ArticleiScience2024
Lamin chromatin binding is modulated by interactions of different LAP2α domains with lamins and chromatin.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- The responsive nucleus: morphological signatures of cellular state.Nucleus (Austin, Tex.) · 2026Review
- Review
- LBR and LAP2 mediate heterochromatin tethering to the nuclear periphery to preserve genome homeostasis.Nature cell biology · 2026Article
- Barrier-to-Autointegration Factor 1: a key regulator of nuclear envelope integrity, genome stability, and disease progression.Frontiers in immunology · 2026Review
- Nuclear envelope and chromatin choreography direct cellular differentiation.Nucleus (Austin, Tex.) · 2025Review
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- LAP2alpha facilitates myogenic gene expression by preventing nucleoplasmic lamin A/C from spreading to active chromatin regions.Nucleic acids research · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Lamins A and C are components of the lamina at the nuclear periphery and associate with heterochromatin. A distinct, relatively mobile pool of lamin A/C in the nuclear interior associates with euchromatic regions and with lamin-associated polypeptide 2α (LAP2α). Here we show that phosphorylation-dependent impairment of lamin assembly had no effect on its chromatin association, while LAP2α depletion was sufficient to increase chromatin association of lamins. This suggests that complex interactions between LAP2α, chromatin, and lamins regulate lamin chromatin binding. Both the C terminus of LAP2α and its N-terminal LAP2-Emerin-MAN1 (LEM) domain, mediating interaction with lamin A/C indirectly via barrier-to-autointegration factor (BAF), are required for binding to lamins. The N-terminal LEM-like domain of LAP2α, but not its LEM domain, mediates chromatin association of LAP2α and requires LAP2α dimerization via its C terminus. Our data suggest that formation of several LAP2α-, lamin A/C-, and BAF-containing complexes in the nucleoplasm and on chromatin affects lamin chromatin association.
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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.