Eric S. Levine

This study investigates the role of UBE3A in Dup15q syndrome using CRISPR-corrected patient-derived neurons, showing UBE3A overexpression is necessary for most neuronal deficits but not synaptic phenotypes.

This study shows that antisense oligonucleotides targeting UBE3A-ATS restore UBE3A expression by removing transcriptional interference in Angelman syndrome neurons.

The paper investigates the abundance and localization of human UBE3A protein isoforms and their impact on Angelman Syndrome phenotypes using CRISPR/Cas9-generated isogenic cells.

The paper investigates molecular differences in neural cultures derived from iPSCs with GRIK1 rs2832407 genotypes and their response to topiramate exposure.

The paper investigates the role of Kalirin-7 interactions with PSD-95 and GluN2B in synaptic plasticity using knockout mice and blocking peptides.

This study investigates hyperexcitability in iPSC-derived neurons from Dup15q patients, identifying mechanisms like delayed action potential maturation and KCNQ2 channel disruption.