
Julien Prudent
Articles
-
Oct 16, 2024 |
nature.com | Mayuko Segawa |Julien Prudent
AbstractMitochondria not only synthesize energy required for cellular functions but are also involved in numerous cellular pathways including apoptosis, calcium homoeostasis, inflammation and immunity. Mitochondria are dynamic organelles that undergo cycles of fission and fusion, and these transitions between fragmented and hyperfused networks ensure mitochondrial function, enabling adaptations to metabolic changes or cellular stress.
-
Mar 10, 2024 |
nature.com | Emma Wilson |Yizhou Yu |Nikolaos Patikas |Julien Prudent |L. Martins |Georgina E. Lindop | +1 more
AbstractOrganelles 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 mitochondria and ER membranes. They have been implicated in many diseases, including neurodegenerative, metabolic, and cardiac diseases. Although MERCS have been extensively studied, much remains to be explored.
-
Mar 7, 2024 |
nature.com | Daniel M. Virga |Stevie Hamilton |Abigail Daisy Morgan |Victoria Hewitt |D. Grahame Hardie |Julien Prudent | +2 more
AbstractNeuronal mitochondria play important roles beyond ATP generation, including Ca2+ uptake, and therefore have instructive roles in synaptic function and neuronal response properties. Mitochondrial morphology differs significantly between the axon and dendrites of a given neuronal subtype, but in CA1 pyramidal neurons (PNs) of the hippocampus, mitochondria within the dendritic arbor also display a remarkable degree of subcellular, layer-specific compartmentalization.
-
Apr 17, 2023 |
biorxiv.org | Timo Rey |Julien Prudent |Michal Minczuk |Luis Carlos Tabara
Thank you for your interest in spreading the word about bioRxiv. NOTE: Your email address is requested solely to identify you as the sender of this article. Your Email * Your Name * Send To * Enter multiple addresses on separate lines or separate them with commas. Message Subject (Your Name) has forwarded a page to you from bioRxiv Message Body (Your Name) thought you would like to see this page from the bioRxiv website.
-
Mar 8, 2023 |
nature.com | Vincent Roberto Zecchini |Gonçalo Pereira |Laura Tronci |Shamith A. Samarajiwa |Thomas Mitchell |Julien Prudent | +1 more
AbstractMutations in fumarate hydratase (FH) cause hereditary leiomyomatosis and renal cell carcinoma1. Loss of FH in the kidney elicits several oncogenic signalling cascades through the accumulation of the oncometabolite fumarate2. However, although the long-term consequences of FH loss have been described, the acute response has not so far been investigated. Here we generated an inducible mouse model to study the chronology of FH loss in the kidney.
Try JournoFinder For Free
Search and contact over 1M+ journalist profiles, browse 100M+ articles, and unlock powerful PR tools.
Start Your 7-Day Free Trial →