Net synthesis of ATP by reversal of the sodium pump.
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Adenosine Triphosphate↗
Biomedical subjects
J C Ellory
Publications and source records attributed to J C Ellory.
The binding of cardiac glycosides to bull spermatozoa.
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Adenosine Triphosphatases↗
Active potassium transport and the L and M antigens of sheep and goat red cells.
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Adenosine Triphosphatases↗
The binding of ouabain to spermatozoa of boar and ram.
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Adenosine Triphosphatases↗
Sodium pump reversal in the erythrocytes of various species.
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Animals↗
Active potassium transport in the immature red cells of anaemic sheep.
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Anemia↗
Short-term measurements of amino acid and sodium fluxes across the mucosal border of goldfish intestine.
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Alanine↗
Volume and electrophoretic mobility distribution patterns in a reticulocyte-enriched fraction from the blood of anaemic sheep.
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Anemia↗
Deoxycholate stimulation of goldfish intestinal (Na positive plus K positive)-ATPase and its relation to digoxin binding.
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Adenosine Triphosphatases↗
Effect of tetrodotoxin on Ascaris somatic muscle.
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Action Potentials↗
Shape, volume and integrity of reconstituted human red cell ghosts.
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Biological Transport↗
Stimulation of the potassium transport system in low potassium type sheep red cells by a specific antigen antibody reaction.
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Animals↗
Binding of tritiated digoxin to human red cell ghosts.
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Adenosine Triphosphatases↗
Cardiac glycoside binding and alkali cation transport in mature and epididymal bull spermatozoa.
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Animals↗
Active potassium transport and the development of m antigen on red cells of LK type lambs.
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Animals↗
Ion movements in the somatic muscle cells of Ascaris lumbricoides.
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Animals↗
Membrane transport in sickle cell disease.
We have reviewed here a number of membrane transport events in red cells from normal individuals and sickle cell patients which respond to changes in O(2) tension. Some deoxygenation-induced changes in membrane permeability are unique to HbS cells and contribute to their dehydration and subsequent sickling. Polymerization of HbS, or specific oxidant damage (or altered redox potential), is a likely factor underlying the abnormal behavior. The key regulatory sites within the membrane or associated proteins remain uncertain and their identity will form the focus of future research. A model for sickle cell dehydration is presented. Inhibition of these permeability changes represents possible avenues for future chemotherapy to ameliorate the condition.
Anemia, Sickle Cell↗
Amino acid transport systems.
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Amino Acids↗