The de Bruin lab focuses on two main lines of investigation: (1) elucidating the mechanism and functional importance of the regulation of the cell cycle transcriptional program by the checkpoints that ensure maintenance of genome integrity, and (2) obtaining a better understanding of fundamental regulatory pathways that cause changes in cell cycle-regulated gene expression and the importance of this regulation for the maintenance of genome integrity.
Our work is aimed at understanding, at the molecular level, why defects in proteins ranging from gene-specific transcriptional regulators to global regulators of transcription are associated with human disease, most notably with cancer.
Bertoli C, et al (2016). Sustained E2F-Dependent Transcription Is a Key Mechanism to Prevent Replication-Stress-Induced DNA Damage. Cell Reports, 15 (7), 1412-1422. doi:10.1016/j.celrep.2016.04.036
Caetano C, et al (2014). Tolerance of deregulated G1/S transcription depends on critical G1/S regulon genes to prevent catastrophic genome instability. Cell Rep, 9 (6), 2279-2289. doi:10.1016/j.celrep.2014.11.039
Bertoli C, et al (2013). Chk1 inhibits E2F6 repressor function in response to replication stress to maintain cell cycle transcription.Current Biology.
Bertoli C, et al (2013). Control of cell cycle transcription during G1 and S phases. Nat Rev Mol Cell Biol, 14 (8), 518-528. doi:10.1038/nrm3629
de Oliveira FMB, et al (2012). Linking DNA replication checkpoint to MBF cell-cycle transcription reveals a distinct class of G1/S genes. EMBO JOURNAL, 31 (7), 1798-1810. doi:10.1038/emboj.2012.27
About the lab
Cancer Research UK