GENETIC-BASIS OF MULTIDRUG RESISTANCE OF TUMOR-CELLS

被引：142
作者：
KANE, SE
PASTAN, I
GOTTESMAN, MM
机构：
[1] NCI,CELL BIOL LAB,BETHESDA,MD 20892
[2] NCI,MOLEC BIOL LAB,BETHESDA,MD 20892
来源：
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES | 1990年 / 22卷 / 04期
关键词：
actinomycin D; ATP; Chemotherapy; colchicine; doxorubicin; drug transport; evolution; introns; MDR1; gene; P-glycoprotein; transmembrane domains; vinblastine; vincristine;
D O I：
10.1007/BF00762963
中图分类号：
Q6 [生物物理学];
学科分类号：
071011 ;
摘要：
Multidrug resistance in animal cells is defined as the simultaneous resistance to a variety of compounds which appear to be structurally and mechanistically unrelated. One type of multidrug resistance is characterized by the decreased accumulation of hydrophobic natural product drugs, a phenotype which is mediated by an ATP-dependent integral membrane multidrug transporter termed P-glycoprotein or P170. The gene coding for P170 is called MDR. The nucleotide-binding domain of P-glycoprotein shares sequence homology with a family of bacterial permease ATP-binding components. In addition, P170 as a whole is structurally very similar to a number of prokaryotic and eukaryotic proteins believed to be involved in transport activities. This review summarizes our current knowledge of the molecular biology and clinical significance of MDR expression and P-glycoprotein transport activity, as well as some theories about the function of this protein in normal cells. © 1990 Plenum Publishing Corporation.
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页码：593 / 618
页数：26
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