Mouse models of Angelman syndrome, a neurodevelopmental disorder, display different brain regional GABA A receptor alterations

Angelman syndrome is a severe neurodevelopmental disorder with cognitive impairment and neurological deficits. It results from a maternal deletion of human chromosome 15q11–13 containing two candidate genes E6–P ubiquitin-protein ligase (UBE3A) and GABA A receptor β3 subunit (GABRB3), the latter of...

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Veröffentlicht in:	Neuroscience letters 2003-04, Vol.340 (3), p.205-208
Hauptverfasser:	Sinkkonen, S.T, Homanics, G.E, Korpi, E.R
Format:	Artikel
Sprache:	eng
Schlagworte:	Angelman syndrome Angelman Syndrome - genetics Angelman Syndrome - metabolism Animals Brain - metabolism Disease Models, Animal E6–P ubiquitin-protein ligase gene Female Knockout mice Ligand autoradiography Ligases - deficiency Ligases - genetics Ligases - metabolism Male Mice Mice, Mutant Strains Protein Binding - physiology Receptors, GABA-A - deficiency Receptors, GABA-A - genetics Receptors, GABA-A - metabolism Ubiquitin-Protein Ligases γ-aminobutyric acid type A receptor γ-aminobutyric acid type β3
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