In the laboratory, our research focuses on the regulation of DNA replication, genome stability, and the chromatin response to DNA damage. We investigate how chromatin regulators influence the progression of replication forks and prevent conflicts between replication and transcription, which is crucial for maintaining genome integrity. Studies conducted by our team have demonstrated that INO80 is essential for the resolution of R-loops, which can hinder DNA replication and contribute to genomic instability in cancer cells.

We investigate the regulation of DNA repair processes, particularly double-strand break (DSB) repair mechanisms and ways to exploit these for therapeutic purposes.

A different facet investigates protein-drug interactions for targeted cancer therapy, focusing on lectins as carriers for cytotoxic compounds, such as metal-based anticancer drugs.

Selected publications:

Hristova, RH., et al. “Deregulated Levels of RUVBL1 Induce Transcription-Dependent Replication Stress.” The International Journal of Biochemistry & Cell Biology, vol. 128, 2020, p. 105839.
Prendergast, L., et al. “Resolution of R-Loops by INO80 Promotes DNA Replication and Maintains Cancer Cell Proliferation and Viability.” Nature Communications, vol. 11, no. 1, 2020, p. 4534.
Aleksandrov, R. et al. “The Chromatin Response to Double-Strand DNA Breaks and Their Repair.” Cells, vol. 9, no. 8, 2020, p. 1853.
Gospodinov, A., et al. “Mammalian Ino80 Mediates Double-Strand Break Repair through Its Role in DNA End Strand Resection.” Molecular and Cellular Biology, vol. 31, no. 23, Dec. 2011, pp. 4735–45.
Bogoeva, V., et al. “Ruthenium Porphyrin-Induced Photodamage in Bladder Cancer Cells.” Photodiagnosis and Photodynamic Therapy, vol. 14, June 2016, pp. 9–17. ScienceDirect
D’Auria, S., et al. “Tumor-Specific Protein Human Galectin-1 Interacts with Anticancer Agents.” Molecular bioSystems, vol. 5, no. 11, 2009, pp. 1331–36.