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Matthew C. Judson

University of North Carolina at Chapel Hill

18

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789

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Dual-isoform hUBE3A gene transfer improves behavioral and seizure outcomes in Angelman syndrome model mice.

2021 JCI insight
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Delayed loss of UBE3A reduces the expression of Angelman syndrome-associated phenotypes

2019 Molecular Autism
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Subcellular organization of UBE3A in human cerebral cortex

2018 Molecular Autism
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Enhanced Operant Extinction and Prefrontal Excitability in a Mouse Model of Angelman Syndrome

2018 The Journal of Neuroscience
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Decreased axon caliber underlies loss of fiber tract integrity, disproportional reductions in white matter volume, and microcephaly in angelman syndrome model mice

2017 The Journal of Neuroscience
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Subcellular organization of UBE3A in neurons

2017 The Journal of Comparative Neurology
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Loss of UBE3A from TH-expressing neurons suppresses GABA co-release and enhances VTA-NAc optical self-stimulation

2016 Nature Communications
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Angelman syndrome (AS) is a severe neurological disorder that is associated with prominent movement and balance impairments that are widely considered to be due to defects of cerebellar origin. Here, using the cerebellar-specific vestibulo- ocular reflex (VOR) paradigm, we determined that cerebellar function is only mildly impaired in the Ube3a

2015
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Dissociation of locomotor and cerebellar deficits in a murine Angelman syndrome model

2015 Journal of Clinical Investigation
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Allelic Specificity of Ube3a Expression in the Mouse Brain during Postnatal Development

2014 The Journal of Comparative Neurology
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Citations (81)