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Whether the the sodium-potassium exchange pump is vulnerable to cardiac glycoside toxins depends upon whether the toxins can bind to the pump proteins.
These substances act by specifically binding to proteins embedded in cell membranes known as the sodium-potassium exchange pump (Na+/K+-ATPase).
These animo acid replacements significantly reduce the ability of cardiac glycosides from binding to, and thereby inhibiting, the action of the sodium-potassium exchange pump.
The glial membrane was either "passive", incorporating only leak channels and an ion exchange pump, or it had rectifying K+ channels.
Using electrophysiological and biochemical functional assays on the same preparation of prokaryotic ClC proteins (ClC-ec1) that had been used for X-ray crystallography, this study came to the shocking conclusion that ClC-ec1 is a Cl/H exchange pump, rather than the Cl ion channel initially assumed.
However, in these epithelia, active Na+ transport seems to be not exclusively mediated by the Na+/K+ exchange pump.
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When cardiac glycosides bind to these exchange pumps, they stop the pumps' function.
When the price of Bitcoin goes down, activity on an influential exchange pumps it back up.
So the researchers measured the isoelectric point for the sodium-potassium exchange pumps of resistant and susceptible animals.
For example, snakes and lizards have evolved resistance to frog toxins that results from just two, very specific, amino acid changes in the structure of their sodium-potassium exchange pumps.
Heat exchange pumps above ground extract energy from water to provide building heat in winter and cooling in summer.
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