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Biochimica Et Biophysica Acta|February 7, 2012
Metabolically induced heteroplasmy shifting and l-arginine treatment reduce the energetic defect in a neuronal-like model of MELASValerie Desquiret-Dumas, Naig Gueguen, Magalie Barth, et al.
Molecular Vision|March 28, 2009
Acute and late-onset optic atrophy due to a novel OPA1 mutation leading to a mitochondrial coupling defectYannick Nochez, Sophie Arsene, Naig Gueguen, et al.
Mitochondrion|May 23, 2021
Optic neuropathy linked to ACAD9 pathogenic variants: A potentially riboflavin-responsive disorder?Naig Gueguen, Julie Piarroux, Emmanuelle Sarzi, et al.
Biochimica Et Biophysica Acta. Molecular Basis of Disease|November 6, 2016
The addition of ketone bodies alleviates mitochondrial dysfunction by restoring complex I assembly in a MELAS cellular modelSamuel Frey, Guillaume Geffroy, Valerie Desquiret-Dumas, et al.
Plos Biology|October 28, 2024
MICU2 up-regulation enhances tumor aggressiveness and metabolic reprogramming during colorectal cancer developmentAlison Robert, David Crottès, Jérôme Bourgeais, et al.
FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology|March 1, 2019
Phostine 3.1a as a pharmacological compound with antiangiogenic properties against diseases with excess vascularizationSimon Bousseau, Marion Marchand, Raffaella Soleti, et al.
Mitochondrion|February 21, 2022
Cancer/Testis Antigen 55 is required for cancer cell proliferation and mitochondrial DNA maintenanceJade Aurrière, David Goudenege, Simone A Baechler, et al.
Biochimica Et Biophysica Acta. Molecular Basis of Disease|February 18, 2018
The accumulation of assembly intermediates of the mitochondrial complex I matrix arm is reduced by limiting glucose uptake in a neuronal-like model of MELAS syndromeGuillaume Geffroy, Rayane Benyahia, Samuel Frey, et al.
Clinical Genetics|July 21, 2022
Expanding the phenotype of DNAJC30-associated Leigh syndromeMarta Zawadzka, Magdalena Krygier, Małgorzata Pawłowicz, et al.
The Journal of Pathology|June 3, 2011
Methyl donor deficiency induces cardiomyopathy through altered methylation/acetylation of PGC-1α by PRMT1 and SIRT1Maira Moreno Garcia, Rosa-Maria Guéant-Rodriguez, Shabnam Pooya, et al.
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