title: IF(1): setting the pace of the F(1)F(o)-ATP synthase.
abstract: When mitochondrial function is compromised and the mitochondrial membrane potential (Deltapsi(m)) falls below a threshold, the F(1)F(o)-ATP synthase can reverse, hydrolysing ATP to pump protons out of the mitochondrial matrix. Although this activity can deplete ATP and precipitate cell death, it is limited by the mitochondrial protein IF(1), an endogenous F(1)F(o)-ATPase inhibitor. IF(1), therefore, preserves ATP at the expense of Deltapsi(m). Despite a wealth of detailed knowledge on the biochemistry of the interaction of IF(1) and the F(1)F(o)-ATPase, little is known about its physiological activity. Emerging research suggests that IF(1) has a wider ranging impact on mitochondrial structure and function than previously thought.
authors: Department of Cell and Developmental Biology, University College London, UK.
authors: Michelangelo
authors: M
authors: Campanella
authors: Nadeene
authors: N
authors: Parker
authors: Choon Hong
authors: CH
authors: Tan
authors: Andrew M
authors: AM
authors: Hall
authors: Michael R
authors: MR
authors: Duchen
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000502:physiology; D008928:Mitochondria / Q000201:enzymology* / Q000648:ultrastructure; D025261:Mitochondrial Proton-Translocating ATPases / Q000737:chemistry / Q000172:deficiency / Q000378:metabolism*; D011506:Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D000097795:ATPase Inhibitory Protein
chemical_list: D000255:Adenosine Triphosphate; D025261:Mitochondrial Proton-Translocating ATPases; D011506:Proteins; D000097795:ATPase Inhibitory Protein