ArticleNucleus (Austin, Tex.)2016
Prelamin A processing, accumulation and distribution in normal cells and laminopathy disorders.
Article 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 22 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
22 citing papers in PubMed, 39 citations in OpenAlex.
- The Underexplored Mechanobiology of Lamin A Biogenesis and Homeostasis.Biology of the cell · 2026Review
- Article
- Endothelial Nuclear and Cytoskeletal Responses to Mechanical Stresses.Advances in experimental medicine and biology · 2026Article
- Reversal of perturbed DNA damage response and HIV latency by a histone methyltransferase inhibitor in virally suppressed individuals living with HIV.Frontiers in aging · 2025Article
- Effect of β-Estradiol on Adipogenesis in a 3T3-L1 Cell Model of Prelamin A Accumulation.International journal of molecular sciences · 2024Article
- Case Report: ConcurrentFrontiers in genetics · 2024Article
- Discovery of a Small-Molecule Modulator of the Autophagy-Lysosome Pathway That Targets Lamin A/C and LAMP1, Induces Autophagic Flux, and Affects Lysosome Positioning in Neurons.ACS chemical neuroscience · 2023Article
- Knockdown ofCell adhesion & migration · 2023Article
- Hepatic hydrogen sulfide levels are reduced in mouse model of Hutchinson-Gilford progeria syndrome.Aging · 2023Article
- Lamin A precursor localizes to the Z-disc of sarcomeres in the heart and is dynamically regulated in muscle cell differentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- The E262K mutation in Lamin A links nuclear proteostasis imbalance to laminopathy-associated premature aging.Aging cell · 2022Article
- Lamin A to Z in normal aging.Aging · 2022Article
- Drosophila p38 MAPK interacts with BAG-3/starvin to regulate age-dependent protein homeostasis.Aging cell · 2021Article
- Post-translational Modifications of the Protein Termini.Frontiers in cell and developmental biology · 2021Review
- Review
- The nuclear envelope: LINCing tissue mechanics to genome regulation in cardiac and skeletal muscle.Biology letters · 2020Article
- Lamin A/C Mechanotransduction in Laminopathies.Cells · 2020Review
- The tripartite architecture of the eukaryotic integral membrane protein zinc metalloprotease Ste24.Proteins · 2020Article
- Biology, pathology, and therapeutic targeting of RAS.Advances in cancer research · 2020Review
- A new laminopathy caused by an Arg133/Leu mutation inAdipocyte · 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Lamin A is part of a complex structural meshwork located beneath the nuclear envelope and is involved in both structural support and the regulation of gene expression. Lamin A is initially expressed as prelamin A, which contains an extended carboxyl terminus that undergoes a series of post-translational modifications and subsequent cleavage by the endopeptidase ZMPSTE24 to generate lamin A. To facilitate investigations of the role of this cleavage in normal and disease states, we developed a monoclonal antibody (PL-1C7) that specifically recognizes prelamin A at the intact ZMPSTE24 cleavage site, ensuring prelamin A detection exclusively. Importantly, PL-1C7 can be used to determine prelamin A localization and accumulation in cells where lamin A is highly expressed without the use of exogenous fusion proteins. Our results show that unlike mature lamin A, prelamin A accumulates as discrete and localized foci at the nuclear periphery. Furthermore, whereas treatment with farnesylation inhibitors of cells overexpressing a GFP-prelamin A fusion protein results in the formation of large nucleoplasmic clumps, these aggregates are not observed upon similar treatment of cells expressing endogenous prelamin A or in cells lacking ZMPSTE24 expression and/or activity. Finally, we show that specific laminopathy-associated mutations exhibit both positive and negative effects on prelamin A accumulation, indicating that these mutations affect prelamin A processing efficiency in different manners.
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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.