ArticleThe Journal of cell biology2002
Alteration of nuclear lamin organization inhibits RNA polymerase II-dependent transcription.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 267 citations in OpenAlex.
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Deregulated miR-145 and miR-27b in Hutchinson-Gilford progeria syndrome: implications for adipogenesis.Aging · 2025Article
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
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- Nascent RNA scaffolds contribute to chromosome territory architecture and counter chromatin compaction.Molecular cell · 2021Article
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- Article
- Lamin A/C and Emerin depletion impacts chromatin organization and dynamics in the interphase nucleus.BMC molecular and cell biology · 2019Article
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- Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging.The Journal of cell biology · 2018Review
- The Genomic Health of Human Pluripotent Stem Cells: Genomic Instability and the Consequences on Nuclear Organization.Frontiers in genetics · 2018Review
- Exploring the Crosstalk BetweenFrontiers in genetics · 2018Review
- Laminopathies: what can humans learn from fruit flies.Cellular & molecular biology letters · 2018Review
- Mechanotransduction, nuclear architecture and epigenetics in Emery Dreifuss Muscular Dystrophy: tous pour un, un pour tous.Nucleus (Austin, Tex.) · 2018Review
- G2/M-Phase Checkpoint Adaptation and Micronuclei Formation as Mechanisms That Contribute to Genomic Instability in Human Cells.International journal of molecular sciences · 2017Review
- Aberrant Compartment Formation by HSPB2 Mislocalizes Lamin A and Compromises Nuclear Integrity and Function.Cell reports · 2017Article
- Chromosomal aneuploidies induced upon Lamin B2 depletion are mislocalized in the interphase nucleus.Chromosoma · 2017Article
- Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.Current treatment options in cardiovascular medicine · 2017Review
- Comparing lamin proteins post-translational relative stability using a 2A peptide-based system reveals elevated resistance of progerin to cellular degradation.Nucleus (Austin, Tex.) · 2016Article
- A potential role for genome structure in the translation of mechanical force during immune cell development.Nucleus (Austin, Tex.) · 2016Review
30 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Regulation of gene activity is mediated by alterations in chromatin organization. In addition, chromatin organization may be governed in part by interactions with structural components of the nucleus. The nuclear lamins comprise the lamina and a variety of nucleoplasmic assemblies that together are major structural components of the nucleus. Furthermore, lamins and lamin-associated proteins have been reported to bind chromatin. These observations suggest that the nuclear lamins may be involved in the regulation of gene activity. In this report, we test this possibility by disrupting the normal organization of nuclear lamins with a dominant negative lamin mutant lacking the NH2-terminal domain. We find that this disruption inhibits RNA polymerase II activity in both mammalian cells and transcriptionally active embryonic nuclei from Xenopus laevis. The inhibition appears to be specific for polymerase II as disruption of lamin organization does not detectably inhibit RNA polymerases I and III. Furthermore, immunofluorescence observations indicate that this selective inhibition of polymerase II-dependent transcription involves the TATA binding protein, a component of the basal transcription factor TFIID.
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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.