ArticleMolecular biology of the cell2016
Lamin B1 protein is required for dendrite development in primary mouse cortical neurons.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- The Influence of Short Peptides on Cell Senescence and Neuronal Differentiation.Current issues in molecular biology · 2025Article
- Rapid and high-purity differentiation of human medium spiny neurons reveals LMNB1 hypofunction and subtype necessity in modeling Huntington's disease.Inflammation and regeneration · 2024Article
- Understanding the Ultra-Rare Disease Autosomal Dominant Leukodystrophy: an Updated Review on Morpho-Functional Alterations Found in Experimental Models.Molecular neurobiology · 2023Review
- Dose imbalance of DYRK1A kinase causes systemic progeroid status in Down syndrome by increasing the un-repaired DNA damage and reducing LaminB1 levels.EBioMedicine · 2023Article
- Decoding degeneration: the implementation of machine learning for clinical detection of neurodegenerative disorders.Neural regeneration research · 2023Review
- Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023Review
- From cradle to grave: neurogenesis, neuroregeneration and neurodegeneration in Alzheimer's and Parkinson's diseases.Neural regeneration research · 2022Review
- The wide and growing range of lamin B-related diseases: from laminopathies to cancer.Cellular and molecular life sciences : CMLS · 2022Review
- Age-dependent changes in nuclear-cytoplasmic signaling in skeletal muscle.Experimental gerontology · 2021Article
- Cell signaling pathways in autosomal-dominant leukodystrophy (ADLD): the intriguing role of the astrocytes.Cellular and molecular life sciences : CMLS · 2021Article
- The Nucleoskeleton: Crossroad of Mechanotransduction in Skeletal Muscle.Frontiers in physiology · 2021Review
- De Novo Variants in LMNB1 Cause Pronounced Syndromic Microcephaly and Disruption of Nuclear Envelope Integrity.American journal of human genetics · 2020Article
- Homogenous generation of dopaminergic neurons from multiple hiPSC lines by transient expression of transcription factors.Cell death & disease · 2019Article
- In vivo epigenetic editing of Sema6a promoter reverses transcallosal dysconnectivity caused by C11orf46/Arl14ep risk gene.Nature communications · 2019Article
- Glucose metabolism in the brain in LMNB1-related autosomal dominant leukodystrophy.Acta neurologica Scandinavica · 2019Article
- LMNB1-Related Adult-Onset Autosomal Dominant Leukodystrophy Presenting as Movement Disorder: A Case Report and Review of the Literature.Frontiers in neuroscience · 2019Article
- Autosomal Dominant Leukodystrophy: A Disease of the Nuclear Lamina.Frontiers in cell and developmental biology · 2019Review
- A new TAO kinase inhibitor reduces tau phosphorylation at sites associated with neurodegeneration in human tauopathies.Acta neuropathologica communications · 2018Article
- Mice overexpressing lamin B1 in oligodendrocytes recapitulate the age-dependent motor signs, but not the early autonomic cardiovascular dysfunction of autosomal-dominant leukodystrophy (ADLD).Experimental neurology · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Lamin B1, a key component of the nuclear lamina, plays an important role in brain development and function. A duplication of the human lamin B1 (LMNB1) gene has been linked to adult-onset autosomal dominant leukodystrophy, and mouse and human loss-of-function mutations in lamin B1 are susceptibility factors for neural tube defects. In the mouse, experimental ablation of endogenous lamin B1 (Lmnb1) severely impairs embryonic corticogenesis. Here we report that in primary mouse cortical neurons, LMNB1 overexpression reduces axonal outgrowth, whereas deficiency of endogenous Lmnb1 results in aberrant dendritic development. In the absence of Lmnb1, both the length and complexity of dendrites are reduced, and their growth is unresponsive to KCl stimulation. This defective dendritic outgrowth stems from impaired ERK signaling. In Lmnb1-null neurons, ERK is correctly phosphorylated, but phospho-ERK fails to translocate to the nucleus, possibly due to delocalization of nuclear pore complexes (NPCs) at the nuclear envelope. Taken together, these data highlight a previously unrecognized role of lamin B1 in dendrite development of mouse cortical neurons through regulation of nuclear shuttling of specific signaling molecules and NPC distribution.
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