May J M
Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232.
FEBS Lett. 1988 Dec 5;241(1-2):188-90. doi: 10.1016/0014-5793(88)81058-5.
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.
已知ATP耗竭会抑制人类红细胞中的葡萄糖转运,但其作用的动力学机制存在争议。在细胞外钙存在的情况下,用10微克/毫升的A23187对人类红细胞进行选择性ATP耗竭,非竞争性地抑制了3 - O - 甲基葡萄糖的内流,并竞争性地抑制了其外流。ATP耗竭还降低了平衡态的3 - O - 甲基葡萄糖或细胞外麦芽糖抑制完整细胞中细胞松弛素B结合的能力,而总的高亲和力细胞松弛素B结合及其解离常数均未受影响。在己糖转运的单位点模型下,这些数据表明ATP耗竭既降低了向内的葡萄糖载体对底物的亲和力,也降低了其在完整细胞中外向重定向的能力。