Uncovering a Role for SK2 in Angelman Syndrome

Sofia B Lizarraga; Eric M Morrow

doi:10.1016/j.celrep.2015.07.009

Uncovering a Role for SK2 in Angelman Syndrome

Cell Rep. 2015 Jul 21;12(3):359-60. doi: 10.1016/j.celrep.2015.07.009.

Authors

Sofia B Lizarraga¹, Eric M Morrow²

Affiliations

¹ Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA; Center for Childhood Neurotherapeutics, University of South Carolina, Columbia SC 29208, USA. Electronic address: lizarras@mailbox.sc.edu.
² Department of Molecular Biology, Cell Biology and Biochemistry, Brown Institute for Brain Science and Laboratories for Molecular Medicine, Brown University, 70 Ship Street, Providence, RI 02912, USA; Developmental Disorders Genetics Research Program, Emma Pendleton Bradley Hospital, 1011 Veterans Memorial Parkway, East Providence, RI 02912, USA; Department of Psychiatry and Human Behavior, Alpert Medical School, Brown University, Providence, RI 02912, USA. Electronic address: eric_morrow@brown.edu.

PMID: 26200312
DOI: 10.1016/j.celrep.2015.07.009

Abstract

Angelman syndrome is a severe neurodevelopmental disorder caused by mutations in UBE3A. Sun et al. (2015) report SK2 as a UBE3A substrate and provide insight into the molecular mechanisms that might underlie impaired neuronal function in individuals affected by Angelman syndrome.

Publication types

Comment

MeSH terms

Animals
Learning / physiology*
Male
Memory / physiology*
Neuronal Plasticity / physiology*
Small-Conductance Calcium-Activated Potassium Channels / metabolism*
Ubiquitin-Protein Ligases / physiology*

Substances

Small-Conductance Calcium-Activated Potassium Channels
Ubiquitin-Protein Ligases