Stimulation and inhibition of human platelet membrane high-affinity GTPase by neomycin.
The effect of the inositol phospholipid-binding antibiotic neomycin was studied on high-affinity GTPase in human platelet membranes. At low concentrations (up to 1 mM), neomycin by itself stimulated a high-affinity GTPase. This GTPase stimulation was additive with that caused by the hormonal factors, prostaglandin E1 and epinephrine, but not with thrombin. At concentrations higher than 1 mM, neomycin reduced control GTPase activity and eliminated the stimulation caused by thrombin. The data suggest that neomycin by a presently unknown mechanism can regulate activity states of signal transducing GTP-binding proteins.
Herrmann
E
E
Pharmakologisches Institut der Universität Heidelberg, FRG.
Jakobs
K H
KH
D001792:Blood Platelets / Q000187:drug effects / Q000201:enzymology*; D002462:Cell Membrane / Q000187:drug effects / Q000201:enzymology; D004533:Egtazic Acid / Q000494:pharmacology; D020558:GTP Phosphohydrolases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007700:Kinetics; D009355:Neomycin / Q000494:pharmacology*; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism*; D013917:Thrombin / Q000494:pharmacology
D004533:Egtazic Acid; D010744:Phosphoric Monoester Hydrolases; D013917:Thrombin; D020558:GTP Phosphohydrolases; D009355:Neomycin; D007213:Indomethacin