ArticleHuman molecular genetics2011
Striatal neurons expressing full-length mutant huntingtin exhibit decreased N-cadherin and altered neuritogenesis.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- A small-molecule stabilizer of the calpastatin-calpain-2 complex restores mitochondrial function and mitigates neurodegeneration.Science advances · 2026Article
- N-cadherin facilitates trigeminal sensory neuron outgrowth and target tissue innervation.Development (Cambridge, England) · 2025Article
- Nuclear proteasomes buffer cytoplasmic proteins during autophagy compromise.Nature cell biology · 2024Article
- Article
- CAG repeat expansion in the Huntington's disease gene shapes linear and circular RNAs biogenesis.PLoS genetics · 2023Article
- Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.Matrix biology plus · 2021Review
- Altered microRNA expression in animal models of Huntington's disease and potential therapeutic strategies.Neural regeneration research · 2021Review
- Innovative Therapeutic Approaches for Huntington's Disease: From Nucleic Acids to GPCR-Targeting Small Molecules.Frontiers in cellular neuroscience · 2021Review
- mGluR5 regulates REST/NRSF signaling through N-cadherin/β-catenin complex in Huntington's disease.Molecular brain · 2020Article
- The long non-coding RNA NEAT1 is elevated in polyglutamine repeat expansion diseases and protects from disease gene-dependent toxicities.Human molecular genetics · 2018Article
- A patient-derived cellular model for Huntington's disease reveals phenotypes at clinically relevant CAG lengths.Molecular biology of the cell · 2018Article
- Huntington Disease as a Neurodevelopmental Disorder and Early Signs of the Disease in Stem Cells.Molecular neurobiology · 2018Review
- Cancer: From Wild-Type to Mutant Huntingtin.Journal of Huntington's disease · 2018Review
- Reduced cell size, chromosomal aberration and altered proliferation rates are characteristics and confounding factors in the STHdh cell model of Huntington disease.Scientific reports · 2017Article
- The Ubiquitin Receptor ADRM1 Modulates HAP40-Induced Proteasome Activity.Molecular neurobiology · 2017Article
- Network analysis of human post-mortem microarrays reveals novel genes, microRNAs, and mechanistic scenarios of potential importance in fighting huntington's disease.Computational and structural biotechnology journal · 2016Article
- Genomic Analysis Reveals Disruption of Striatal Neuronal Development and Therapeutic Targets in Human Huntington's Disease Neural Stem Cells.Stem cell reports · 2015Article
- Mutant huntingtin impairs immune cell migration in Huntington disease.The Journal of clinical investigation · 2012Article
- Induced pluripotent stem cells from patients with Huntington's disease show CAG-repeat-expansion-associated phenotypes.Cell stem cell · 2012Article
- Genetic correction of Huntington's disease phenotypes in induced pluripotent stem cells.Cell stem cell · 2012Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
The expanded CAG repeat that causes striatal cell vulnerability in Huntington's disease (HD) encodes a polyglutamine tract in full-length huntingtin that is correlated with cellular [ATP] and [ATP/ADP]. Since striatal neurons are vulnerable to energy deficit, we have investigated, in Hdh CAG knock-in mice and striatal cells, the hypothesis that decreased energetics may affect neuronal (N)-cadherin, a candidate energy-sensitive adhesion protein that may contribute to HD striatal cell sensitivity. In vivo, N-cadherin was sensitive to ischemia and to the effects of full-length mutant huntingtin, progressively decreasing in Hdh(Q111) striatum with age. In cultured striatal cells, N-cadherin was decreased by ATP depletion and STHdh(Q111) striatal cells exhibited dramatically decreased N-cadherin, due to decreased Cdh2 mRNA and enhanced N-cadherin turnover, which was partially normalized by adenine supplementation to increase [ATP] and [ATP/ADP]. Consistent with decreased N-cadherin function, STHdh(Q111) striatal cells displayed profound deficits in calcium-dependent N-cadherin-mediated cell clustering and cell-substratum adhesion, and primary Hdh(Q111) striatal neuronal cells exhibited decreased N-cadherin and an abundance of immature neurites, featuring diffuse, rather than clustered, staining for N-cadherin and synaptic vesicle markers, which was partially rescued by adenine treatment. Thus, mutant full-length huntingtin, via energetic deficit, contributes to decreased N-cadherin levels in striatal neurons, with detrimental effects on neurite maturation, strongly suggesting that N-cadherin-mediated signaling merits investigation early in the HD pathogenic disease process.
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