Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incorporation of the fluorescent, nonpermeant pH indicator pyranine into submitochondrial particles (pyranine-SMP) permitted monitoring of intravesicular pH changes brought about by proton translocation due to oxidation of respiratory chain substrates or to hydrolysis of ATP. Addition of oligomycin to beef heart pyranine-SMP was followed by a pH-independent quenching of pyranine fluorescence. Quenching was influenced by the presence of adenine nucleotides both inside and outside the submitochondrial particles. The nature of the nucleotides required for quenching resembled the specificity of the adenine nucleotide translocase rather than F1-ATPase. Removal of F1 from pyranine-SMP by treatment of the particles with urea did not alter oligomycin-induced quenching. Atractyloside, a specific inhibitor of the adenine nucleotide translocase, prevented oligomycin-induced quenching when the inhibitor was coincorporated into submitochondrial particles with pyranine. Bongkrekic acid prevented or reversed the oligomycin-dependent quenching when added to pyranine-SMP either before or after oligomycin, respectively, but only when ATP was present within the particles. A mutant of Saccharomyces cerevisiae, lacking translocase genes, exhibited oligomycin-dependent fluorescence quenching which was not inhibited by bongkrekic acid. The results support the interpretation that oligomycin promotes sequestration of the fluorescent probe in a region of the submitochondrial particle, probably the F0F1 complex, that leads to a quenching of fluorescence. The observed quenching can be modulated in a way that suggests an interaction between the translocase and F0.
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PMID:The adenine nucleotide translocase modulates oligomycin-induced quenching of pyranine fluorescence in submitochondrial particles. 824 63

The oxidative phosphorylation inhibitor DBCT (dibutylchloromethyltin chloride) inhibits state 3 respiration at a concentration less than that which stimulates K+ flux into respiring rat liver mitochondria. Inhibition of ADP-stimulated respiration by DBCT can be reversed or blocked by the dithiol 2,3-dimercaptopropanol. The data are consistent with previous suggestions that DBCT may interact with the ATP synthase via reaction with a dithiol group. The stimulation of K+ influx by DBCT is partially reversed by concentrations of 2-mercaptoethanol which fail to affect the inhibition of state 3 respiration by DBCT. The combination of DBCT plus 2,3-dimercaptopropanol inhibits mitochondrial K+ influx. The inhibitory effect of dicyclohexylcarbodiimide on K+ influx is not expressed in the presence of DBCT. Atractyloside has little effect on K+ influx in the presence or absence of DBCT. The combination of DBCT plus uncoupler induces a net loss of endogenous K+. Consideration is given to the alternative hypotheses that the acceleration of K+ influx by DBCT may involve either a direct link to the energy transduction apparatus, or may occur via separate activation of a passive transport mechanism.
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PMID:Interacting effects of dibutylchloromethyltin chloride, 2,3-dimercaptopropanol, and other reagents on mitochondrial respiration and K+ flux. 1825 Nov 11