ReviewMolecular and cellular biology2014
Nuclear lamins and neurobiology.
Review in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Trauma context exerts intergenerational effects on child mental health via DNA methylation.Epigenetics · 2024Article
- Review
- Progerin, an Aberrant Spliced Form of Lamin A, Is a Potential Therapeutic Target for HGPS.Cells · 2023Review
- Regulatory role of cathepsin L in induction of nuclear laminopathy in Alzheimer's disease.Aging cell · 2022Article
- Lamin A/C missense variants: from discovery to functional validation.NPJ genomic medicine · 2021Article
- Clinical and genetic features of arrhythmogenic cardiomyopathy: diagnosis, management and the heart failure perspective.Progress in pediatric cardiology · 2021Article
- A geroscience motivated approach to treat Alzheimer's disease: Senolytics move to clinical trials.Mechanisms of ageing and development · 2021Review
- A novel biallelicClinical case reports · 2021Article
- Increased expression of LAP2β eliminates nuclear membrane ruptures in nuclear lamin-deficient neurons and fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- De Novo Variants in LMNB1 Cause Pronounced Syndromic Microcephaly and Disruption of Nuclear Envelope Integrity.American journal of human genetics · 2020Article
- Mechanical Regulation of Nuclear Translocation in Migratory Neurons.Frontiers in cell and developmental biology · 2020Review
- An absence of lamin B1 in migrating neurons causes nuclear membrane ruptures and cell death.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Physiological and pathological roles of LRRK2 in the nuclear envelope integrity.Human molecular genetics · 2019Article
- Recapitulation of molecular regulators of nuclear motion during cell migration.Cell adhesion & migration · 2019Review
- Diagnostic and therapeutic strategies for arrhythmogenic right ventricular dysplasia/cardiomyopathy patient.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2019Review
- Phenotypic and Genetic Characteristics of Lipodystrophy: Pathophysiology, Metabolic Abnormalities, and Comorbidities.Current diabetes reports · 2018Review
- Unweaving the role of nuclear Lamins in neural circuit integrity.Cell stress · 2018Article
- NeuronalCell stress · 2018Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Much of the work on nuclear lamins during the past 15 years has focused on mutations in LMNA (the gene for prelamin A and lamin C) that cause particular muscular dystrophy, cardiomyopathy, partial lipodystrophy, and progeroid syndromes. These disorders, often called "laminopathies," mainly affect mesenchymal tissues (e.g., striated muscle, bone, and fibrous tissue). Recently, however, a series of papers have identified important roles for nuclear lamins in the central nervous system. Studies of knockout mice uncovered a key role for B-type lamins (lamins B1 and B2) in neuronal migration in the developing brain. Also, duplications of LMNB1 (the gene for lamin B1) have been shown to cause autosome-dominant leukodystrophy. Finally, recent studies have uncovered a peculiar pattern of nuclear lamin expression in the brain. Lamin C transcripts are present at high levels in the brain, but prelamin A expression levels are very low-due to regulation of prelamin A transcripts by microRNA 9. This form of prelamin A regulation likely explains why "prelamin A diseases" such as Hutchinson-Gilford progeria syndrome spare the central nervous system. In this review, we summarize recent progress in elucidating links between nuclear lamins and neurobiology.
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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.