ArticleIBRO reports2018
Differential expression of nuclear lamin subtypes in the neural cells of the adult rat cerebral cortex.
Article in IBRO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Synchronisation of apical constriction and cell cycle progression is a conserved behaviour of pseudostratified neuroepithelia informed by their tissue geometry.Developmental biology · 2023Article
- Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023Review
- Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases.Frontiers in pharmacology · 2022Review
- Multiscale Mechanobiology in Brain Physiology and Diseases.Frontiers in cell and developmental biology · 2022Review
- A geroscience motivated approach to treat Alzheimer's disease: Senolytics move to clinical trials.Mechanisms of ageing and development · 2021Review
- In Silico and In Vivo Analysis of Amino Acid Substitutions That Cause Laminopathies.International journal of molecular sciences · 2021Article
- A novel biallelicClinical case reports · 2021Article
- Mislocalization of Nucleocytoplasmic Transport Proteins in Human Huntington's Disease PSC-Derived Striatal Neurons.Frontiers in cellular neuroscience · 2021Article
- Review
- Perinuclear Lamin A and Nucleoplasmic Lamin B2 Characterize Two Types of Hippocampal Neurons through Alzheimer's Disease Progression.International journal of molecular sciences · 2020Article
- Dynamic Lamin B1-Gene Association During Oligodendrocyte Progenitor Differentiation.Neurochemical research · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamins are type V intermediate filament proteins that are located beneath the inner nuclear membrane. In mammalian somatic cells, LMNB1 and LMNB2 encode somatic lamins B1 and B2, respectively, and the LMNA gene is alternatively spliced to generate somatic lamins A and C. Mutations in lamin genes have been linked to many human hereditary diseases, including neurodegenerative disorders. Knowledge about lamins in the nervous system has been accumulated recently, but a precise analysis of lamin subtypes in glial cells has not yet been reported. In this study we investigated the composition of lamin subtypes in neurons, astrocytes, oligodendrocyte-lineage cells, and microglia in the adult rat cerebral cortex using an immunohistochemical staining method. Lamin A was not observed in neurons and glial cells. Lamin C was observed in astrocytes, mature oligodendrocytes and neurons, but not observed in oligodendrocyte progenitor cells. Microglia also did not stain positive for lamin C which differed from macrophages, with lamin C positive. Lamin B1 and B2 were observed in all glial cells and neurons. Lamin B1 was intensely positive in oligodendrocyte progenitor cells compared with other glial cells and neurons. Lamin B2 was weakly positive in all glial cells compared to neurons. Our current study might provide useful information to reveal how the onset mechanisms of human neurodegenerative diseases are associated with mutations in genes for nuclear lamin proteins.
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