Diamond D L, Carruthers A
Program in Molecular Medicine, University of Massachusetts Medical Center, Worcester 01606.
J Biol Chem. 1993 Mar 25;268(9):6437-44.
Protein-mediated sugar transport is nominally absent in normoxic pigeon erythrocytes. Following exposure to metabolic inhibitors (cyanide or carbonyl-cyanide-p-trifluoromethoxyphenylhydrazone), pigeon red cells transport sugars by a saturable stereoselective pathway that is inhibited by cytochalasin B or forskolin. The sugar transport capacity of fully poisoned cells is consistent with a transporter density of approximately 30 carriers/erythrocyte. Immunoblot analyses and competition enzyme-linked immunosorbent assay indicate that pigeon red cells contain approximately 200 copies of an integral plasma membrane protein immunologically related to the glucose transporter isoform GLUT1. GLUT1 is quantitatively restricted to the plasma membrane at all times. Pigeon red cells and brain lack proteins immunologically related to the sugar transporter isoforms GLUT3 and GLUT4. Specific immunodepletion of red cell GLUT1 content results in the subsequent loss of reconstitutable protein-mediated sugar transport. These findings demonstrate that avian erythrocyte sugar transport is mediated by a GLUT1-like sugar transport protein and that sugar transport stimulation by metabolic depletion results from derepression of cell surface sugar transport proteins.
在正常氧合的鸽红细胞中，蛋白质介导的糖转运通常并不存在。在暴露于代谢抑制剂（氰化物或羰基氰 - 对 - 三氟甲氧基苯腙）后，鸽红细胞通过一种可饱和的立体选择性途径转运糖类，该途径会被细胞松弛素B或福斯高林抑制。完全中毒细胞的糖转运能力与约30个载体/红细胞的转运体密度一致。免疫印迹分析和竞争酶联免疫吸附测定表明，鸽红细胞含有约200个与葡萄糖转运体异构体GLUT1免疫相关的整合质膜蛋白拷贝。GLUT1在任何时候都定量地局限于质膜。鸽红细胞和大脑缺乏与糖转运体异构体GLUT3和GLUT4免疫相关的蛋白质。红细胞GLUT1含量的特异性免疫耗竭导致随后可重构的蛋白质介导的糖转运丧失。这些发现表明，鸟类红细胞糖转运由一种GLUT1样糖转运蛋白介导，并且代谢耗竭引起的糖转运刺激是由于细胞表面糖转运蛋白的去阻遏所致。
