ReviewFrontiers in cell and developmental biology2019
Autosomal Dominant Leukodystrophy: A Disease of the Nuclear Lamina.
Review in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- LMNB1 reduction is a potential therapeutic strategy in a mouse model of autosomal dominant leukodystrophy.JCI insight · 2026Article
- Clinical Practice Guidelines for the Diagnosis, Management, and Surveillance ofNeurology. Genetics · 2025Review
- 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
- Review
- Article
- Adult-onset autosomal dominant leukodystrophy and neuronal intranuclear inclusion disease: lessons from two new Chinese families.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Pan-cancer analysis identifies LMNB1 as a target to redress Th1/Th2 imbalance and enhance PARP inhibitor response in human cancers.Cancer cell international · 2022Article
- The wide and growing range of lamin B-related diseases: from laminopathies to cancer.Cellular and molecular life sciences : CMLS · 2022Review
- Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases.Frontiers in pharmacology · 2022Review
- Review
- Cell signaling pathways in autosomal-dominant leukodystrophy (ADLD): the intriguing role of the astrocytes.Cellular and molecular life sciences : CMLS · 2021Article
- Neuron type-specific increase in lamin B1 contributes to nuclear dysfunction in Huntington's disease.EMBO molecular medicine · 2021Article
- Review
- Dynamic Lamin B1-Gene Association During Oligodendrocyte Progenitor Differentiation.Neurochemical research · 2020Article
- Novel missense alleles of SIGMAR1 as tools to understand emerin-dependent gene silencing in response to cocaine.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- LMNB1-Related Adult-Onset Autosomal Dominant Leukodystrophy Presenting as Movement Disorder: A Case Report and Review of the Literature.Frontiers in neuroscience · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The nuclear lamina is a fibrous meshwork of proteins found adjacent to the inner nuclear membrane that plays a critical role in the maintenance of nuclear architecture. Made up of A and B type lamins, the nuclear lamina has recently been shown to contribute to numerous cellular functions such as chromatin organization, DNA replication, cellular proliferation, senescence, and aging. While at least a dozen disorders are associated with
Indexed as
Identifiers
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.