ArticleNucleus (Austin, Tex.)2016
Comparing lamin proteins post-translational relative stability using a 2A peptide-based system reveals elevated resistance of progerin to cellular degradation.
Article in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- The p.R249W Mutation inCells · 2026Article
- Article
- RNA-coupled CRISPR screens reveal ZNF207 as a regulator of LMNA aberrant splicing in progeria.Molecular cell · 2026Article
- Selection of specific and efficient siRNAs in new cellular model for Hutchinson-Gilford progeria syndrome therapy.Molecular therapy. Nucleic acids · 2025Article
- Development of an accelerated cellular model for early changes in Alzheimer's disease.Scientific reports · 2023Article
- Gene-specific nonsense-mediated mRNA decay targeting for cystic fibrosis therapy.Nature communications · 2022Article
- Exon-skipping antisense oligonucleotides for cystic fibrosis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A targeted antisense therapeutic approach for Hutchinson-Gilford progeria syndrome.Nature medicine · 2021Article
- SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome.Nature communications · 2020Article
- Diminished Canonical β-Catenin Signaling During Osteoblast Differentiation Contributes to Osteopenia in Progeria.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Lamin A and microtubules collaborate to maintain nuclear morphology.Nucleus (Austin, Tex.) · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Nuclear lamins are the major components of the nuclear lamina at the periphery of the nucleus, supporting the nuclear envelope and participating in many nuclear processes, including DNA replication, transcription and chromatin organization. A group of diseases, the laminopathies, is associated with mutations in lamin genes. One of the most striking cases is Hutchinson-Gilford progeria syndrome (HGPS) which is the consequence of a lamin A dominant negative mutant named progerin. Due to the abnormal presence of a permanent C-terminal farnesyl tail, progerin gradually accumulates on the nuclear membrane, perturbing a diversity of signalings and transcriptional events. The accumulation of progerin has led to the speculation that progerin possesses higher stability than the wild type lamin A protein. However, the low solubility of lamin proteins renders traditional immunoprecipitation-dependent methods such as pulse-chase analysis ineffective for comparing the relative stabilities of mutant and wild type lamins. Here, we employ a novel platform for inferring differences in lamin stability, which is based on normalization to a co-translated reporter protein following porcine teschovirus-1 2A peptide-mediated co-translational cleavage. The results obtained using this method support the notion that progerin is more stable than lamin A. Moreover, treatment of FTI reduces progerin relative stability to the level of wild type lamin A.
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Registered trials
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