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A10 - Cell death and inflammation modulated by the ubiquitin E3 ligase activities within LUBAC in metabolic inflammation

Nieves Peltzer

Department of Translational Genomics, University of Cologne
Contact: m.peltzer(at)uni-koeln.de
For more information visit: Peltzer lab

Abstract

Receptor-ligand-mediated signalling in cell death, inflammation and immunity is regulated by a fine-tuned system of post-translational modifications by phosphorylation, ubiquitination and their respective reversals. The linear ubiquitin chain assembly complex (LUBAC) modulates signalling via the tumour necrosis factor (TNF) – TNF receptor 1 (TNFR1) system. We found LUBAC and the linear ubiquitin chains it creates to be crucial for the different TNFR1 signalling outputs by enabling full gene activation and preventing cell death. These studies contributed to establishing cell death as a trigger of inflammation and inflammatory disease. In this project we aim to understand and further dissect the biochemistry and function of LUBAC and and its individual components in physiology and in various disease settings. 

Recent Publications

2024

Albert MC, Uranga-Murillo I, Arias M, De Miguel D, Peña N, Montinaro A, Varanda AB, Theobald SJ, Areso I, Saggau J, Koch M, Liccardi G, Peltzer N, Rybniker J, Hurtado-Guerrero R, Merino P, Monzón M, Badiola JJ, Reindl-Schwaighofer R, Sanz-Pamplona R, Cebollada-Solanas A, Megyesfalvi Z, Dome B, Secrier M, Hartmann B, Bergmann M, Pardo J, Walczak H. Identification of FasL as a crucial host factor driving COVID-19 pathology and lethality. Cell Death Differ. 2024 Mar 21. doi: 10.1038/s41418-024-01278-6. Epub ahead of print. PMID: 38514848

Project A10 Publications 2020 - 2023

Project related Publications

Project A10 First funding period 2020 - 2023