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Akademický článek

Genome-wide CRISPR/Cas9 screen shows that loss of GET4 increases mitochondria-endoplasmic reticulum contact sites and is neuroprotective

Autor: Emma L. Wilson, Yizhou Yu, Nuno S. Leal, James A. Woodward, Nikolaos Patikas, Jordan L. Morris, Sarah F. Field, William Plumbly, Vincent Paupe, Suvagata R. Chowdhury, Robin Antrobus, Georgina E. Lindop, Yusuf M. Adia, Samantha H. Y. Loh, Julien Prudent, L. Miguel Martins, Emmanouil Metzakopian

Publikováno v: Cell Death and Disease, Vol 15, Iss 3, Pp 1-16 (2024)

Abstract Organelles form membrane contact sites between each other, allowing for the transfer of molecules and signals. Mitochondria-endoplasmic reticulum (ER) contact sites (MERCS) are cellular subdomains characterized by close apposition of mitocho

Externí odkaz: https://doaj.org/article/2914aeb333b24972878c1604812247ee

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Akademický článek

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Akademický článek

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Akademický článek

SLC25A46 is required for mitochondrial lipid homeostasis and cristae maintenance and is responsible for Leigh syndrome

Autor: Alexandre Janer, Julien Prudent, Vincent Paupe, Somayyeh Fahiminiya, Jacek Majewski, Nicolas Sgarioto, Christine Des Rosiers, Anik Forest, Zhen‐Yuan Lin, Anne‐Claude Gingras, Grant Mitchell, Heidi M McBride, Eric A Shoubridge

Publikováno v: EMBO Molecular Medicine, Vol 8, Iss 9, Pp 1019-1038 (2016)

Abstract Mitochondria form a dynamic network that responds to physiological signals and metabolic stresses by altering the balance between fusion and fission. Mitochondrial fusion is orchestrated by conserved GTPases MFN1/2 and OPA1, a process coordi

Externí odkaz: https://doaj.org/article/22810f2315b34bb8997e0edcfcab588d

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AMPK-dependent phosphorylation of MTFR1L regulates mitochondrial morphology

Autor: Tilokani, Lisa, Russell, Fiona M, Hamilton, Stevie, Virga, Daniel M, Segawa, Mayuko, Paupe, Vincent, Gruszczyk, Anja V, Protasoni, Margherita, Tabara, Luis-Carlos, Johnson, Mark, Anand, Hanish, Murphy, Michael P, Hardie, D Grahame, Polleux, Franck, Prudent, Julien

Mitochondria are dynamic organelles that undergo membrane remodeling events in response to metabolic alterations to generate an adequate mitochondrial network. Here, we investigated the function of mitochondrial fission regulator 1-like protein (MTFR

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1f0493c3de3b889168bb0808643e8599