ReviewNucleus (Austin, Tex.)2016
Lamin B1 mediated demyelination: Linking Lamins, Lipids and Leukodystrophies.
Review in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- LMNB1 reduction is a potential therapeutic strategy in a mouse model of autosomal dominant leukodystrophy.JCI insight · 2026Article
- A high throughput, high content screen for non-toxic small molecules that reduce levels of the nuclear lamina protein, Lamin B1.Scientific reports · 2025Article
- An oligodendrocyte silencer element underlies the pathogenic impact of lamin B1 structural variants.Nature communications · 2025Article
- Case report:Frontiers in neuroscience · 2025Article
- Understanding the Ultra-Rare Disease Autosomal Dominant Leukodystrophy: an Updated Review on Morpho-Functional Alterations Found in Experimental Models.Molecular neurobiology · 2023Review
- The stability of the myelinating oligodendrocyte transcriptome is regulated by the nuclear lamina.Cell reports · 2023Article
- Dodecyl creatine ester improves cognitive function and identifies key protein drivers including KIF1A and PLCB1 in a mouse model of creatine transporter deficiency.Frontiers in molecular neuroscience · 2023Article
- Article
- Disease Modeling with Human Neurons Reveals LMNB1 Dysregulation Underlying DYT1 Dystonia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Cell signaling pathways in autosomal-dominant leukodystrophy (ADLD): the intriguing role of the astrocytes.Cellular and molecular life sciences : CMLS · 2021Article
- Dynamic Lamin B1-Gene Association During Oligodendrocyte Progenitor Differentiation.Neurochemical research · 2020Article
- Differential Expression of LaminB1 in the Developing Rat Cochlea.The journal of international advanced otology · 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
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Autosomal Dominant Leukodystrophy (ADLD), a fatal adult onset demyelinating disorder, is the only human disease that has been linked to mutations of the nuclear lamina protein, lamin B1, and is primarily caused by duplications of the LMNB1 gene. Why CNS myelin is specifically targeted and the mechanisms underlying ADLD are unclear. Recent work from our group has demonstrated that over expression of lamin B1 in oligodendrocytes, the myelin producing cells in the CNS, resulted in age dependent epigenetic modifications, transcriptional down-regulation of lipogenic gene expression and significant reductions of myelin-enriched lipids. Given the high lipid content of meylin, we hypothesize that lipid loss is one of the primary drivers of the demyelination phenotype. These results can, at least partially, explain the age dependence and cell type specificity in ADLD and are discussed in the context of the existing literature, in an attempt to delineate potential pathways underlying the disease phenotype.
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What OpenQuestion holds
Registered trials
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.