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Targeting mitochondrial health for healthy ageing and prevention of neurodegeneration. Co-founder, Automera.
Michael Lazarou








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Mechanism of #autophagy initiation by transmembrane selective autophagy receptors @elias-adriaenssens.bsky.social & @martenslab.bsky.social review emerging mechanistic differences between soluble and transmembrane autophagy receptors www.embopress.org/doi/full/10....
7mo
Abstract deadline approaching! Apply for a short/spotlight talk bsky.app/profile/sato...
New from us! Had a question about mitophagy but were afraid to ask? 😂 Excited to review the latest advances in beta cell mitophagy research as a key adaptive response in all forms of diabetes in @cp-trendsendomet.bsky.social. We'd be honored if you have it a read! #T1D #T2D
7mo
7mo
Excited to share our latest research, out today in Cell (@cellpress.bsky.social) Using cryo-EM and cell-based studies, we reveal how large nutrient sensing protein complexes form at the lysosomal membrane to turn off mTORC1 and halt anabolic signalling. Read the paper here: doi.org/10.1016/j.ce...
CRN Team Hurley developed AI-directed voxel extraction (AIVE), a segmentation strategy that refines AI-based organelle boundary predictions. Using AIVE, they identified a previously unknown mitochondrial contact termed the mitochondrial intrusion 🧪 🔗 Read the #publication: bit.ly/4qeZiOY
5mo
5mo
⚡️Mitochondria make ATP, the energy that powers life. But in neurons, with axons up to a meter long, how do these tiny power plants stay functional in the right places? We went looking. 1/n www.biorxiv.org/content/10.6...
6mo
Mitochondrial ATP production is essential for life. Mitochondrial function depends on the spatio-temporal coordination of nuclear and mitochondrial genome expression, yet how this coordination occurs ...
www.biorxiv.org
The EMBO Journal
Self-renewal of neuronal mitochondria through asymmetric division
Updated preprint 🧵 We mapped how loss of 23 LSD genes reshapes neuronal proteomes in cortical (iN) and dopaminergic (iDA) neurons New in v2: We added a computational PPI pipeline assessing KO-dependent vulnerability at the interaction and complex level.
Scott Soleimanpour
2mo
Explore emerging research with field leaders @keystoneSymposia.bsky.social #Autophagy : Mechanisms to Therapy, this February in Keystone! keysym.us/KSAutophagy26 #KSAutophagy26 www.keystonesymposia.org/conferences/...
Aligning Science Across Parkinson's
Thrilled to share that the final piece of my PhD work is now on bioRxiv! biorxiv.org/content/10.1... With support from @nvidia and the @NSF, we used AlphaFold to screen 1.6M+ protein pairs, revealing thousands of potential novel PPIs. All data can be viewed at predictomes.org/hp
Andrew Ellisdon
How do nanoparticles traverse the endothelial barrier in a living organism? We explored this fundamental question using the zebrafish and PEG-based nanoparticles (NPs) in our latest article: (pubs.acs.org/doi/10.1021/...).
Sam Lewis, Ph.D.
8mo
7mo
Online Now: Mitophagy in the adaptation to pancreatic β cell stress in diabetes #trends #endocrinology #metabolism
4mo
Felix Kraus
Join us at the Keystone Symposia on Autophagy: Mechanisms to Therapy, February 2026, in Keystone, with field leaders!
keysym.us
Autophagy: Mechanisms to Therapy | Keystone Symposia
8mo
Protein-protein interactions (PPIs) drive virtually all biological processes, yet most PPIs have not been identified and even more remain structurally unresolved. We developed a two-step computational...
biorxiv.org
Proteome-wide in silico screening for human protein-protein interactions
Trans-endothelial transport of nanoparticles remains poorly characterized in live organisms. The zebrafish is a well-established model for direct in vivo imaging; however, standardized controls have n...
pubs.acs.org
Trans-Endothelial Trafficking in Zebrafish: Nanobio Interactions of Polyethylene Glycol-Based Nanoparticles in Live Vasculature
Mitophagy is a crucial quality control process that preserves metabolic efficiency by selectively targeting damaged mitochondria for removal. Given the high metabolic demand of pancreatic β cells’ insulin secretion, disruption of mitophagy contributes to the mitochondrial dysfunction and β cell failure that are a common feature of both type 1 and type 2 diabetes (T1D and T2D). We review the impact of mitophagy on β cell responses to (patho)physiologic stressors that underlie the development of T1D and T2D. We examine how β cells engage mitophagy in the adaptive response to metabolic, inflammatory, and oxidative damage. We also dissect the importance of ubiquitin- and receptor-mediated mitophagy, methodological advances to quantify mitophagy in β cells, and ongoing efforts to pharmacologically target mitophagy to preserve β cell health and improve glycemic control.
Mitophagy in the adaptation to pancreatic β cell stress in diabetes
dlvr.it
Trends in Endocrinology and Metabolism
Ernst Schmid
Rob Parton