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

Genetically modified rodent models of SCA17.

Journal of neuroscience research - 1 Aug 2017

Cui Yiting, Yang Su, Li Xiao-Jiang, Li Shihua

Abstract excerpt

Spinocerebellar ataxia type 17 (SCA17) is a type of autosomal dominant cerebellar ataxia (ADCA) characterized by variable manifestations, including cerebellar ataxia, dementia, and psychiatric symptoms. Since the identification of a CAG repeat expansion in the TATA-box binding protein (TBP) gene in a patient with ataxia in 1999 and then verification of this expansion in patients with SCA17 in 2001, several SCA17...

Read the complete abstract on PubMed

Topics

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

Share to Animals, Genetically Modified
Share to Disease Models, Animal
Share to TBP gene

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Phenotype

Share to Rodentia

Share to Spinocerebellar Ataxias

Share to TATA-Box Binding Protein

Share to Trinucleotide Repeats

Source

Open in PubMed Open full text

Identifiers

PMID: 27859490
DOI: 10.1002/jnr.23984
PMCID: PMC5508981

Genes

TBP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetically modified rodent models of SCA17.PMID 27859490Read ↗

A novel transgenic rat model for spinocerebellar ataxia type 17 recapitulates neuropathological changes and supplies in vivo imaging biomarkers.Semantic proximity Read ↗

Neuroprotective effects of granulocyte-colony stimulating factor in a novel transgenic mouse model of SCA17.Semantic proximity Read ↗

Phenotypic defects from the expression of wild-type and pathogenic TATA-Binding Proteins in new <i>Drosophila</i> models of Spinocerebellar Ataxia Type 17Semantic proximity Read ↗

SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein.Semantic proximity Read ↗

Spinocerebellar ataxia type 17 is caused by mutations in the TATA-box binding protein.Semantic proximity Read ↗

An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disordersSemantic proximity Read ↗

Practical considerations of genetic rodent models for neurodegenerative diseases.Semantic proximity Read ↗

ERK activation precedes Purkinje cell loss in mice with Spinocerebellar ataxia type 17.Semantic proximity Read ↗

The SCA17 phenotype can include features of MSA-C, PSP and cognitive impairment.Semantic proximity Read ↗

A transgenic model of a familial prion disease.Semantic proximity Read ↗

An overview on the generation of BAC transgenic mice for neuroscience research.Semantic proximity Read ↗

Age-dependent decrease in chaperone activity impairs MANF expression, leading to Purkinje cell degeneration in inducible SCA17 mice.Semantic proximity Read ↗

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