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

N-type Ca2+ channels are affected by full-length mutant huntingtin expression in a mouse model of Huntington's disease.

Neurobiology of aging - 1 Jul 2017

Silva Flavia R, Miranda Artur S, Santos Rebeca P M, Olmo Isabella G, Zamponi Gerald W, Dobransky Tomas, Cruz Jader S, Vieira Luciene B, Ribeiro Fabiola M

Abstract excerpt

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a polyglutamine expansion in the amino-terminal region of the huntingtin (htt) protein. In addition to facilitating neurodegeneration, mutant htt is implicated in HD-related alterations of neurotransmission. Previous data showed that htt can modulate N-type voltage-gated Ca2+ channels (Cav2.2), which are essential for...

Read the complete abstract on PubMed

Topics

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

Share to Calcium Channels, N-Type
Share to Glutamates

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Huntingtin Protein

Share to Huntington Disease

Share to Neurotransmitter Agents

Share to Synapses

Share to Synaptic Transmission

Share to Syntaxin 1

Source

Identifiers

PMID: 28391067
DOI: 10.1016/j.neurobiolaging.2017.03.015

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

N-type Ca2+ channels are affected by full-length mutant huntingtin expression in a mouse model of Huntington's disease.PMID 28391067Read ↗

Alterations of Calcium Channels in a Mouse Model of Huntington’s Disease and Neuroprotection by Blockage of Ca V 1 ChannelsSemantic proximity Read ↗

Mutant Huntingtin Causes a Selective Decrease in the Expression of Synaptic Vesicle Protein 2C.Semantic proximity Read ↗

Expression of a modified astrocytic glutamate transporter alleviates Huntington’s hypokinesia, promotes synaptic glutamate clearance and counteracts potentially adverse EAAT2 interactionsSemantic proximity Read ↗

Huntington's disease and Group I metabotropic glutamate receptors.Semantic proximity Read ↗

Altered NMDA Receptor Trafficking in a Yeast Artificial Chromosome Transgenic Mouse Model of Huntington's DiseaseSemantic proximity Read ↗

Huntingtin is essential for synaptic plasticity in the adult hippocampusSemantic proximity Read ↗

Control of Huntington's Disease-Associated Phenotypes by the Striatum-Enriched Transcription Factor Foxp2.Semantic proximity Read ↗

Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm.Semantic proximity Read ↗

Neuronal targets for reducing mutant huntingtin expression to ameliorate disease in a mouse model of Huntington's disease.Semantic proximity Read ↗

Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 miceSemantic proximity Read ↗

Role of NR2B-type NMDA receptors in selective neurodegeneration in Huntington disease.Semantic proximity Read ↗

Enhanced Ca(2+)-dependent glutamate release from astrocytes of the BACHD Huntington's disease mouse model.Semantic proximity Read ↗

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