ArticleHuman molecular genetics2010
The Huntington's disease mutation impairs Huntingtin's role in the transport of NF-κB from the synapse to the nucleus.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 92 citations in OpenAlex.
- Identification of Age-Associated Upstream Regulators to Promote Neuronal Resilience in HD Patient-Derived Neurons.Neuroscience bulletin · 2026Article
- Network-based stratification of allele-specific expression reveals patient subgroups in Huntington's disease.Bioinformatics (Oxford, England) · 2026Article
- Exploration of the genetic neuroinflammatory environment in the human midcingulate cortex in Huntington's disease.Communications medicine · 2026Article
- Decoding Non-Neuronal Mechanisms and Therapeutic Targets in Huntington's Disease Through Integrative Transcriptomics and Machine Learning.Journal of molecular neuroscience : MN · 2026Article
- Huntingtin reduction results in altered nuclear structure and heterochromatic instability.Human molecular genetics · 2025Article
- Protein kinases in neurodegenerative diseases: current understandings and implications for drug discovery.Signal transduction and targeted therapy · 2025Review
- Pathophysiological role of high mobility group box-1 signaling in neurodegenerative diseases.Inflammopharmacology · 2025Review
- RNA-Targeting CRISPR/CasRx system relieves disease symptoms in Huntington's disease models.Molecular neurodegeneration · 2025Article
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- The regulating effect of curcumin on NF-κB pathway in neurodegenerative diseases: a review of the underlying mechanisms.Inflammopharmacology · 2024Review
- Revisiting the Mitochondrial Function and Communication in Neurodegenerative Diseases.Current pharmaceutical design · 2024Review
- Research advances in huntingtin-associated protein 1 and its application prospects in diseases.Frontiers in neuroscience · 2024Review
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- The Emerging Landscape of Natural Small-molecule Therapeutics for Huntington's Disease.Current neuropharmacology · 2023Review
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Synaptic and functional alterations in the development of mutant huntingtin expressing hiPSC-derived neurons.Frontiers in molecular biosciences · 2022Article
- Adaptor protein APPL1 links neuronal activity to chromatin remodeling in cultured hippocampal neurons.Journal of molecular cell biology · 2021Article
- Overexpression of the ubiquitin-editing enzyme A20 in the brain lesions of Multiple Sclerosis patients: moving from systemic to central nervous system inflammation.Brain pathology (Zurich, Switzerland) · 2021Article
- Mislocalization of Nucleocytoplasmic Transport Proteins in Human Huntington's Disease PSC-Derived Striatal Neurons.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Expansion of a polyglutamine (polyQ) tract in the Huntingtin (Htt) protein causes Huntington's disease (HD), a fatal inherited neurodegenerative disorder. Loss of the normal function of Htt is thought to be an important pathogenetic component of HD. However, the function of wild-type Htt is not well defined. Htt is thought to be a multifunctional protein that plays distinct roles in several biological processes, including synaptic transmission, intracellular transport and neuronal transcription. Here, we show with biochemical and live cell imaging studies that wild-type Htt stimulates the transport of nuclear factor κ light-chain-enhancer of activated B cells (NF-κB) out of dendritic spines (where NF-κB is activated by excitatory synaptic input) and supports a high level of active NF-κB in neuronal nuclei (where NF-κB stimulates the transcription of target genes). We show that this novel function of Htt is impaired by the polyQ expansion and thus may contribute to the etiology of HD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.