Andrew T. Ferenbach

This study investigates OGA inhibition as a potential therapy for OGT-CDG by creating a mouse model and showing partial restoration of O-GlcNAc homeostasis.

This study presents multi-domain OGA structures from Trichoplax adhaerens and human, revealing allosteric regulatory mechanisms involving the pHAT domain.

This paper introduces a triple fluorescence stem cell sorting approach to measure O-GlcNAc dyshomeostasis and demonstrates its utility for high-throughput screening.

The paper identifies O-GlcNAcylation of DDX3X as a regulator of the G1/S-phase transition and shows its role in cell cycle control and neurogenesis in OGT-CDG.

This study identifies synaptogenesis and sleep stability defects in a Drosophila model of OGT intellectual disability and shows partial rescue by modulating OGA activity.

This paper describes mouse models with OGT mutations that exhibit neurodevelopmental defects, including microcephaly and cognitive impairments, to study OGT-CDG mechanisms and potential treatments.

This study investigates OGT-CDG using stem cells, finding disrupted O-GlcNAc homeostasis and morphology during neuroectoderm differentiation but preserved stemness and differentiation potential.

The paper shows that an OGT variant causes reduced pluripotent stem cell self-renewal and lower stem cell marker levels in mouse embryonic stem cells.

This study shows that OGT mutations impair cognitive function in Drosophila by disrupting O-GlcNAcylation, and that blocking OGA can correct the deficit.