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Updated: Mar 7, 2026

F1FO ATPase Vesicle Preparation and Technique for Performing Patch Clamp Recordings of Submitochondrial Vesicle Membranes
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F1FO ATPase Vesicle Preparation and Technique for Performing Patch Clamp Recordings of Submitochondrial Vesicle Membranes

Published on: May 4, 2013

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Control of Mitochondrial Remodeling by the ATPase Inhibitory Factor 1 Unveils a Pro-survival Relay via OPA1

Danilo Faccenda1, Junji Nakamura2, Giulia Gorini3

  • 1Department of Comparative Biomedical Sciences, The Royal Veterinary College London and UCL Consortium for Mitochondrial Research, Royal College Street, NW1 0TU London, UK; Department of Biology, University of Rome "Tor Vergata," 00133 Rome, Italy.

Cell Reports
|February 24, 2017
PubMed

Insights

ATPase inhibitory factor 1 (IF1) maintains cellular ATP levels, suppressing apoptosis and tumor progression. This mitochondrial protein impacts cancer cell proliferation by regulating redox balance and mitochondrial structure.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • ATPase inhibitory factor 1 (IF1) is a mitochondrial protein that inhibits F1Fo-ATP synthase, preventing ATP depletion during ischemia.
  • IF1 is upregulated in various human cancers, where it promotes tumor invasion and chemoresistance by suppressing programmed cell death.

Purpose of the Study:

  • To investigate the role of IF1 in regulating mitochondrial redox balance and apoptotic cristae remodeling.
  • To elucidate the molecular mechanisms by which IF1 influences cancer cell survival and proliferation.

Main Methods:

  • Assessing glutathione (GSH) consumption and peroxiredoxin 3 (Prx3) inactivation during apoptosis.
  • Analyzing the processing of optic atrophy 1 (OPA1) by metallopeptidase OMA1.
  • Evaluating the impact of IF1 on mitochondrial structure and ATP levels.

Main Results:

  • IF1 maintains ATP levels, leading to reduced GSH consumption and Prx3 inactivation during apoptosis.
  • IF1 inhibits OMA1-mediated OPA1 processing, stabilizing OPA1 and impeding cristae remodeling.
  • Stabilization of OPA1 by IF1 delays the completion of apoptosis and preserves mitochondrial integrity.

Conclusions:

  • IF1 influences both mitochondrial bioenergetics and structure, playing a critical role in cancer cell survival.
  • IF1's modulation of redox balance and OPA1 stability contributes to its pro-tumorigenic effects.
  • IF1 represents a potential therapeutic target for inhibiting cancer cell proliferation and overcoming chemoresistance.
Keywords:
IF(1)OMA1OPA1PrxsROScancermitochondria

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