ArticleScientific reports2016
In silico synchronization reveals regulators of nuclear ruptures in lamin A/C deficient model cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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Who cites it
60 citing papers in PubMed, 89 citations in OpenAlex.
- Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.Biochemical Society transactions · 2026Review
- URGCP promotes osteosarcoma progression by regulating the ESCRT-III subunit CHMP4B.Translational cancer research · 2026Article
- LRRC59 cooperates with nuclear transporters to restrain the nuclear envelope repair machinery and safeguard genome integrity.Nature communications · 2025Article
- Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity.Molecular biology of the cell · 2025Article
- Engineered Nanotopographies Induce Transient Openings in the Nuclear Membrane.Advanced functional materials · 2025Article
- Crosstalk between mitotic reassembly and repair of the nuclear envelope.Nucleus (Austin, Tex.) · 2024Review
- Roles of the lamin A-specific tail region in the localization to sites of nuclear envelope rupture.PNAS nexus · 2024Article
- Lamin B1 curtails early human papillomavirus infection by safeguarding nuclear compartmentalization and autophagic capacity.Cellular and molecular life sciences : CMLS · 2024Article
- A high-content screen reveals new regulators of nuclear membrane stability.Scientific reports · 2024Article
- Actin contraction controls nuclear blebbing and rupture independent of actin confinement.Molecular biology of the cell · 2024Article
- Nuclear shape is affected differentially by loss of lamin A, lamin C, or both lamin A and C.microPublication biology · 2024Article
- Transcription inhibition suppresses nuclear blebbing and rupture independently of nuclear rigidity.Journal of cell science · 2023Article
- A high-content screen reveals new regulators of nuclear membrane stability.bioRxiv : the preprint server for biology · 2023Article
- Small lipid droplets are rigid enough to indent a nucleus, dilute the lamina, and cause rupture.The Journal of cell biology · 2023Article
- Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS.The Journal of cell biology · 2022Article
- The BAF A12T mutation disrupts lamin A/C interaction, impairing robust repair of nuclear envelope ruptures in Nestor-Guillermo progeria syndrome cells.Nucleic acids research · 2022Article
- Genome instability from nuclear catastrophe and DNA damage.Seminars in cell & developmental biology · 2022Review
- Nuclear lamins: Structure and function in mechanobiology.APL bioengineering · 2022Review
- The functional impact of nuclear reorganization in cellular senescence.Briefings in functional genomics · 2022Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear lamina is a critical regulator of nuclear structure and function. Nuclei from laminopathy patient cells experience repetitive disruptions of the nuclear envelope, causing transient intermingling of nuclear and cytoplasmic components. The exact causes and consequences of these events are not fully understood, but their stochastic occurrence complicates in-depth analyses. To resolve this, we have established a method that enables quantitative investigation of spontaneous nuclear ruptures, based on co-expression of a firmly bound nuclear reference marker and a fluorescent protein that shuttles between the nucleus and cytoplasm during ruptures. Minimally invasive imaging of both reporters, combined with automated tracking and in silico synchronization of individual rupture events, allowed extracting information on rupture frequency and recovery kinetics. Using this approach, we found that rupture frequency correlates inversely with lamin A/C levels, and can be reduced in genome-edited LMNA knockout cells by blocking actomyosin contractility or inhibiting the acetyl-transferase protein NAT10. Nuclear signal recovery followed a kinetic that is co-determined by the severity of the rupture event, and could be prolonged by knockdown of the ESCRT-III complex component CHMP4B. In conclusion, our approach reveals regulators of nuclear rupture induction and repair, which may have critical roles in disease development.
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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.