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Antisense Oligonucleotide Therapy Targeted Against ATXN3 Improves Potassium Channel-Mediated Purkinje Neuron Dysfunction in Spinocerebellar Ataxia Type 3.

Cerebellum (London, England) - 1 Feb 2021

Bushart David D, Zalon Annie J, Zhang Hongjiu, Morrison Logan M, Guan Yuanfang, Paulson Henry L, Shakkottai Vikram G, McLoughlin Hayley S

Abstract excerpt

Spinocerebellar ataxia type 3 (SCA3) is the second-most common CAG repeat disease, caused by a glutamine-encoding expansion in the ATXN3 protein. SCA3 is characterized by spinocerebellar degeneration leading to progressive motor incoordination and early death. Previous studies suggest that potassium channel dysfunction underlies early abnormalities in cerebellar cortical Purkinje neuron firing in SCA3. However,...

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Share to Ataxin-3
Share to Behavior, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Injections, Intraventricular

Share to Machado-Joseph Disease

Share to Oligonucleotides, Antisense

Share to Patch-Clamp Techniques

Share to Potassium Channels, Voltage-Gated

Share to Purkinje Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 32789747
DOI: 10.1007/s12311-020-01179-7
PMCID: PMC7930886

Genes

ATXN3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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Antisense Oligonucleotide Therapy Targeted Against ATXN3 Improves Potassium Channel-Mediated Purkinje Neuron Dysfunction in Spinocerebellar Ataxia Type 3.PMID 32789747Read ↗

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