🧐 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...
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...
I’d take a full review from a grumpy Reviewer #2 any day over student teaching evaluations. Students are savage.
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.
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