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- W2052844218 abstract "When mitochondrial respiration is compromised, the F(1)F(o)-ATP synthase reverses and consumes ATP, serving to maintain the mitochondrial membrane potential (Delta psi(m)). This process is mitigated by IF(1). As little is known of the cell biology of IF(1), we have investigated the functional consequences of varying IF(1) expression. We report that, (1) during inhibition of respiration, IF(1) conserves ATP at the expense of Delta psi(m); (2) overexpression of IF(1) is protective against ischemic injury; (3) relative IF(1) expression level varies between tissues and cell types and dictates the response to inhibition of mitochondrial respiration; (4) the density of mitochondrial cristae is increased by IF(1) overexpression and decreased by IF(1) suppression; and (5) IF(1) overexpression increases the formation of dimeric ATP synthase complexes and increases F(1)F(o)-ATP synthase activity. Thus, IF(1) regulates mitochondrial function and structure under both physiological and pathological conditions." @default.
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- W2052844218 date "2008-07-01" @default.
- W2052844218 modified "2023-10-15" @default.
- W2052844218 title "Regulation of Mitochondrial Structure and Function by the F1Fo-ATPase Inhibitor Protein, IF1" @default.
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- W2052844218 doi "https://doi.org/10.1016/j.cmet.2008.06.001" @default.
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