Lukasz J. Bugaj

This paper uses optogenetic control of RET signaling to induce controlled budding in human kidney organoids.

This paper introduces Aviatar, a single-component optogenetic system for inducible protein translocation to various subcellular compartments, demonstrating its utility in regulating actin polymerization and cancer-related signaling.

This study shows that low-order RTK fusions can drive oncogenic signaling without forming condensates, challenging the role of condensation in signal transmission.

The paper shows that RTK fusions suppress EGFR and sequester Grb2, and targeted therapies reverse this suppression, enhancing EGFR signaling and drug response.

This study shows nuclear-import receptors suppress RNA-binding protein phase transitions by remodeling the dilute phase, preventing disease-linked aggregation.

The paper quantifies how cancer and drug treatments affect the information capacity of RTK signaling pathways using optogenetic stimulation and information theory.

The paper shows that proteins can dynamically encode environmental information through domain interactions, with pulsatory responses shaped by light, temperature, and evolution.

This paper introduces a temperature-inducible protein module called Melt that allows reversible control of mammalian cell processes through temperature changes, demonstrating its utility in cell death control in a mouse cancer model.

The paper introduces thermoPlate, a device for dynamic temperature control in cell culture, and uses it to study temperature-dependent cellular responses like phase separation and stress granule dynamics.

The paper introduces an open-source device for high-throughput optogenetic experiments in microwell plates, enabling automated stimulation, spectroscopy, and feedback control in E. coli.

The paper introduces CLASP, an optogenetic tool to control TF localization, and shows differential promoter responses to pulsatile vs. continuous TF inputs.