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

Inclusion formation by ataxins -1, -2, -3, and -7.

The International journal of neuroscience - 1 Sept 2007

Tarlac Volga, Turnbull Victor, Stefani Daniela, Kelly Louise, Walsh Renae, Storey Elsdon

Abstract excerpt

The authors studied inclusion formation in vitro using transiently transfected PC12 cells, with epitope-tagged and untagged full-length and truncated wild-type and expanded ataxins -1, -2, -3, and -7. At 72 hours, no inclusions were seen with wild-type full-length or truncated ataxins -2, -3, or...

Read the complete abstract on PubMed

Topics

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

Share to Ataxin-1
Share to Ataxin-3
Share to Ataxin-7

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Ataxins

Share to Inclusion Bodies

Share to Nerve Tissue Proteins

Share to Nuclear Proteins

Share to PC12 Cells

Source

Identifiers

PMID: 17654093
DOI: 10.1080/00207450600936668

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17654093-2026-09-02.2. 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 · 8 closest

Inclusion formation by ataxins -1, -2, -3, and -7.PMID 17654093Read ↗

Similarities between spinocerebellar ataxia type 7 (SCA7) cell models and human brain: proteins recruited in inclusions and activation of caspase-3.Semantic proximity Read ↗

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death.Semantic proximity Read ↗

Differential degradation of full-length and cleaved ataxin-7 fragments in a novel stable inducible SCA7 model.Semantic proximity Read ↗

PML clastosomes prevent nuclear accumulation of mutant ataxin-7 and other polyglutamine proteins.Semantic proximity Read ↗

Expansion of the polyQ repeat in ataxin-2 alters its Golgi localization, disrupts the Golgi complex and causes cell death.Semantic proximity Read ↗

Time-lapse analysis of aggregate formation in an inducible PC12 cell model of Huntington's disease reveals time-dependent aggregate formation that transiently delays cell deathSemantic proximity Read ↗

Ataxin-2 mediated cell death is dependent on domains downstream of the polyQ repeat.Semantic proximity Read ↗

Adenovirus-mediated expression of mutant DRPLA proteins with expanded polyglutamine stretches in neuronally differentiated PC12 cells. Preferential intranuclear aggregate formation and apoptosis.Semantic proximity Read ↗

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