Effects of ATP depletion on the mechanism of hexose transport in intact human erythrocytes.
Depletion of ATP is known to inhibit glucose transport in human erythrocytes, but the kinetic mechanism of this effect is controversial. Selective ATP depletion of human erythrocytes by 10 micrograms/ml A23187 in the presence of extracellular calcium inhibited 3-O-methylglucose influx noncompetitively and efflux competitively. ATP depletion also decreased the ability of either equilibrated 3-O-methylglucose or extracellular maltose to inhibit cytochalasin B binding in intact cells, whereas neither total high-affinity cytochalasin B binding nor its Kd was affected. Under the one-site model of hexose transport these data indicate that ATP depletion decreases both the affinity of the inward-facing glucose carrier for substrate and its ability to reorient outwardly in intact cells.
D019325:3-O-Methylglucose; D000255:Adenosine Triphosphate / Q000097:blood*; D000001:Calcimycin / Q000494:pharmacology; D003571:Cytochalasin B / Q000097:blood; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D008320:Maltose / Q000097:blood; D008757:Methylglucosides / Q000097:blood; D009004:Monosaccharide Transport Proteins / Q000097:blood*
D008757:Methylglucosides; D009004:Monosaccharide Transport Proteins; D019325:3-O-Methylglucose; D000001:Calcimycin; D003571:Cytochalasin B; D008320:Maltose; D000255:Adenosine Triphosphate