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Effects of ATP depletion on the mechanism of hexose transport in intact human erythrocytes
Author(s) -
May James M.
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)81058-5
Subject(s) - chemistry , hexose , mechanism (biology) , biochemistry , erythrocyte membrane , biophysics , microbiology and biotechnology , biology , enzyme , membrane , philosophy , epistemology
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 μg/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 K d 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.

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