Cód. SSPA: IBiS-C-17
Our lab is focused on investigating the formation, detection, and repair of DNA lesions associated with gene expression. This is a crucial question in both basic research and biomedicine, as transcription is a major endogenous source of DNA damage, leading to cell death and genome instability. Thus, understanding transcription-associated DNA breaks presents the added value of well-established connections with human prevalent disease.
We are specially focused in the formation and repair of DNA double-strand breaks (DSBs) that arise during gene expression by the action of DNA topoisomerases, essential enzymes that catalyze the release of DNA torsional stress and remove DNA tangles or knots by cutting the DNA. These enzymes are common targets of chemotherapy and their aberrant activity is linked to progressive neurodegenerative diseases. Strikingly, transcription-associated DSBs are a major and poorly understood source of genome instability in eukaryotic cells.
Our laboratory has significantly contributed to understand the repair process of TOP1 and TOP2-induced DSBs revealing the threat posed by these DSBs during transcription and demonstrating the importance of TDP1 and TDP2-dependent end-joining in protecting both gene transcription and genome stability
Lines of research:
- DNA repair mechanisms of topoisomerase-induced DSBs.
- Transcriptional stress induced by endogenous sources of DNA damage.
- Novel therapeutic targets based on the synthetic lethality of DNA damage repair factors.
More details about us in this LINK
