Molecular Neurobiology Laboratory

On the other hand, we aimed to understand molecular processes underlying neurological disorders and established their genetic models ranging from Drosophila to human patient-derived neurons. Importantly, we expanded our original research on the ATAXIN-2 protein complex for circadian translation to ATAXIN-2 relevant neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS; also known as Lou Gehrig’s disease). It led to our discovery of the novel molecular machinery that protects ALS patients’ neurons from degeneration. In particular, we demonstrated that ALS-causing proteins induce ribosomal stalling during their translation and a dedicated pathway called ribosome-associated quality control (RQC) co-translationally triages the neurodegenerative translation intermediates. Equipped with broad ranges of research expertise and experimental models, we are uniquely positioned in the field. Our findings will have a high impact on science and clear implications for developing therapeutic strategies, given their strong relevance to neurological disorders and aging in humans.