Cell Stress & Inflammation - CSI - is my group's new name. We are still incredibly interested in ubiquitin, but our new name reflects a broadening scope in the lab, in part based on our recent paper (www.nature.com/articles/s41...). Visit our new website here: www.bioengineering.dtu.dk/csi
Cell Stress & Inflammation - CSI - is my group's new name. We are still incredibly interested in ubiquitin, but our new name reflects a broadening scope in the lab, in part based on our recent paper (www.nature.com/articles/s41...). Visit our new website here: www.bioengineering.dtu.dk/csi
Receptor clustering is a common theme in viral detection, but whether detection directly hinders genome replication is less clear.
Excited to share the Z in RZ-type E3s: ZNFX1 is an RNA helicase that builds ubiquitin chains leading to aggregates that ensnare viral RNA.
www.cell.com/molecular-ce...
I’d take a full review from a grumpy Reviewer #2 any day over student teaching evaluations. Students are savage.
More evidence that LUBAC has functions beyond inflammation: Our study shows that LUBAC regulates AMPK signalling to control metabolic adaptation, autophagy, and cell death. This might explain the metabolic problems observed in LUBAC deficiency and ORAS patients. www.nature.com/articles/s41...
More evidence that LUBAC has functions beyond inflammation: Our study shows that LUBAC regulates AMPK signalling to control metabolic adaptation, autophagy, and cell death. This might explain the metabolic problems observed in LUBAC deficiency and ORAS patients. www.nature.com/articles/s41...
This project started with confusion 🤔 www.nature.com/articles/s41...
Loss of LUBAC or OTULIN causes severe inflammatory disease. But patients also show clear metabolic defects.
Neither LUBAC nor OTULIN had been linked to metabolic regulation.
So where do these metabolic manifestations come from?
We turned to proteomics 📊 and found that LUBAC and OTULIN regulate AMPK.
This suggests the metabolic defects may not simply be secondary to inflammation. Rather, they may be central in to the pathogenesis.
This project started with confusion 🤔 www.nature.com/articles/s41...
Loss of LUBAC or OTULIN causes severe inflammatory disease. But patients also show clear metabolic defects.
Neither LUBAC nor OTULIN had been linked to metabolic regulation.
So where do these metabolic manifestations come from?
🧐 What if metabolic defects are not just a consequence of inflammatory disease - but actively contribute to it?
Inflammation and metabolism are deeply intertwined, but the molecular links remain unclear.
Our new paper in Cell Death & Differentiation uncovers one. 🧵👇
nature.com/articles/s41...
M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress
www.nature.com/articles/s41...
Thanks, Leo
...Brent Ryan, Joern Dengjel, @gyrd-lab.bsky.social, @elliottlab.bsky.social, Lisa Frankel, @nievespeltzer.bsky.social, and Geert van Loo.
Huge congratulations to Camilla Elbæk, co-authors, and amazing collaborators on this effort 👏 @keisakamoto.bsky.social @labsakamoto.bsky.social, @annikameinander.bsky.social, Grahame Hardie...
💡 This links inflammatory ubiquitin signalling directly to metabolic control.
Could metabolic dysfunction be a driver - not just a consequence - of inflammatory disease?
🔬 Using cell lines 🧫, mice 🐁, flies 🪰, and patient cells 🏥, we found:
✔️ LUBAC + OTULIN regulate AMPK during energetic stress
✔️ M1-linked ubiquitination promotes AMPK activity and metabolic adaptation
✔️ Loss of this axis reduces cell and organism resilience to starvation
👉 We show that M1-linked ubiquitination by LUBAC directly regulates AMPK, the master energy sensor of the cell.
LUBAC and M1-linked ubiquitin are best known for regulating inflammatory signalling and cell death 💀☠️.
But they also control metabolic signalling and adaptation.
🧐 What if metabolic defects are not just a consequence of inflammatory disease - but actively contribute to it?
Inflammation and metabolism are deeply intertwined, but the molecular links remain unclear.
Our new paper in Cell Death & Differentiation uncovers one. 🧵👇
nature.com/articles/s41...
M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress
#Drosophila
Tomato? or tomahto?
Interesting article and accompanying spotlight on the cross-talk between ciliary homeostasis and ubiquitination (written by Jonathan Pruneda and @rbdamgaard.bsky.social).
www.nature.com/articles/s41...
www.nature.com/articles/s41...
💡 Ciliary homeostasis turns out to depend on an unexpected tug-of-war between UFMylation and ubiquitination.
In a recent editorial in Cell Death & Differentiation,
@jnpruneda.bsky.social and I highlight new work from Wang et al. 🧵👇
This work expands the landscape of PTM crosstalk and raises the possibility that ciliary dysfunction contributes to neurological and developmental disorders linked to the UFM1 pathway.
🔗 www.nature.com/articles/s41...
Mechanistically, UFMylation and ubiquitination compete for the same lysine on IFT88, forming a mutually exclusive modification switch that controls protein stability and ciliary integrity across tissues.
While ubiquitination is a well-known regulator of protein stability, the roles of many ubiquitin-like modifiers remain unclear. Here, UFL1-mediated UFMylation emerges as a protective signal for the ciliary protein IFT88.
💡 Ciliary homeostasis turns out to depend on an unexpected tug-of-war between UFMylation and ubiquitination.
In a recent editorial in Cell Death & Differentiation,
@jnpruneda.bsky.social and I highlight new work from Wang et al. 🧵👇
🚨 Postdoc position in my lab!
A project on protein binder discovery for K6-linked #ubiquitin to investigate their role in infection is available.
📍 DTU, Copenhagen, Denmark
⏰ Deadline: 18 December 2025
Apply here: efzu.fa.em2.oraclecloud.com/hcmUI/Candid...
🚨 Postdoc position in my lab!
A project on protein binder discovery for K6-linked #ubiquitin to investigate their role in infection is available.
📍 DTU, Copenhagen, Denmark
⏰ Deadline: 18 December 2025
Apply here: efzu.fa.em2.oraclecloud.com/hcmUI/Candid...
A #postdoc position in atypical #ubiquitin signalling and protein binder engineering is opening soon in my lab at DTU Bioengineering! Get in touch if you are interested.
🚀 Off to our Research Retreat with the Section for Medical Biotechnology, DTU Biotechnology and Biomedicine.
Two days of science, ideas & innovation 🧬💡
12 faculty pitches, 30+ PhDs & postdocs, and endless opportunities for new collaborations 🔬🤝✨