1. Inhibition of Na,K-ATPase and sodium pump by anticancer ether lipids and protein kinase C inhibitors ET-18-OCH3 and BM 41.440
- Author
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J.F. Kuo, Bin Zheng, J F White, William R. Vogler, and K Oishi
- Subjects
Erythrocytes ,ATPase ,Biophysics ,Diaphragm pump ,Antineoplastic Agents ,Biochemistry ,Ouabain ,Sodium Channels ,chemistry.chemical_compound ,medicine ,Tumor Cells, Cultured ,Animals ,Humans ,Na+/K+-ATPase ,Protein kinase A ,Molecular Biology ,Protein kinase C ,Protein Kinase C ,Cerebral Cortex ,Leukemia ,biology ,Chemistry ,Sodium Radioisotopes ,Cell Membrane ,Lysophosphatidylcholines ,Phospholipid Ethers ,Cell Biology ,Molecular biology ,Rats ,Ether lipid ,Enzyme inhibitor ,biology.protein ,Sodium-Potassium-Exchanging ATPase ,medicine.drug ,Synaptosomes - Abstract
The anticancer ether lipid analogs ET-18-OCH 3 and BM 41.440 inhibited Na,K-ATPase in the purified rat brain membrane fragments, with a potency comparable to that of their inhibition of protein kinase C. They also inhibited Na,K-ATPase in the crude membrane fraction of HL60 cells. Kinetic analysis indicated that the lipids had a mode of action different from that of ouabain, a classic inhibitor of the ATPase. The lipids also blocked 22 Na uptake in the inside-out membrane vesicles of human erythrocytes. It is suggested that Na,K-ATPase might represent an additional site with which certain protein kinase C inhibitors can interact to alter cellular activities.
- Published
- 1988