| 초록 |
The artificial assembly of synthetic building units inside a living cell and the interaction of these units with the cellular components have rarely been studied, but are emerging as an intriguing strategy to control cellular fate. Considering the role of vicious mitochondrial fibril proteins such as amyloid beta (Aβ) in Alzheimer’s disease, we hypothesized that artificial induction of fibril formation inside the mitochondria could promote mitochondrial dysfunction and induce cell damage. Amphiphilic peptides with a mitochondrial targeting unit selectively accumulate in the mitochondria and self-assemble into an ordered structure because inside the confined organelle, the concentration of the peptides is significantly increased over their critical aggregation concentration. The fibrous structure inside the mitochondria then disrupts the mitochondrial membrane to cause leakage of the mitochondrial contents into the cytosol, resulting in severe damage to the cells. |
