🚨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...

ZNFX1 uses two-component ubiquitin circuitry to quarantine viral RNA

Squair et al. show that ZNFX1 restricts ssRNA virus replication by integrating SF1 helicase activity with dual E3 ligase mechanisms. ATP-dependent RNA binding activates E3 function, driving self-propa...

cell.com

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...

M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress - Cell Death & Differentiation

Cell Death & Differentiation - M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress

nature.com

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...

M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress - Cell Death & Differentiation

Cell Death & Differentiation - M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress

nature.com

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?

Rune Busk Damgaard@rbdamgaard.bsky.social · 6mo ago

🧐 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?

Rune Busk Damgaard@rbdamgaard.bsky.social · 6mo ago

🧐 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...

M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress www.nature.com/articles/s41...

M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress - Cell Death & Differentiation

Cell Death & Differentiation - M1-linked ubiquitination by LUBAC regulates AMPK signalling and the response to energetic stress

nature.com

🧐 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

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...

A tale of two tags: UFMylation counters ubiquitination for ciliary homeostasis - Cell Death & Differentiation

Cell Death & Differentiation - A tale of two tags: UFMylation counters ubiquitination for ciliary homeostasis

nature.com

💡 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. 🧵👇

🚨 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....

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.

Jeg er godt træt af måden regeringens spareplan rammer universiteterne.

Regeringens sult efter at afskaffe bureaukratiet er gået for vidt, når den nu rammer forskerne

Regeringen hævder, at der med de nye besparelser på universiteterne ikke vil gå midler fra forskning. Men forskere arbejder ikke i et vakuum. Når administrationen fjernes, ryger tiden fra forskningen

klik1.information.dk

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....

it’s a global contest, whether we want to compete or watch from the sidelines

Mordecai-Mark Mac Low@astrocurator.bsky.social · last yr.

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...

Postdoc Position (f/m/x)

We are looking to support our rapidly growing team as soon as possible:

jobs-uk-koeln.onlyfy.jobs