It is well established that when mitochondrial respiration is impaired,the H+ATP synthase can function in reverse acting as an ATP hydrolase for maintaining the proton motive force[1].This process is regulated by an inhibitor peptide called ATPase inhibitory factor 1 or IF1,a highly conserved nuclearly encoded protein[2].Since IF1 is highly expressed in most tumors,the significance of IF1 in tumor cells has also been widely studied[3].
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