ArticleEMBO molecular medicine2021
Neuron type-specific increase in lamin B1 contributes to nuclear dysfunction in Huntington's disease.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- A sub-set of guanine- and cytosine-rich genes are actively transcribed at the nuclear lamin B1 region.Cellular and molecular life sciences : CMLS · 2026Article
- Zinc finger protein Zfp335 is required for T cell homeostatic proliferation through regulating Lmnb1.Cell & bioscience · 2025Article
- Sertraline treatment prevents motor dysfunction in a Huntington's disease mouse model and functional decline in patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Huntingtin reduction results in altered nuclear structure and heterochromatic instability.Human molecular genetics · 2025Article
- Interventionally targeting somatic CAG expansions can be a rapid disease-modifying therapeutic avenue: Preclinical evidence.bioRxiv : the preprint server for biology · 2025Article
- Identifying G-quadruplex-interacting proteins in cancer-related gene promoters.Communications chemistry · 2025Article
- Beneficial Antioxidant Effects of Coenzyme Q10 in In Vitro and In Vivo Models of CDKL5 Deficiency Disorder.International journal of molecular sciences · 2025Article
- The nuclear envelope and nuclear pore complexes in neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
- Nuclear poly-glutamine aggregates rupture the nuclear envelope and hinder its repair.The Journal of cell biology · 2024Article
- Manipulation of the nuclear envelope-associated protein SLAP during mammalian brain development affects cortical lamination and exploratory behavior.Biology open · 2024Article
- Lamin B1 overexpression alters chromatin organization and gene expression.Nucleus (Austin, Tex.) · 2023Article
- Reevaluating the cause of laminopathy in Alzheimer's disease.Neural regeneration research · 2023Article
- Age-associated reduction of nuclear shape dynamics in excitatory neurons of the visual cortex.Aging cell · 2023Article
- Integration of nuclear CaCellular and molecular life sciences : CMLS · 2023Article
- Functional Characterisation of the Circular RNA,Cells · 2023Article
- Review
- Lamin B1 and nuclear morphology in peripheral cells as new potential biomarkers to follow treatment response in Huntington's disease.Clinical and translational medicine · 2023Article
- Region-specific heterogeneity in neuronal nuclear morphology in young, aged and in Alzheimer's disease mouse brains.Frontiers in cell and developmental biology · 2023Article
- Mechanism and Therapeutic Prospect of miRNAs in Neurodegenerative Diseases.Behavioural neurology · 2023Review
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Lamins are crucial proteins for nuclear functionality. Here, we provide new evidence showing that increased lamin B1 levels contribute to the pathophysiology of Huntington's disease (HD), a CAG repeat-associated neurodegenerative disorder. Through fluorescence-activated nuclear suspension imaging, we show that nucleus from striatal medium-sized spiny and CA1 hippocampal neurons display increased lamin B1 levels, in correlation with altered nuclear morphology and nucleocytoplasmic transport disruption. Moreover, ChIP-sequencing analysis shows an alteration of lamin-associated chromatin domains in hippocampal nuclei, accompanied by changes in chromatin accessibility and transcriptional dysregulation. Supporting lamin B1 alterations as a causal role in mutant huntingtin-mediated neurodegeneration, pharmacological normalization of lamin B1 levels in the hippocampus of the R6/1 mouse model of HD by betulinic acid administration restored nuclear homeostasis and prevented motor and cognitive dysfunction. Collectively, our work points increased lamin B1 levels as a new pathogenic mechanism in HD and provides a novel target for its intervention.
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