Associate Professor, Section for Medical Biotechnology, Technical University of Denmark. Studies ubiquitin signalling in inflammation, metabolism, and disease.
🚨New preprint!🚨
Lack of specific affinity reagents hinders studies of signalling mechanisms. We show that sdAbs provide a robust scaffold for making linkage-specific ubiquitin binders, exemplified by 2A6, a versatile reagent for M1-linked ubiquitin chains.
www.biorxiv.org/content/10.6...
🚨New preprint!🚨
Lack of specific affinity reagents hinders studies of signalling mechanisms. We show that sdAbs provide a robust scaffold for making linkage-specific ubiquitin binders, exemplified by 2A6, a versatile reagent for M1-linked ubiquitin chains.
www.biorxiv.org/content/10.6...
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...
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?
🧐 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...
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...
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.
🧐 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...
🧐 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...
🧐 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...
🔬 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
💡 This links inflammatory ubiquitin signalling directly to metabolic control.
Could metabolic dysfunction be a driver - not just a consequence - of inflammatory disease?
🧐 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...
👉 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.
💡 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. 🧵👇
💡 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. 🧵👇
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.
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...
💡 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. 🧵👇
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.
🚨 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 🔬🤝✨
A few months ago, our review “The Molecular Toolbox for Linkage Type-Specific Analysis of Ubiquitin Signaling” 🧬🧰🛠️ came out in ChemBioChem. Time to give it a spotlight!
chemistry-europe.onlinelibrary.wiley.com/doi/full/10....
A few months ago, our review “The Molecular Toolbox for Linkage Type-Specific Analysis of Ubiquitin Signaling” 🧬🧰🛠️ came out in ChemBioChem. Time to give it a spotlight!
chemistry-europe.onlinelibrary.wiley.com/doi/full/10....
We also highlight:
✅ Trade-offs between specificity, throughput, & sensitivity
✅ Gaps in the current toolbox where innovation is needed
✅ The value of combining orthogonal methods for robust insight
Hope this serves as a useful overview for anyone working on ubiquitin signalling or PTMs. Big thanks to those who did the heavy lifting in the writing process: Julian Koch, Camilla Reiter Elbæk & @dompri.bsky.social 🙌😊
A few months ago, our review “The Molecular Toolbox for Linkage Type-Specific Analysis of Ubiquitin Signaling” 🧬🧰🛠️ came out in ChemBioChem. Time to give it a spotlight!
chemistry-europe.onlinelibrary.wiley.com/doi/full/10....
A few months ago, our review “The Molecular Toolbox for Linkage Type-Specific Analysis of Ubiquitin Signaling” 🧬🧰🛠️ came out in ChemBioChem. Time to give it a spotlight!
chemistry-europe.onlinelibrary.wiley.com/doi/full/10....
Why this matters ⬇️
Ubiquitin chain diversity, i.e. different linkage types, mixed or branched chains, is central to cell signalling.
But analysing these chain types specifically remains a big challenge.
Is it still useful to insist that authors spell out every protein name in research papers? Many names are long, obscure, and say nothing about function... we might as well call them James, Joan, and John.
The goal of a PhD is not to learn some facts or read a few papers or learn a bunch of techniques. The goal of a PhD is to learn independence, problem solving, how to finish things you start, resilience, & gain the ability to adapt & think creatively. Learning these things is hard.
the really key number to remember is that biorxiv serves the entire global science community, posting thousands of papers per month for millions of readers, and it's entire running costs ( a few $M/year) are less than some single labs....
The journal @nature.com compiles a list of leading research institutions ranked by counts of "high-quality research outputs." (www.nature.com/nature-index...) Surely not definitive, but the change over the six years from 2018 to 2024 is astonishing. (1/5)
Special day for our group @cbmr.science as we celebrate the successful defense of our (first) freshly minted PhD, Dr. Conchita Bringas 🥳 Her thesis was based on characterizing novel #AMPK inhibitors. Special thanks to the great committee @rbdamgaard.bsky.social ,Dave Carling & Lykke Sylow.
We have a 4-year postdoc position open in our Research Unit on proteostasis!
The project explores inter-tissue regulation using advanced proteomics approaches.
Collaborative & interdisciplinary environment. More details & application here:
jobs-uk-koeln.onlyfy.jobs/job/pktg6ivj...
Haven’t shared this in a while. But the #ubiquitin and #ubl Starter Pack now includes 116 profiles to follow if you’re interested in the field: signalling, structure and biochemistry, biology, mechanisms, proteostasis, TPD, chemical biology… Check out the list and let me know if you are missing.
Happy to see our review out in ChemBioChem @chemistryeurope.bsky.social in which we describe the tools and strategies for deciphering linkage type-specific #ubiquitin signalling: doi.org/10.1002/cbic.... Thanks to Julian for spearheading this, and to Camilla and Dominik for important contributions.
Happy to see our review out in ChemBioChem @chemistryeurope.bsky.social in which we describe the tools and strategies for deciphering linkage type-specific #ubiquitin signalling: doi.org/10.1002/cbic.... Thanks to Julian for spearheading this, and to Camilla and Dominik for important contributions.
Excited to report our latest research on new “molecular glues” that specifically lock the BRCC36 isopeptidase complex (BRISC) in an autoinhibited state and reduce interferon signalling. This first-of-its-kind approach could reshape how we target large deubiquitylase (DUB) complexes.
rdcu.be/edRwF