We are excited to welcome Dr. Kristyna Pluhackova as our next speaker in the Atomistic Modeling Seminar!

Dr. Kristyna Pluhackova is an Independent Junior Research Group Leader at the Cluster of Excellence SimTech at the University of Stuttgart, where her team and herself use and boost multiscaling molecular dynamic simulations to investigate complex biological and material processes, including protein interactions, biomembranes, signaling pathways, nanoporous materials, and molecular processes behind cell death.

In her talk, “Killing to survive – how protein-lipid interactions drive programmed cell death”, Dr. Pluhackova will discuss programmed cell death as an essential process of eukaryotic life and its role in development, regeneration, and defense against pathogens.

She will present molecular details of protein-lipid interactions using multiscaling molecular dynamics simulations, including how lipids interact with membrane pores formed by gasdermin and how lipid composition influences pore formation. Furthermore, she will address the mechanism by which ninjurin-1 disrupts membranes during plasma membrane rupture.

Date: Tuesday, April 21, 2026, 10:30 am

Location: MIBE Lecture Hall

Abstract:

Programmed cell death is an essential process of eukaryotic life, enabling e.g., embryonic development, regeneration, or fighting pathogens. Depending on the needs of an organism, diverse molecular mechanisms of cell death exist, determining among others the speed of cell death, its extent and the impact on surrounding cells. Not surprisingly, dysregulation of cell death culminates in diverse diseases, the most prominent of all being cancer.

Here, molecular details of protein-lipid interactions in programmed cell death are revealed by multiscaling molecular dynamics simulations. First, it is unveiled how lipids unplug medium-sized membrane pores formed by a pyroptotic agent gasdermin and astonishing adaptability of the pore shape is revealed. Next, it is demonstrated how the gasdermin species and the lipid composition determine the process of gasdermin pore formation. At last, the mechanism through which ninjurin-1 disrupts membranes during plasma membrane rupture, the terminal event of many cell-death processes, is resolved.