ArticleNucleus (Austin, Tex.)2018
Progerin phosphorylation in interphase is lower and less mechanosensitive than lamin-A,C in iPS-derived mesenchymal stem cells.
Article in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- A study on the nutritional status and body composition of children with Hutchinson-Gilford progeria syndrome.Orphanet journal of rare diseases · 2026Article
- The accumulation of progerin underlies the loss of aortic smooth muscle cells in Hutchinson-Gilford progeria syndrome.Cell death & disease · 2025Article
- Decreased DNA density is a better indicator of a nuclear bleb than lamin B loss.Journal of cell science · 2025Article
- Roles of the lamin A-specific tail region in the localization to sites of nuclear envelope rupture.PNAS nexus · 2024Article
- Crosstalk between mitotic reassembly and repair of the nuclear envelope.Nucleus (Austin, Tex.) · 2024Review
- Optimized simple culture protocol for inducing mature myotubes from MYOD1-overexpressed human iPS cells.Scientific reports · 2024Article
- Cellular reprogramming as a tool to model human aging in a dish.Nature communications · 2024Review
- DNA density is a better indicator of a nuclear bleb than lamin B loss.bioRxiv : the preprint server for biology · 2024Article
- Mechanotransduction of the vasculature in Hutchinson-Gilford Progeria Syndrome.Frontiers in physiology · 2024Review
- Premature aging of skeletal stem/progenitor cells rather than osteoblasts causes bone loss with decreased mechanosensation.Bone research · 2023Article
- Article
- Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS.The Journal of cell biology · 2022Article
- Gaussian curvature dilutes the nuclear lamina, favoring nuclear rupture, especially at high strain rate.Nucleus (Austin, Tex.) · 2022Article
- Progerin-expressing endothelial cells are unable to adapt to shear stress.Biophysical journal · 2022Article
- Alterations to Genome Organisation in Stem Cells, Their Differentiation and Associated Diseases.Results and problems in cell differentiation · 2022Article
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- A Unified Linear Viscoelastic Model of the Cell Nucleus Defines the Mechanical Contributions of Lamins and Chromatin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Stem Cell Mechanobiology and the Role of Biomaterials in Governing Mechanotransduction and Matrix Production for Tissue Regeneration.Frontiers in bioengineering and biotechnology · 2020Review
- The Role of Phosphatases in Nuclear Envelope Disassembly and Reassembly and Their Relevance to Pathologies.Cells · 2019Review
- Mechanosensing by the Lamina Protects against Nuclear Rupture, DNA Damage, and Cell-Cycle Arrest.Developmental cell · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Interphase phosphorylation of lamin-A,C depends dynamically on a cell's microenvironment, including the stiffness of extracellular matrix. However, phosphorylation dynamics is poorly understood for diseased forms such as progerin, a permanently farnesylated mutant of LMNA that accelerates aging of stiff and mechanically stressed tissues. Here, fine-excision alignment mass spectrometry (FEA-MS) is developed to quantify progerin and its phosphorylation levels in patient iPS cells differentiated to mesenchymal stem cells (MSCs). The stoichiometry of total A-type lamins (including progerin) versus B-type lamins measured for Progeria iPS-MSCs prove similar to that of normal MSCs, with total A-type lamins more abundant than B-type lamins. However, progerin behaves more like farnesylated B-type lamins in mechanically-induced segregation from nuclear blebs. Phosphorylation of progerin at multiple sites in iPS-MSCs cultured on rigid plastic is also lower than that of normal lamin-A and C. Reduction of nuclear tension upon i) cell rounding/detachment from plastic, ii) culture on soft gels, and iii) inhibition of actomyosin stress increases phosphorylation and degradation of lamin-C > lamin-A > progerin. Such mechano-sensitivity diminishes, however, with passage as progerin and DNA damage accumulate. Lastly, transcription-regulating retinoids exert equal effects on both diseased and normal A-type lamins, suggesting a differential mechano-responsiveness might best explain the stiff tissue defects in Progeria.
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