Liwen Li

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 p63 uses a skin keratinization mechanism for enamel organ development, revealing a shared pathway in tissue specialization.