ArticleHistochemistry and cell biology2013
Cytoplasmic localization of PML particles in laminopathies.
Article in Histochemistry and cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Variable A-type lamin expression in Merkel cell carcinoma cell lines and its association with nuclear integrity.Scientific reports · 2026Article
- A high-content screen reveals new regulators of nuclear membrane stability.Scientific reports · 2024Article
- A high-content screen reveals new regulators of nuclear membrane stability.bioRxiv : the preprint server for biology · 2023Article
- Filamentous nuclear actin regulation of PML NBs during the DNA damage response is deregulated by prelamin A.Cell death & disease · 2022Article
- Effects of arsenic on the topology and solubility of promyelocytic leukemia (PML)-nuclear bodies.PloS one · 2022Article
- Phosphorylation of Lamin A/C at serine 22 modulates NaPhysiological reports · 2021Article
- Review
- Assessment of fibroblast nuclear morphology aids interpretation of LMNA variants.European journal of human genetics : EJHG · 2019Article
- MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation.EMBO molecular medicine · 2017Article
- Bursting the Bubble - Nuclear Envelope Rupture as a Path to Genomic Instability?Trends in cell biology · 2017Review
- Accurate Detection of Dysmorphic Nuclei Using Dynamic Programming and Supervised Classification.PloS one · 2017Article
- In silico synchronization reveals regulators of nuclear ruptures in lamin A/C deficient model cells.Scientific reports · 2016Article
- Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates.Nucleus (Austin, Tex.) · 2015Article
- The Histochem Cell Biol conspectus: the year 2013 in review.Histochemistry and cell biology · 2014Review
- Lysosome-mediated processing of chromatin in senescence.The Journal of cell biology · 2013Article
- Emerging Cellular Functions of Cytoplasmic PML.Frontiers in oncology · 2013Article
- Soft substrates normalize nuclear morphology and prevent nuclear rupture in fibroblasts from a laminopathy patient with compound heterozygous LMNA mutations.Nucleus (Austin, Tex.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is growing evidence that laminopathies, diseases associated with mutations in the LMNA gene, are caused by a combination of mechanical and gene regulatory distortions. Strikingly, there is a large variability in disease symptoms between individual patients carrying an identical LMNA mutation. This is why classical genetic screens for mutations appear to have limited predictive value for disease development. Recently, the widespread occurrence of repetitive nuclear ruptures has been described in fibroblast cultures from various laminopathy patients. Since this phenomenon was strongly correlated with disease severity, the identification of biomarkers that report on these rupture events could have diagnostic relevance. One such candidate marker is the PML nuclear body, a structure that is normally confined to the nuclear interior, but leaks out of the nucleus upon nuclear rupture. Here, we show that a variety of laminopathies shows the presence of these cytoplasmic PML particles (PML CPs), and that the amount of these protein aggregates increases with severity of the disease. In addition, between clinically healthy individuals, carrying LMNA mutations, significant differences can be found. Therefore, we postulate that detection of PML CPs in patient fibroblasts could become a valuable marker for diagnosis of disease development.
Indexed as
Identifiers
22918509What 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.