PubMed:10229326 JSONTXT

{"project":"bionlp-st-cg-2013-training","denotations":[{"id":"T1","span":{"begin":19,"end":40},"obj":"Gene_or_gene_product"},{"id":"T2","span":{"begin":42,"end":48},"obj":"Gene_or_gene_product"},{"id":"T3","span":{"begin":104,"end":111},"obj":"Simple_chemical"},{"id":"T4","span":{"begin":115,"end":120},"obj":"Organism"},{"id":"T5","span":{"begin":121,"end":135},"obj":"Cell"},{"id":"T6","span":{"begin":222,"end":229},"obj":"Simple_chemical"},{"id":"T7","span":{"begin":243,"end":249},"obj":"Gene_or_gene_product"},{"id":"T8","span":{"begin":309,"end":320},"obj":"Simple_chemical"},{"id":"T9","span":{"begin":325,"end":332},"obj":"Simple_chemical"},{"id":"T10","span":{"begin":346,"end":351},"obj":"Organism"},{"id":"T11","span":{"begin":352,"end":376},"obj":"Cell"},{"id":"T12","span":{"begin":378,"end":382},"obj":"Cell"},{"id":"T13","span":{"begin":387,"end":391},"obj":"Cell"},{"id":"T14","span":{"begin":408,"end":419},"obj":"Simple_chemical"},{"id":"T15","span":{"begin":452,"end":466},"obj":"Simple_chemical"},{"id":"T16","span":{"begin":553,"end":560},"obj":"Simple_chemical"},{"id":"T17","span":{"begin":592,"end":605},"obj":"Cell"},{"id":"T18","span":{"begin":607,"end":611},"obj":"Cell"},{"id":"T19","span":{"begin":616,"end":626},"obj":"Cell"},{"id":"T20","span":{"begin":637,"end":643},"obj":"Gene_or_gene_product"},{"id":"T21","span":{"begin":670,"end":680},"obj":"Cell"},{"id":"T22","span":{"begin":681,"end":687},"obj":"Gene_or_gene_product"},{"id":"T23","span":{"begin":740,"end":744},"obj":"Cell"},{"id":"T24","span":{"begin":749,"end":759},"obj":"Cell"},{"id":"T25","span":{"begin":826,"end":836},"obj":"Cell"},{"id":"T26","span":{"begin":842,"end":853},"obj":"Simple_chemical"},{"id":"T27","span":{"begin":908,"end":920},"obj":"Gene_or_gene_product"},{"id":"T28","span":{"begin":999,"end":1009},"obj":"Cell"},{"id":"T29","span":{"begin":1011,"end":1022},"obj":"Simple_chemical"},{"id":"T30","span":{"begin":1126,"end":1136},"obj":"Cell"},{"id":"T31","span":{"begin":1156,"end":1162},"obj":"Gene_or_gene_product"},{"id":"T32","span":{"begin":1212,"end":1223},"obj":"Simple_chemical"},{"id":"T33","span":{"begin":1267,"end":1278},"obj":"Simple_chemical"},{"id":"T34","span":{"begin":1323,"end":1336},"obj":"Simple_chemical"},{"id":"T35","span":{"begin":1341,"end":1352},"obj":"Simple_chemical"},{"id":"T36","span":{"begin":1381,"end":1392},"obj":"Simple_chemical"},{"id":"T37","span":{"begin":1432,"end":1435},"obj":"Simple_chemical"},{"id":"T38","span":{"begin":1453,"end":1458},"obj":"Cell"},{"id":"T39","span":{"begin":1495,"end":1509},"obj":"Cell"},{"id":"T40","span":{"begin":1529,"end":1535},"obj":"Gene_or_gene_product"}],"text":"N-glycosylation of glucose transporter-1 (Glut-1) is associated with increased transporter affinity for glucose in human leukemic cells.\nTo elucidate the role of N-glycosylation in the functional activity of the universal glucose transporter, Glut-1, we investigated effects of the N-glycosylation inhibitor, tunicamycin, on glucose transport by human leukemic cell lines K562, U937 and HL60. Treatment with tunicamycin produced a 40-50% inhibition of 2-deoxyglucose uptake and this was associated with a 2-2.5-fold decrease in transporter affinity for glucose (Km) without a change in Vmax. Leukemic K562, U937 and HL60 cells expressed Glut-1 transporter protein. With K562 cells Glut-1 appeared as a broad band of 50-60 kDa, whereas with U937 and HL60 cells a diffuse band was observed at approximately 55 kDa. Treatment of K562 cells with tunicamycin for 18 h, resulted in extensive loss of the 50-60 kDa glycoprotein, appearance of a 30-40 kDa band and increased staining of a 45 kDa band. With U937 cells, tunicamycin treatment resulted in the appearance of a 30-40 kDa band and increased staining of a 45 kDa band. With HL60 cells loss of the 55 kDa Glut-1 band was observed and a band of 45 kDa appeared. Tunicamycin-treatment resulted in 75-90% inhibition in [3H]mannose incorporation but only 20-25% inhibition in [3H]thymidine and [3H]leucine incorporation. In contrast, tunicamycin had little effect on the viability and MTT responses of the cells used. These results suggest that in leukemic cells N-glycosylation of Glut-1 plays an important role in maintaining its structure and functional integration."}