ReviewNucleus (Austin, Tex.)2018
Invertebrate models of lamin diseases.
Review in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Integrated analysis of tumor mechanical microenvironment-based signature reveals prognostic risk and immune landscape in endometrial carcinoma.Genes & diseases · 2026Article
- Revealing the Mechanisms of Alzheimer's, Parkinson's and Huntington's Diseases Through Invertebrate Models.Biology · 2026Review
- Review
- Developmental changes in nuclear lamina components during germ cell differentiation.Nucleus (Austin, Tex.) · 2024Article
- Aligning with the 3Rs: alternative models for research into muscle development and inherited myopathies.BMC veterinary research · 2024Review
- Nuclear reassembly defects after mitosis trigger apoptotic and p53-dependent safeguard mechanisms in Drosophila.PLoS biology · 2024Article
- Use of Farnesyl Transferase Inhibitors in an Ageing Model inJournal of developmental biology · 2023Article
- Drosophila Models Reveal Properties of Mutant Lamins That Give Rise to Distinct Diseases.Cells · 2023Article
- Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance.Nature reviews. Molecular cell biology · 2022Review
- Effects of mutant lamins on nucleo-cytoskeletal coupling inFrontiers in cell and developmental biology · 2022Article
- Reorganization of the nuclear architecture in theNucleus (Austin, Tex.) · 2020Article
- Article
- Laminopathies: what can humans learn from fruit flies.Cellular & molecular biology letters · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamins are evolutionarily conserved nuclear intermediate filament proteins. They provide structural support for the nucleus and help regulate many other nuclear activities. Mutations in human lamin genes, and especially in the LMNA gene, cause numerous diseases, termed laminopathies, including muscle, cardiac, metabolic, neuronal and early aging diseases. Most laminopathies arise from autosomal dominant missense mutations. Many of the mutant residues are conserved in the lamin genes of the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Our current understanding of the mechanisms leading to these diseases is mostly based on patients cell lines and animal models including C. elegans and D. melanogaster. The simpler lamin system and the powerful genetic tools offered by these invertebrate organisms greatly contributed to such studies. Here we provide an overview of the studies of laminopathies in Drosophila and C. elegans models.
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.