F
Frédéric Darios
Researcher at University of Paris
Publications - 50
Citations - 3702
Frédéric Darios is an academic researcher from University of Paris. The author has contributed to research in topics: Vesicle fusion & Hereditary spastic paraplegia. The author has an hindex of 28, co-authored 48 publications receiving 3266 citations. Previous affiliations of Frédéric Darios include Centre national de la recherche scientifique & Laboratory of Molecular Biology.
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Journal ArticleDOI
Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-dependent cell death
Frédéric Darios,Olga Corti,Christoph B. Lücking,Cornelia Hampe,Marie-Paule Muriel,Nacer Abbas,Wen-Jie Gu,Etienne C. Hirsch,Thomas Rooney,Merle Ruberg,Alexis Brice +10 more
TL;DR: Results suggest that Parkin may promote the degradation of substrates localized in mitochondria and involved in the late mitochondrial phase of ceramide-mediated cell death, which may underlie the degeneration of nigral dopaminergic neurons in patients with Parkin mutations.
Journal ArticleDOI
Omega-3 and omega-6 fatty acids stimulate cell membrane expansion by acting on syntaxin 3
Frédéric Darios,Bazbek Davletov +1 more
TL;DR: It is shown that syntaxin 3 (STX3), a plasma membrane protein, has an important role in the growth of neurites, and also serves as a direct target for omega-6 arachidonic acid, and the first identification of a single effector molecule for these essential nutrients.
Journal ArticleDOI
The p38 subunit of the aminoacyl-tRNA synthetase complex is a Parkin substrate: linking protein biosynthesis and neurodegeneration
Olga Corti,Cornelia Hampe,Hana Koutnikova,Frédéric Darios,Sandrine Jacquier,Annick Prigent,Jean-Charles Robinson,Laurent Pradier,Merle Ruberg,Marc Mirande,Etienne C. Hirsch,Thomas Rooney,Alain Fournier,Alexis Brice +13 more
TL;DR: It is demonstrated that Parkin interacts with, ubiquitylates and promotes the degradation of p38, a key structural component of the mammalian aminoacyl-tRNA synthetase complex, opening the way for a detailed examination of its potential non-canonical role in neurodegeneration.
Journal ArticleDOI
Alpha-synuclein, lipids and Parkinson's disease.
TL;DR: It is proposed that association of alpha-synuclein with oxidized lipid metabolites can lead to mitochondrial dysfunction in turn leading to dopaminergic neuron death and thus to Parkinson's disease.
Journal ArticleDOI
Alteration of fatty-acid-metabolizing enzymes affects mitochondrial form and function in hereditary spastic paraplegia
Christelle Tesson,Magdalena Nawara,Magdalena Nawara,Magdalena Nawara,Mustafa A. Salih,Rodrigue Rossignol,Maha S. Zaki,Mohammed Al Balwi,Rebecca Schüle,Cyril Mignot,Emilie Obre,Ahmed Bouhouche,Filippo M. Santorelli,Christelle M. Durand,Andrés Caballero Oteyza,Khalid H. El-Hachimi,Abdulmajeed Al Drees,Naima Bouslam,Foudil Lamari,Salah A. Elmalik,Mohammad M. Kabiraj,Mohammed Zain Seidahmed,Typhaine Esteves,Typhaine Esteves,Typhaine Esteves,Marion Gaussen,Marion Gaussen,Marion Gaussen,Marie Lorraine Monin,Marie Lorraine Monin,Marie Lorraine Monin,Gabor Gyapay,Doris Lechner,Michael A. Gonzalez,Christel Depienne,Fanny Mochel,Julie Lavie,Ludger Schöls,Didier Lacombe,Mohamed Yahyaoui,Ibrahim Al Abdulkareem,Stephan Züchner,Atsushi Yamashita,Ali Benomar,Cyril Goizet,Alexandra Durr,Joseph G. Gleeson,Frédéric Darios,Frédéric Darios,Frédéric Darios,Alexis Brice,Giovanni Stevanin +51 more
TL;DR: It is demonstrated in human cells that the HSP pathophysiology includes alteration of mitochondrial architecture and bioenergetics with increased oxidative stress and focus attention on lipid metabolism as a critical HSP pathway with a deleterious impact on mitochondrial bioenergetic function.