CORDIS Project
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This project investigates how certain mutations can help cells survive when key DNA repair proteins are lost, focusing on mechanisms related to DNA double-strand breaks. By using advanced genetic techniques, it aims to identify suppressor mutations that could inform new strategies for treating diseases like cancer.
DNA double-strand breaks (DSBs) occur frequently during a cell’s lifetime and constitute the most cytotoxic DNA lesion. DSBs compromise genetic integrity and have the potential to trigger cell death and generate pathological mutations.
To counteract such threat, cells possess a complex protein network termed DSB response (DSBR) which senses, signals and repairs DSBs.
Two predominant mechanisms repair DSBs: homologous recombination (HR) and non-homologous end joining (NHEJ).
While loss of DSBR fa…
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