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International Journal of Cell Biology
Volume 2012, Article ID 367934, 12 pages
Review Article

Molecular Regulation of the Mitochondrial F1Fo-ATPsynthase: Physiological and Pathological Significance of the Inhibitory Factor 1 (IF 1 )

1The Royal Veterinary College, University of London and UCL Consortium for Mitochondrial Research, Royal College Street, London NW1 0TU, UK
2European Brain Research Institute, Rita Levi-Montalcini Foundation, 00143 Rome, Italy

Received 17 February 2012; Revised 19 April 2012; Accepted 19 April 2012

Academic Editor: Giuseppe Filomeni

Copyright © 2012 Danilo Faccenda and Michelangelo Campanella. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In mammals, the mitochondrial F1Fo-ATPsynthase sets out the energy homeostasis by producing the bulk of cellular ATP. As for every enzyme, the laws of thermodynamics command it; however, it is privileged to have a dedicated molecular regulator that controls its rotation. This is the so-called ATPase Inhibitory Factor 1 (IF1) that blocks its reversal to avoid the consumption of cellular ATP when the enzyme acts as an ATP hydrolase. Recent evidence has also demonstrated that IF1 may control the alignment of the enzyme along the mitochondrial inner membrane, thus increasing the interest for the molecule. We conceived this review to outline the fundamental knowledge of the F1Fo-ATPsynthase and link it to the molecular mechanisms by which IF1 regulates its way of function, with the ultimate goal to highlight this as an important and possibly unique means to control this indispensable enzyme in both physiological and pathological settings.