Research Focus
Andreas Villunger's research focuses on the role of pro-apoptotic BH3-only proteins in lymphocyte transformation and anti-cancer treatment responses, revealing for the first time that cell death induced by radiotherapy can have pro-tumorigenic effects. In recent years, his team has begun to explore the interplay between the cell cycle and programmed cell death pathways, with a particular focus on mitotic cell death and post-mitotic cell fate decisions. These investigations also uncovered a previously overlooked role of the PIDDosome signaling platform in the activation of the tumor suppressor p53 in cells harboring supernumerary centrosomes. This discovery laid the foundation for ongoing ERC-funded research into the function of the PIDDosome multi-protein complex in ploidy control during organ development and cellular transformation, with the long-term goal of establishing the PIDDosome as a potential therapeutic target in diseases associated with centrosome abnormalities, including cancer and age-related disorders.
Major Research Interests
- BCL2 family proteins in tissue homeostasis
- DNA damage response & checkpoint signaling
- Cell cycle – cell death cross-talk
- Polyploidization in health and disease
Biosketch
Andreas Villunger is a full professor at the Medical University of Innsbruck, Austria, where he heads the Division of Developmental Immunology at the MUI Biocenter. He joined CeMM in November 2018 as an adjunct PI aiming to develop PIDDosome inhibitors. He studied biology at the Universities of Salzburg and Innsbruck, completing his PhD and early postdoctoral studies in Innsbruck before moving to the Walter and Eliza Hall Institute in Melbourne, Australia. There, he investigated the role of BCL2 family proteins in immune cell development and immune tolerance together with his mentor Professor Andreas Strasser. Back in Innsbruck, he established his own research group supported by the FWF START Prize in 2003 and became a full professor in 2009. In the more recent past, his team has begun to explore the crosstalk between the cell-cycle and cell-death machineries, focusing on mitotic cell death and post-mitotic cell fate after failed cell division, leading to polyploidy. His work is funded by the Austrian Science Fund (FWF) and the European Research Council (ERC).
Top 5 Publications
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Rizzotto D, Vigorito V, Rieder P, et al. Caspase-2 kills cells with extra centrosomes. Sci Adv. 2024;10(44):eado6607. doi:10.1126/sciadv.ado6607. (published paper)
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Braun VZ, Karbon G, Schuler F, et al. Extra centrosomes delay DNA damage-driven tumorigenesis. Sci Adv. 2024;10(13):eadk0564. doi:10.1126/sciadv.adk0564. (published paper)
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Garcia-Carpio I, Braun VZ, Weiler ES, et al. Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance. EMBO J. 2023;42(20):e113510. doi:10.15252/embj.2023113510. (published paper)
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Kim JY, Wang LQ, Sladky VC, et al. PIDDosome-SCAP crosstalk controls high-fructose-diet-dependent transition from simple steatosis to steatohepatitis. Cell Metab. 2022;34(10):1548-1560.e6. doi:10.1016/j.cmet.2022.08.005. (published paper)
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Sladky VC, Knapp K, Soratroi C, et al. E2F-family members engage the PIDDosome to limit hepatocyte ploidy in liver development and regeneration. Dev Cell. 2020;52(3):335-349.e7. doi:10.1016/j.devcel.2019.12.016. (published paper)
Please visit Andreas Villunger's Google Scholar profile for a complete list of publications.