ArticleNucleus (Austin, Tex.)2020
Impairment of nuclear F-actin formation and its relevance to cellular phenotypes in Hutchinson-Gilford progeria syndrome.
Article in Nucleus (Austin, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 15 citations in OpenAlex.
- Expression of progerin enhances disease-related endpoints in a tau seeding reporter cell system.GeroScience · 2026Article
- Roles of DNA Damage Response Pathway in the Regulation of the Nuclear Envelope.Current issues in molecular biology · 2026Review
- Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025Review
- Microhand Platform Equipped with Plate-Shaped End-Effectors Enables Precise Probing of Intracellular Structure Contribution to Whole-Cell Mechanical Properties.Micromachines · 2025Article
- Actin from within - how nuclear myosins and actin regulate nuclear architecture and mechanics.Journal of cell science · 2025Review
- Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation.Nature communications · 2024Article
- Nuclear actin structure regulates chromatin accessibility.Nature communications · 2024Article
- Architectural control of mesenchymal stem cell phenotype through nuclear actin.Nucleus (Austin, Tex.) · 2022Article
- Nuclear envelope mechanobiology: linking the nuclear structure and function.Nucleus (Austin, Tex.) · 2021Review
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Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder caused by a mutation of lamin A, which contributes to nuclear architecture and the spatial organization of chromatin in the nucleus. The expression of a lamin A mutant, named progerin, leads to functional and structural disruption of nuclear organization. Since progerin lacks a part of the actin-binding site of lamin A, we hypothesized that nuclear actin dynamics and function are altered in HGPS cells. Nuclear F-actin is required for the organization of nuclear shape, transcriptional regulation, DNA damage repair, and activation of Wnt/β-catenin signaling. Here we show that the expression of progerin decreases nuclear F-actin and impairs F-actin-regulated transcription. When nuclear F-actin levels are increased by overexpression of nuclear-targeted actin or by using jasplakinolide, a compound that stabilizes F-actin, the irregularity of nuclear shape and defects in gene expression can be reversed. These observations provide evidence for a novel relationship between nuclear actin and the etiology of HGPS.
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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.