ATPase},
  author={E. V. Lopatina and V. A. Pennyaynen and I. V. Rogachevskyi and Boris V. Krylov},
  journal={Bulletin of Experimental Biology and Medicine},
  year={2008},
  volume={146},
  pages={436-438},
  url={https://api.semanticscholar.org/CorpusID:31472463}
}
It is experimentally proven that ouabain is incapable of inhibiting neurite growth in sensory neuron and heart tissue explants after removal of free calcium from the nutrient medium with EGTA.
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Modulation of the transducer function of Na+,K+-ATPase: new mechanism of heart remodeling.

The results indicate that the cardiac glycoside ouabain applied in endogenous concentrations can modulate transducer function of Na+,K+-ATPase and control the cell growth and proliferation.

4 References

Molecular Mechanisms of Na/K‐ATPase‐Mediated Signal Transduction

It is shown that in addition to pumping ions, Na/K‐ATPase acts as a signal transducer and the signaling function of the enzyme is also pivotal to ouabain‐induced nongenomic effects on cardiac myocytes.

Identification of a Pool of Non-pumping Na/K-ATPase*

Experimental evidence is presented demonstrating that over half of the plasma membrane Na/K-ATPase in LLC-PK1 cells is performing cellular functions other than ion pumping, suggesting that a substantial amount of surface-expressed Na/k-ATpase, at least in some types of cells, may function as non-canonical ouabain-binding receptors.

Endogenous cardiac glycosides: hormones using the sodium pump as signal transducer.

General atomic and molecular electronic structure system

A description of the ab initio quantum chemistry package GAMESS, which can be treated with wave functions ranging from the simplest closed‐shell case up to a general MCSCF case, permitting calculations at the necessary level of sophistication.