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PMID: 1977744 Published · ppublish English Journal Article Review

Genetic basis of multidrug resistance of tumor cells.

Journal of bioenergetics and biomembranes ·Vol. 22 ·No. 4 ·1990-08-00 ·Pages 593-618

Kane SE, Pastan I, Gottesman MM

Abstract

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.

MeSH Terms
ATP Binding Cassette Transporter, Subfamily B, Member 1 Animals Antineoplastic Agents/pharmacology,therapeutic use Biological Evolution Drug Resistance/genetics Genes Humans Membrane Glycoproteins/genetics,metabolism Neoplasms/drug therapy,genetics Tumor Cells, Cultured
Chemicals
ATP Binding Cassette Transporter, Subfamily B, Member 1 Antineoplastic Agents Membrane Glycoproteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Kane S E
Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Pastan I
Gottesman M M
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Article Info
Journal
Journal of bioenergetics and biomembranes
Abbr.
J Bioenerg Biomembr
ISSN
0145-479X
DOI
10.1007/BF00762963
Published
1990-08-00
Pages
593-618
Language
English
Region
United States
NLM ID
7701859
Subset
IM
External Links
PubMed source DOI: 10.1007/BF00762963 View journal details
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