Soo‐Kyung Lee

This study shows that delivering FOXG1 to neurons via AAV vectors improves oligodendrocyte maturation, myelination, and hippocampal structure in mouse models of FOXG1 syndrome.

This study creates a patient-specific mouse model of FOXG1 syndrome and identifies disrupted protein homeostasis and neuroinflammation as key factors in the disorder's pathogenesis.

This study creates a patient-specific mouse model with a Foxg1 frameshift mutation to investigate FOXG1 syndrome, revealing cellular and behavioral phenotypes and the role of the mutant protein fragment.

This study shows that MLL4 is critical for midpalatal suture development and palate growth, with loss of MLL4 causing hypoplasia, widened suture, and disrupted cartilage development.