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What happens when ATP synthesis is inhibited?
Inhibition of the ATP synthase compromises the output of ATP by OXPHOS and rewires energy metabolism to an enhanced glycolysis.
Does synthesis require ATP?
The two stages of biosynthesis—the formation of building blocks and their specific assembly into macromolecules—are energy-consuming processes and thus require ATP. Although the ATP is derived from catabolism, catabolism does not “drive” biosynthesis.
What is the function of ATP synthesis?
The function of ATP synthase is to synthesize ATP from ADP and inorganic phosphate (Pi) in the F1 sector. This is possible due to energy derived from a gradient of protons which cross the inner mitochondrial membrane from the intermembrane space into the matrix through the Fo portion of the enzyme.
What decreases ATP synthesis?
Thus, the cells are able to partially compensate for the atractyloside-induced reduction of mitochondrial ATP supply by nonmitochondrial ATP generation. Consequently, ATP synthesis is affected more than 30%.
How can ATP synthesis be reduced?
Antibiotics efrapeptins and aurovertins inhibit both synthesis and hydrolysis of ATP by ATP synthase. The efrapeptins bind to ATP synthase at a site extending from the rotor, across the central cavity of the enzyme, into the specific β-subunit catalytic site.
How ATP synthesis is stopped?
The mode of inhibition by efrapeptin during ATP synthesis is competitive with ADP and phosphate (83). Efrapeptin also binds to the nonmitochondrial ATP synthase of endothelial cells and inhibits extracellular ATP synthesis (17).
How is ATP synthesized in the cell?
The ATP synthase is a mitochondrial enzyme localized in the inner membrane, where it catalyzes the synthesis of ATP from ADP and phosphate, driven by a flux of protons across a gradient generated by electron transfer from the proton chemically positive to the negative side.
What happens if ATP is decreased?
The effect of ATP-depletion or its consequence, by metabolic inhibition, on the inhibition of glucose transport by various inhibitors was studied in human red cells. In cells depleted of ATP, glucose exit times were longer than in normal cells and the times increased with the duration of depletion.