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

Transcriptional dysregulation of TrkA associates with neurodegeneration in spinocerebellar ataxia type 17.

Human molecular genetics - 1 Nov 2009

Shah Anjali G, Friedman Meyer J, Huang Shanshan, Roberts Meredith, Li Xiao-Jiang, Li Shihua

Abstract excerpt

TATA binding protein (TBP), a universal transcription factor, is broadly required by nuclear RNA polymerases for the initiation of transcription. TBP contains a polymorphic polyglutamine tract in its N-terminal region, and expansion of this tract leads to spinocerebellar ataxia type 17 (SCA17), one of nine dominantly inherited neurodegenerative diseases caused by polyglutamine expansion in the affected proteins....

Read the complete abstract on PubMed

Topics

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

Share to Nerve Degeneration
Share to Neurites

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to PC12 Cells

Share to Purkinje Cells

Share to Receptor, trkA

Share to Spinocerebellar Ataxias

Share to TATA-Box Binding Protein

Share to Trinucleotide Repeat Expansion

Source

Open in PubMed Open full text

Identifiers

PMID: 19643914
DOI: 10.1093/hmg/ddp363
PMCID: PMC2758144

Genes

TBP

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

Transcriptional dysregulation of TrkA associates with neurodegeneration in spinocerebellar ataxia type 17.PMID 19643914Read ↗

Deactivation of TBP contributes to SCA17 pathogenesis.Semantic 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 ↗

Activation of Gene Transcription by Heat Shock Protein 27 May Contribute to Its Neuronal ProtectionSemantic proximity Read ↗

Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration.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 ↗

Spinocerebellar ataxia 17 (SCA17) and Huntington's disease-like 4 (HDL4).Semantic proximity Read ↗

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

Molecular investigation of TBP allele length: a SCA17 cellular model and population study.Semantic proximity Read ↗

Molecular pathogenesis and cellular pathology of spinocerebellar ataxia type 7 neurodegeneration.Semantic proximity Read ↗

Genetically modified rodent models of SCA17.Semantic proximity Read ↗

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

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