ArticleGenes2023
Gene Regulatory Interactions at Lamina-Associated Domains.
Article in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed.
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Article
- The molecular basis of lamin-specific chromatin interactions.Nature structural & molecular biology · 2025Article
- Nuclear stiffness through lamin A/C overexpression differentially modulates chromosomal instability biomarkers.Biology of the cell · 2025Article
- Differential Expression of Lamins and Modulation of Chromatin Architecture in Carcinogenesis: tous pour un et un pour tous.Sub-cellular biochemistry · 2025Review
- PML modulates epigenetic composition of chromatin to regulate expression of pro-metastatic genes in triple-negative breast cancer.Nucleic acids research · 2023Article
- Cellular and Genomic Features of Muscle Differentiation from Isogenic Fibroblasts and Myoblasts.Cells · 2023Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment.
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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.