ArticleMolecular and cellular biology2002
Interaction of Huntington disease protein with transcriptional activator Sp1.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed.
- Article
- Utility of the continuous spectrum formed by pathological states in characterizing disease properties.NPJ systems biology and applications · 2025Article
- Regulation ofInternational journal of molecular sciences · 2024Review
- Huntington's Disease: Complex Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Huntingtin Interacting Proteins and Pathological Implications.International journal of molecular sciences · 2023Review
- Huntingtin S421 phosphorylation increases kinesin and dynein engagement on early endosomes and lysosomes.Biophysical journal · 2023Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- Investigation of the Influence of TBP CAG/CAA Repeats in Conjunction with HTT CAG Repeats on Huntington's Disease Age at Onset in a Brazilian Sample.Journal of molecular neuroscience : MN · 2022Article
- Review
- Review
- MEF2 impairment underlies skeletal muscle atrophy in polyglutamine disease.Acta neuropathologica · 2020Article
- Phosphorylation of myelin regulatory factor by PRKG2 mediates demyelination in Huntington's disease.EMBO reports · 2020Article
- Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17.Nature communications · 2020Article
- The first year.Acta neuropathologica · 2020Article
- Transcriptional Assessment of Striatal mRNAs as Valid Biomarkers of Disease Progression in Three Mouse Models of Huntington's Disease.Journal of Huntington's disease · 2020Article
- Disruption of zinc transporter ZnT3 transcriptional activity and synaptic vesicular zinc in the brain of Huntington's disease transgenic mouse.Cell & bioscience · 2020Article
- Structural and functional features of medium spiny neurons in the BACHDΔN17 mouse model of Huntington's Disease.PloS one · 2020Article
- A protein quality control pathway regulated by linear ubiquitination.The EMBO journal · 2019Article
- Protein Co-Aggregation Related to Amyloids: Methods of Investigation, Diversity, and Classification.International journal of molecular sciences · 2018Review
- Review
61 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
Polyglutamine expansion causes Huntington disease (HD) and at least seven other neurodegenerative diseases. In HD, N-terminal fragments of huntingtin with an expanded glutamine tract are able to aggregate and accumulate in the nucleus. Although intranuclear huntingtin affects the expression of numerous genes, the mechanism of this nuclear effect is unknown. Here we report that huntingtin interacts with Sp1, a transcription factor that binds to GC-rich elements in certain promoters and activates transcription of the corresponding genes. In vitro binding and immunoprecipitation assays show that polyglutamine expansion enhances the interaction of N-terminal huntingtin with Sp1. In HD transgenic mice (R6/2) that express N-terminal-mutant huntingtin, Sp1 binds to the soluble form of mutant huntingtin but not to aggregated huntingtin. Mutant huntingtin inhibits the binding of nuclear Sp1 to the promoter of nerve growth factor receptor and suppresses its transcriptional activity in cultured cells. Overexpression of Sp1 reduces the cellular toxicity and neuritic extension defects caused by intranuclear mutant huntingtin. These findings suggest that the soluble form of mutant huntingtin in the nucleus may cause cellular dysfunction by binding to Sp1 and thus reducing the expression of Sp1-regulated genes.
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