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ATP 耗竭对完整人红细胞中己糖转运机制的影响。

Effects of ATP depletion on the mechanism of hexose transport in intact human erythrocytes.

作者信息

May J M

机构信息

Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232.

出版信息

FEBS Lett. 1988 Dec 5;241(1-2):188-90. doi: 10.1016/0014-5793(88)81058-5.

Abstract

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.

摘要

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。

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