ArticleNature cell biology2020
Nuclear F-actin counteracts nuclear deformation and promotes fork repair during replication stress.
Article in Nature cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 155 citations in OpenAlex.
- The responsive nucleus: morphological signatures of cellular state.Nucleus (Austin, Tex.) · 2026Review
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Efficient spatio-angular reconstruction enables high-fidelity mapping of six-dimensional structures and dynamics with polarized fluorescence microscopy.Nature communications · 2026Article
- Getting nuclear size just right - emerging mechanisms regulating nuclear scaling and morphology.Journal of cell science · 2026Review
- Regulation of chromatin dynamics by a calcium-dependent nucleoskeleton.The Journal of biological chemistry · 2026Article
- Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cruciform-forming AT/TA repeats are acted upon by structure-selective endonucleases and Rad51 prior to repositioning to the nuclear periphery for repair.Nucleic acids research · 2026Article
- Nanoengineered 3D culture substrate enables superior persistence and polyclonal engraftment of genetically engineered hematopoietic stem cells.Cell stem cell · 2026Article
- Nuclear myosin VI cooperates with actin to promote transcriptional cluster formation at androgen receptors.The Journal of biological chemistry · 2026Article
- Integrin-Mediated Mechanosensing of Modeled Lymph Node Microenvironment Promotes T Cell Activation via Nuclear Deformation.Research (Washington, D.C.) · 2026Article
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- Nuclear actin and DNA replication stress regulate telomere maintenance by telomerase.Nature communications · 2025Article
- Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025Review
- Nucleoplasmic Lamin A/C controls replication fork restart upon stress by modulating local H3K9me3 and ADP-ribosylation levels.Nature communications · 2025Article
- Nuclear rupture in confined cell migration triggers nuclear actin polymerization to limit chromatin leakage.The EMBO journal · 2025Article
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Platelet-derived growth factor signaling in porcine testicular tubular somatic cells.Cell and tissue research · 2025Article
- Replication stress-induced nuclear hypertrophy alters chromatin topology and impacts cancer cell fitness.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From Obscurity to Prominence: IPMK's Expanding Role in Cellular Signaling, Physiology, and Disease.Biomolecules · 2025Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Filamentous actin (F-actin) provides cells with mechanical support and promotes the mobility of intracellular structures. Although F-actin is traditionally considered to be cytoplasmic, here we reveal that nuclear F-actin participates in the replication stress response. Using live and super-resolution imaging, we find that nuclear F-actin is polymerized in response to replication stress through a pathway regulated by ATR-dependent activation of mTORC1, and nucleation through IQGAP1, WASP and ARP2/3. During replication stress, nuclear F-actin increases the nuclear volume and sphericity to counteract nuclear deformation. Furthermore, F-actin and myosin II promote the mobility of stressed-replication foci to the nuclear periphery through increasingly diffusive motion and directed movements along the nuclear actin filaments. These actin functions promote replication stress repair and suppress chromosome and mitotic abnormalities. Moreover, we find that nuclear F-actin is polymerized in vivo in xenograft tumours after treatment with replication-stress-inducing chemotherapeutic agents, indicating that this pathway has a role in human disease.
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.