ArticleFEBS letters2010
Loss of a DNA binding site within the tail of prelamin A contributes to altered heterochromatin anchorage by progerin.
Article in FEBS letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Orientia tsutsugamushi targets lamin A using Ank effectors and alters chromatin to inhibit NF-κB.Communications biology · 2026Article
- Advances in research on the relationship between the LMNA gene and human diseases (Review).Molecular medicine reports · 2024Review
- Article
- The role of TEMRA cell-mediated immune senescence in the development and treatment of HIV disease.Frontiers in immunology · 2023Review
- Close to the edge: Heterochromatin at the nucleolar and nuclear peripheries.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Nuclear lamin phosphorylation: an emerging role in gene regulation and pathogenesis of laminopathies.Nucleus (Austin, Tex.) · 2020Review
- Lamin microaggregates lead to altered mechanotransmission in progerin-expressing cells.Nucleus (Austin, Tex.) · 2020Article
- Nuclear filaments: role in chromosomal positioning and gene expression.Nucleus (Austin, Tex.) · 2020Review
- Lamin A/C Mechanotransduction in Laminopathies.Cells · 2020Review
- Phosphorylated Lamin A/C in the Nuclear Interior Binds Active Enhancers Associated with Abnormal Transcription in Progeria.Developmental cell · 2020Article
- SIRT7 mediates L1 elements transcriptional repression and their association with the nuclear lamina.Nucleic acids research · 2019Article
- Kinesin-14 motor protein KIFC1 participates in DNA synthesis and chromatin maintenance.Cell death & disease · 2019Article
- HiPLA: High-throughput imaging proximity ligation assay.Methods (San Diego, Calif.) · 2019Article
- Review
- Assessment of fibroblast nuclear morphology aids interpretation of LMNA variants.European journal of human genetics : EJHG · 2019Article
- Hutchinson-Gilford Progeria Syndrome-Current Status and Prospects for Gene Therapy Treatment.Cells · 2019Review
- Finding Friends in the Crowd: Three-Dimensional Cliques of Topological Genomic Domains.Frontiers in genetics · 2019Review
- Nesprins and Lamins in Health and Diseases of Cardiac and Skeletal Muscles.Frontiers in physiology · 2018Review
- Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.Current treatment options in cardiovascular medicine · 2017Review
- Alzheimer's disease: An acquired neurodegenerative laminopathy.Nucleus (Austin, Tex.) · 2016Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Mutations in the lamin A/C (LMNA) gene that cause Hutchinson-Gilford progeria syndrome (HGPS) lead to expression of a protein called progerin with 50 amino acids deleted from the tail of prelamin A. In cells from patients with HGPS, both the amount and distribution of heterochromatin are altered. We designed in vitro assays to ask whether such alterations might reflect changes in chromatin, DNA and/or histone binding properties of progerin compared to wild-type lamin C-terminal tails. We show that progerin tail has a reduced DNA/chromatin binding capacity and modified trimethylated H3K27 binding pattern, offering a molecular mechanism for heterochromatin alterations related to HGPS.
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