Excited to share our latest preprint, in which we identified the Pml gene as a key genetic interactor in ALS, protecting mice from disease onset by clearing misfolded proteins in motoneurons. We also found that PML-targeting agents hold promise as a potential therapy for ALS 1/10

RT @fenssabanci: Seeking Exceptional Doctoral Candidates! 🌟. Sabancı University Faculty of Engineering and Natural Sciences invites excepti….

RT @JCellBiol: Vertegaal highlights recent work from Jaffray et al. (, describing how a machinery of #ubiquitin, SU….

📢⬇️.

RT @FEBSnews: 📣 ⌛ Deadline reminder: Thursday 13 March 2025, 23:59 (UTC+01:00)!.

RT @DormannL: One more day to apply!.

looking forward !

I finally encountered my share of Reviewer 2 - and quite a harsh one on that - unreasonable and unconstructive. Some reviewers should just relax and tone down the aggression in their feedback.

"SUMOylation: From Discovery to Translation".I am very excited about this upcoming EMBO meeting (France, 2025) and looking forward to presenting my lab's latest work. An outstanding lineup of speakers, as before. #EMBOsumoylation @EMBO_YIP .

A big thank you to @Sciezgin for sharing his incredible work on the biophysical properties of cell and organelle membranes (and their potential use as biomarkers in disease) - and also, congrats on the well-deserved @EMBO_YIP award.

A big thank you to the amazing team for their hard work and dedication.

This work is the product of a successful collaboration with some fantastic groups and friends, including @CytoLabKoc, who is active on here X 10/10.

Our study is the first to show, in vivo, a dramatic.Pml-dependency of mutant protein stability and aggregation, disease incidence, as well as a provocative Pml-dependent clinical response to interferon 9/10.

To our knowledge, this is the most dramatic benefit ever reported in treatment trials initiated presymptomatically in ALS mouse models 8/10.

This intervention dramatically improves ALS-.associated symptoms and muscle strength, and extends survival by nearly 6 months, in a Pml-dependent manner 7/10

Pharmacological intervention aimed at augmenting Pml expression, achieved through interferon alpha (IFN) or poly(I:C) treatment, effectively eliminates NEK1t and.its aggregates from motoneurons in vivo 6/10

Through this novel ALS mouse model, we identified the promyelocytic leukemia (Pml) gene as a key genetic interactor, protecting mice against disease onset by clearing truncated NEK1 within PML nuclear bodies (PML NBs) 5/10

We showed that the resulting mutant truncated NEK1 protein (NEK1t) is highly prone to aggregation, particularly in alpha motoneurons of mice, resulting in major motor function decline, muscle weakness and death 4/10

NEK1 is a key gene associated with ALS (Amyotrophic Lateral Sclerosis). In this study, we engineered the NEK1 Arg812Ter mutation, found in ALS patients, in mice, thereby creating a new ALS mouse model 3/10

ALS driven by mutant NEK1 aggregation is accelerated by Pml loss, but clinically reversed through pharmacologic induction of Pml-mediated degradation 2/10.