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We explore the intersections of biochemistry, cell and molecular biology combined with immunology. The main focus of the lab lies in designing and developing drugs to influence receptor-mediated signal transduction and intercellular signaling, specifically in the context of infection and cancer disease response.

We’ve conducted comprehensive research on a range of cellular pathways, such as GSK3B, Inflammasome, and autophagy—a fundamental process essential for cellular balance—alongside signaling pathways governing crucial cellular processes like apoptosis, known as programmed cell death. Our focus revolves around activating autophagy, a meticulously regulated cellular mechanism responsible for the degradation and recycling of cellular components, aiming to preserve cellular equilibrium without manipulating other vital cellular pathways.

How come we do this?

We aim to explore the triggers by which pathogens activate intricate cellular mechanisms, examining potential commonalities between cancer and infections.

What’s our approach?

We use various OMICs techniques from proteomics, metabolomics, genomics to investigate subcellular compartmentalization, translocation mechanisms, and protein-protein interactions.

What are the questions we’re aiming to address?

  • What causes multidrug resistance in microorganisms and cancer cells?
  • How can we combat multidrug resistance to improve treatment outcomes?
  • What new approaches can be developed to prevent or reverse multidrug resistance?
  • In infection, can we investigate non-autophagy pathways that pathogens utilize to evade host defenses and replicate within host cells?
  • For cancer treatment, are there alternative pathways, distinct from autophagy, that can be targeted to induce apoptosis or inhibit cancer cell proliferation?
  • In the context of both infection and cancer, what non-autophagy pathways can be exploited to develop innovative therapeutic strategies that effectively combat these diseases?