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A06 - Mitochondrial YME1L at the interface of cell death and inflammation

Thomas Langer

Max Planck Institute for Biology of Ageing
Contact: langerSpamProtectionage.mpg.de
For more information visit: Langer Lab

Abstract

Mitochondria play an active role in cell death control and are emerging as central regulators of innate immunity. In addition to their well-described role in apoptosis, mitochondria have also been linked to other modes of regulated cell death, such as necroptosis, ferroptosis and pyroptosis. This project will examine how the mitochondrial i-AAA protease YME1L regulates cell survival, mtDNA release and inflammatory responses on a molecular level and how this relates to neurodegeneration and tissue-specific cell death in vivo. These studies will help define the role of mitochondria at the interface between cell death and inflammation.

Recent Publications

2021

Bahat, A., MacVicar, T., and Langer, T. (2021) Metabolism and Innate Immunity Meet at the Mitochondria.


Sprenger, H.G., MacVicar, T., Bahat, A., Fiedler, K.U., Hermans, S., Ehrentraut, D., Ried, K., Milenkovic, D., Bonekamp, N., Larsson, N.G., Nolte, H., Giavalisco, P. & Langer. T. (2021) Cellular pyrimidine imbalance triggers mitochondrial DNA–dependent innate immunity. Nature Metabolism 26.04.2021 https://doi.org/10.1038/s42255-021-00385-9

Project related Publications