We investigate Neuronal Genomic Instability (NGI) — how DNA damage in neurons drives neurological disorders and opens paths to new therapies.
Our lab explores key mechanisms at the intersection of DNA damage response and neurodegeneration.
The PARP1-TRIM44-MRN axis dictates the response to PARP inhibitors — a critical pathway in DNA damage signaling and therapeutic targeting in neurodegeneration.
Learn more →USP39 promotes NHEJ repair by poly(ADP-ribose)-induced liquid demixing. We study how biomolecular condensates regulate genome integrity in neurons.
Learn more →LC3B drives transcription-associated homologous recombination via direct interaction with R-loops — linking autophagy machinery to DNA repair.
Learn more →Recent work from the NGI Lab.