Francois Godard

Screening strategy using a filamentous fungus model to repurpose drugs for mitochondrial complex I deficiencies.

Journal: Life sciences

Published: September 23, 2025

The copper ionophore disulfiram improves mitochondrial function in various yeast and human cellular models of mitochondrial diseases.

Journal: Human molecular genetics

Published: October 15, 2024

Creation of Yeast Models for Evaluating the Pathogenicity of Mutations in the Human Mitochondrial Gene MT-ATP6 and Discovering Therapeutic Molecules.

Journal: Methods in molecular biology (Clifton, N.J.)

Published: June 30, 2022

Assembly-dependent translation of subunits 6 (Atp6) and 9 (Atp9) of ATP synthase in yeast mitochondria.

Journal: Genetics

Published: September 30, 2021

The pathogenic m.8993 T > G mutation in mitochondrial ATP6 gene prevents proton release from the subunit c-ring rotor of ATP synthase.

Journal: Human molecular genetics

Published: September 14, 2020

Molecular Basis of the Pathogenic Mechanism Induced by the m.9191T>C Mutation in Mitochondrial ATP6 Gene.

Journal: International journal of molecular sciences

Published: June 21, 2020

Deregulating mitochondrial metabolite and ion transport has beneficial effects in yeast and human cellular models for NARP syndrome.

Journal: Human molecular genetics

Published: April 04, 2019

The pathogenic MT-ATP6 m.8851T>C mutation prevents proton movements within the n-side hydrophilic cleft of the membrane domain of ATP synthase.

Journal: Biochimica et biophysica acta. Bioenergetics

Published: October 25, 2018

Functional investigation of an universally conserved leucine residue in subunit a of ATP synthase targeted by the pathogenic m.9176 T>G mutation.

Journal: Biochimica et biophysica acta. Bioenergetics

Published: June 20, 2018

Decreasing cytosolic translation is beneficial to yeast and human Tafazzin-deficient cells.

Journal: Microbial cell (Graz, Austria)

Published: May 26, 2018

Molecular basis of diseases caused by the mtDNA mutation m.8969G>A in the subunit a of ATP synthase.

Journal: Biochimica et biophysica acta. Bioenergetics

Published: February 14, 2018

Biallelic PPA2 Mutations Cause Sudden Unexpected Cardiac Arrest in Infancy.

Journal: American journal of human genetics

Published: April 06, 2016

Screening strategy using a filamentous fungus model to repurpose drugs for mitochondrial complex I deficiencies.

Screening strategy using a filamentous fungus model to repurpose drugs for mitochondrial complex I deficiencies.

The copper ionophore disulfiram improves mitochondrial function in various yeast and human cellular models of mitochondrial diseases.

The copper ionophore disulfiram improves mitochondrial function in various yeast and human cellular models of mitochondrial diseases.

Creation of Yeast Models for Evaluating the Pathogenicity of Mutations in the Human Mitochondrial Gene MT-ATP6 and Discovering Therapeutic Molecules.

Creation of Yeast Models for Evaluating the Pathogenicity of Mutations in the Human Mitochondrial Gene MT-ATP6 and Discovering Therapeutic Molecules.

Assembly-dependent translation of subunits 6 (Atp6) and 9 (Atp9) of ATP synthase in yeast mitochondria.

Assembly-dependent translation of subunits 6 (Atp6) and 9 (Atp9) of ATP synthase in yeast mitochondria.

The pathogenic m.8993 T > G mutation in mitochondrial ATP6 gene prevents proton release from the subunit c-ring rotor of ATP synthase.

The pathogenic m.8993 T > G mutation in mitochondrial ATP6 gene prevents proton release from the subunit c-ring rotor of ATP synthase.

Molecular Basis of the Pathogenic Mechanism Induced by the m.9191T>C Mutation in Mitochondrial ATP6 Gene.

Molecular Basis of the Pathogenic Mechanism Induced by the m.9191T>C Mutation in Mitochondrial ATP6 Gene.

Deregulating mitochondrial metabolite and ion transport has beneficial effects in yeast and human cellular models for NARP syndrome.

Deregulating mitochondrial metabolite and ion transport has beneficial effects in yeast and human cellular models for NARP syndrome.

The pathogenic MT-ATP6 m.8851T>C mutation prevents proton movements within the n-side hydrophilic cleft of the membrane domain of ATP synthase.

The pathogenic MT-ATP6 m.8851T>C mutation prevents proton movements within the n-side hydrophilic cleft of the membrane domain of ATP synthase.

Functional investigation of an universally conserved leucine residue in subunit a of ATP synthase targeted by the pathogenic m.9176 T>G mutation.

Functional investigation of an universally conserved leucine residue in subunit a of ATP synthase targeted by the pathogenic m.9176 T>G mutation.

Decreasing cytosolic translation is beneficial to yeast and human Tafazzin-deficient cells.

Decreasing cytosolic translation is beneficial to yeast and human Tafazzin-deficient cells.

Molecular basis of diseases caused by the mtDNA mutation m.8969G>A in the subunit a of ATP synthase.

Molecular basis of diseases caused by the mtDNA mutation m.8969G>A in the subunit a of ATP synthase.

Biallelic PPA2 Mutations Cause Sudden Unexpected Cardiac Arrest in Infancy.

Biallelic PPA2 Mutations Cause Sudden Unexpected Cardiac Arrest in Infancy.

Functional investigation of an universally conserved leucine residue in subunit a of ATP synthase targeted by the pathogenic m.9176 T>G mutation.

Functional investigation of an universally conserved leucine residue in subunit a of ATP synthase targeted by the pathogenic m.9176 T>G mutation.