Regulation of Cav2.1 by Ankyrin B and its variants

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dc.contributor.authorChoi, Catherine S.W.
dc.contributor.supervisorSwayne, Leigh Anne
dc.date.accessioned2019-08-20T00:07:51Z
dc.date.copyright2019en_US
dc.date.issued2019-08-19
dc.degree.departmentProgram: Neuroscienceen_US
dc.degree.levelMaster of Science M.Sc.en_US
dc.description.abstractAnkyrin B (AnkB) is a scaffolding protein, acting as a bridge between ion channels and cytoskeleton networks. AnkB variants are associated with cognitive disorders including autism spectrum disorder and epilepsy. In the brain, AnkB interacts with Cav2.1, the pore-forming subunit of P/Q type voltage gated calcium channels. However, how AnkB regulates Cav2.1 is not fully understood. Using HEK293T cells, we discovered that AnkB increases Cav2.1 expression levels but does not change Cav2.1 surface levels. AnkB p.S646F increases Cav2.1 to an even greater level of expression, again without impacting Cav2.1 surface levels. Looking at a partial loss of AnkB in glutamatergic neurons, overall Cav2.1 levels decreased at P30 but the synaptosomal fraction was not impacted. Our findings indicate that AnkB plays a role in regulating an intracellular pool of Cav2.1 but does not affect the surface or the synaptosomal pools of Cav2.1. This intracellular pool of Cav2.1 may play an important role in neuronal function and homeostasis, suggesting a mechanism for neuronal pathogenicity of AnkB variants.en_US
dc.description.embargo2020-08-06
dc.description.scholarlevelGraduateen_US
dc.identifier.urihttp://hdl.handle.net/1828/11053
dc.languageEnglisheng
dc.language.isoenen_US
dc.rightsAvailable to the World Wide Weben_US
dc.subjectAnkyrin Ben_US
dc.subjectCav2.1en_US
dc.subjectCACNA1Aen_US
dc.subjectintracellular poolen_US
dc.subjectsurface localizationen_US
dc.subjectsynapseen_US
dc.titleRegulation of Cav2.1 by Ankyrin B and its variantsen_US
dc.typeThesisen_US

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