ArticlePloS one2010
Dynamics of lamin-A processing following precursor accumulation.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- Nuclear envelope mechanobiology: linking the nuclear structure and function.Nucleus (Austin, Tex.) · 2021Review
- Article
- Intermittent treatment with farnesyltransferase inhibitor and sulforaphane improves cellular homeostasis in Hutchinson-Gilford progeria fibroblasts.Oncotarget · 2017Article
- VRK2A is an A-type lamin-dependent nuclear envelope kinase that phosphorylates BAF.Molecular biology of the cell · 2017Article
- Lamin A/C deficiency is an independent risk factor for cervical cancer.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- AKT1-mediated Lamin A/C degradation is required for nuclear degradation and normal epidermal terminal differentiation.Cell death and differentiation · 2015Article
- Article
- Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins.Experimental cell research · 2011Article
- Structure and stability of the lamin A tail domain and HGPS mutant.Journal of structural biology · 2011Article
- Laminopathies: the molecular background of the disease and the prospects for its treatment.Cellular & molecular biology letters · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
Lamin A (LaA) is a component of the nuclear lamina, an intermediate filament meshwork that underlies the inner nuclear membrane (INM) of the nuclear envelope (NE). Newly synthesized prelamin A (PreA) undergoes extensive processing involving C-terminal farnesylation followed by proteolysis yielding non-farnesylated mature lamin A. Different inhibitors of these processing events are currently used therapeutically. Hutchinson-Gilford Progeria Syndrome (HGPS) is most commonly caused by mutations leading to an accumulation of a farnesylated LaA isoform, prompting a clinical trial using farnesyltransferase inhibitors (FTI) to reduce this modification. At therapeutic levels, HIV protease inhibitors (PI) can unexpectedly inhibit the final processing step in PreA maturation. We have examined the dynamics of LaA processing and associated cellular effects during PI or FTI treatment and following inhibitor washout. While PI reversibility was rapid, with respect to both LaA maturation and associated cellular phenotype, recovery from FTI treatment was more gradual. FTI reversibility is influenced by both cell type and rate of proliferation. These results suggest a less static lamin network than has previously been observed.
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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.