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

Targeted deletion of betaIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes.

Proceedings of the National Academy of Sciences of the United States of America - 30 Mar 2010

Stankewich Michael C, Gwynn Babette, Ardito Thomas, Ji Lan, Kim Jung, Robledo Raymond F, Lux Samuel E, Peters Luanne L, Morrow Jon S

Abstract excerpt

The spectrin membrane skeleton controls the disposition of selected membrane channels, receptors, and transporters. In the brain betaIII spectrin binds directly to the excitatory amino acid transporter (EAAT4), the glutamate receptor delta, and other proteins. Mutations in betaIII spectrin link strongly to human spinocerebellar ataxia type 5 (SCA5), correlating with alterations in EAAT4. We have explored the...

Read the complete abstract on PubMed

Topics

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

Share to Ataxia
Share to Gene Targeting

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Microscopy, Electron, Transmission

Share to Nerve Degeneration

Share to Seizures

Share to Spectrin

Share to Spinocerebellar Ataxias

Share to Synapses

Source

Open in PubMed Open full text

Identifiers

PMID: 20231455
DOI: 10.1073/pnas.1001522107
PMCID: PMC2851889

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeted deletion of betaIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes.PMID 20231455Read ↗

Cerebellar ataxias: β-III spectrin's interactions suggest common pathogenic pathways.Semantic proximity Read ↗

Impaired motor activity in a CRISPR SCA5 L253P knock-in mouse is associated with selective β-III-spectrin subcellular redistribution in the cerebellumSemantic proximity Read ↗

Loss of β-III Spectrin Leads to Purkinje Cell Dysfunction Recapitulating the Behavior and Neuropathology of Spinocerebellar Ataxia Type 5 in HumansSemantic proximity Read ↗

β-III Spectrin Is Critical for Development of Purkinje Cell Dendritic Tree and Spine MorphogenesisSemantic proximity Read ↗

Mutant β-III spectrin causes mGluR1α mislocalization and functional deficits in a mouse model of spinocerebellar ataxia type 5.Semantic proximity Read ↗

Posterior cerebellar Purkinje cells in an SCA5/SPARCA1 mouse model are especially vulnerable to the synergistic effect of loss of β-III spectrin and GLAST.Semantic proximity Read ↗

β-III spectrin underpins ankyrin R function in Purkinje cell dendritic trees: protein complex critical for sodium channel activity is impaired by SCA5-associated mutations.Semantic proximity Read ↗

Critical roles of αII spectrin in brain development and epileptic encephalopathy.Semantic proximity Read ↗

Spectrins: molecular organizers and targets of neurological disordersSemantic proximity Read ↗

Spinocerebellar ataxia type 5.Semantic proximity Read ↗

Drosophila alpha- and beta-spectrin mutations disrupt presynaptic neurotransmitter release.Semantic proximity Read ↗

Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3Semantic proximity Read ↗

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