Good signals in bad times: decoding AMPK targets that restore metabolic homeostasis
Given the sanitary situation, talks will be held via ZOOM but also in-person in SV 1717 (participant numbers limited to 30 – first come, first served). Wearing of masks is mandatory. The Sanitary Pass is mandatory and should be presented at the entrance of the meeting room.
Thanks for your understanding.
Eukaryotic cells evolved a very sophisticated system to sense low cellular ATP levels via the serine/threonine kinase AMP-activated protein kinase (AMPK). This energy switch suppresses pro-growth pathways (mTORC1 and fatty acid synthesis) while inducing autophagy and lysosomal function. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, via stimulation of autophagy, mitochondrial fission, and mitochondrial biogenesis. Here will present new data from our lab identifying key new steps and players in the mechanisms of AMPK controls mitochondrial homeostasis.
Thanks for your understanding.
Eukaryotic cells evolved a very sophisticated system to sense low cellular ATP levels via the serine/threonine kinase AMP-activated protein kinase (AMPK). This energy switch suppresses pro-growth pathways (mTORC1 and fatty acid synthesis) while inducing autophagy and lysosomal function. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, via stimulation of autophagy, mitochondrial fission, and mitochondrial biogenesis. Here will present new data from our lab identifying key new steps and players in the mechanisms of AMPK controls mitochondrial homeostasis.
Practical information
- Informed public
- Free
Organizer
- Johan Auwerx, EPFL Sebastien Herzig, NIHS
Contact
- Sebastien Herzig, NIHS [email protected], P +41 21 632 6155