The recent publication of IMol researchers identifies a novel defense mechanism to restore cellular protein homeostasis upon mitochondrial disease stress.
The Chacinska group, with a leading researcher Minji Kim supported by Remigiusz Serwa, a head of the IMol Proteomics Core Facility, discovered a novel stress mechanism activated by defective mitochondria, the powerhouses of the cell. This mechanism is caused by the mitochondrial immature proteins transiting through the cytosol. It involves expression of immune proteasome leading to an increase in protein degradation and clearing protein homeostasis-related defects. This exciting finding demonstrates a causative link between mitochondrial function and cellular protein homeostasis, identifying new strategies to fight civilization diseases, such as dementia or Alzheimer syndrome.
In collaboration with Bettina Warscheid, currently at the University of Wuerzburg.
Read the paper: https://www.nature.com/articles/s41467-023-39642-8