Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Functional effects of spinocerebellar ataxia type 13 mutations are conserved in zebrafish Kv3.3 channels.

BMC neuroscience - 16 Aug 2010

Mock Allan F, Richardson Jessica L, Hsieh Jui-Yi, Rinetti Gina, Papazian Diane M

Abstract excerpt

BACKGROUND: The zebrafish has been suggested as a model system for studying human diseases that affect nervous system function and motor output. However, few of the ion channels that control neuronal activity in zebrafish have been characterized. Here, we have identified zebrafish orthologs of vo...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromosomes
Share to Cloning, Molecular
Share to Conserved Sequence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Electrophysiology

Share to Mutagenesis

Share to Spinocerebellar Ataxias

Share to Zebrafish

Share to Zebrafish Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 20712895
DOI: 10.1186/1471-2202-11-99
PMCID: PMC2933717

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20712895-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Functional effects of spinocerebellar ataxia type 13 mutations are conserved in zebrafish Kv3.3 channels.PMID 20712895Read ↗

Spinocerebellar ataxia type 13 mutant potassium channel alters neuronal excitability and causes locomotor deficits in zebrafish.Semantic proximity Read ↗

Sca13.Semantic proximity Read ↗

Mutations in voltage-gated potassium channel KCNC3 cause degenerative and developmental central nervous system phenotypes.Semantic proximity Read ↗

Novel KCND3 Variant Underlying Nonprogressive Congenital Ataxia or SCA19/22 Disrupt KV4.3 Protein Expression and K+ Currents with Variable Effects on Channel Properties.Semantic proximity Read ↗

Altered Kv3.3 channel gating in early-onset spinocerebellar ataxia type 13.Semantic proximity Read ↗

First de novo KCND3 mutation causes severe Kv4.3 channel dysfunction leading to early onset cerebellar ataxia, intellectual disability, oral apraxia and epilepsySemantic proximity Read ↗

Infant and adult SCA13 mutations differentially affect Purkinje cell excitability, maturation, and viability in vivo.Semantic proximity Read ↗

Structure and Function of Sodium Channel Nav1.3 in Neurological Disorders.Semantic proximity Read ↗

C-terminal proline deletions in KCNC3 cause delayed channel inactivation and an adult-onset progressive SCA13 with spasticity.Semantic proximity Read ↗

Kv3 Channels: Enablers of Rapid Firing, Neurotransmitter Release, and Neuronal EnduranceSemantic proximity Read ↗

An E280K Missense Variant in KCND3/Kv4.3-Case Report and Functional Characterization.Semantic proximity Read ↗

The role of individual subunits in the formation and function of presynaptic Kv3 potassium channelsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.