ArticleAging2016
Permanent farnesylation of lamin A mutants linked to progeria impairs its phosphorylation at serine 22 during interphase.
Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Mechanosensing by the nucleus: From pathways to scaling relationships.The Journal of cell biology · 2017Pooled it
- Mutation-agnostic base editing of the progerin farnesylation site rescues Hutchinson-Gilford progeria syndrome phenotypes in neuromuscular organoids.Nature communications · 2026Article
- Progerin cross-linking stiffens the nucleus and impairs mechanosensation in Hutchinson-Gilford progeria syndrome.Journal of cell science · 2026Article
- Roles of the lamin A-specific tail region in the localization to sites of nuclear envelope rupture.PNAS nexus · 2024Article
- Article
- Recruitment of a splicing factor to the nuclear lamina for its inactivation.Communications biology · 2022Article
- Nuclear Lamins: Key Proteins for Embryonic Development.Biology · 2022Review
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- LAP2alpha maintains a mobile and low assembly state of A-type lamins in the nuclear interior.eLife · 2021Article
- Lamin A/C Mechanotransduction in Laminopathies.Cells · 2020Review
- Nuclear Organization in Stress and Aging.Cells · 2019Review
- Progerin phosphorylation in interphase is lower and less mechanosensitive than lamin-A,C in iPS-derived mesenchymal stem cells.Nucleus (Austin, Tex.) · 2018Article
- Identification of novel RNA isoforms of LMNA.Nucleus (Austin, Tex.) · 2017Article
- MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation.EMBO molecular medicine · 2017Article
- ZP3 is Required for Germinal Vesicle Breakdown in Mouse Oocyte Meiosis.Scientific reports · 2017Article
- Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations.Ageing research reviews · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mutants of lamin A cause diseases including the Hutchinson-Gilford progeria syndrome (HGPS) characterized by premature aging. Lamin A undergoes a series of processing reactions, including farnesylation and proteolytic cleavage of the farnesylated C-terminal domain. The role of cleavage is unknown but mutations that affect this reaction lead to progeria. Here we show that interphase serine 22 phosphorylation of endogenous mutant lamin A (progerin) is defective in cells from HGPS patients. This defect can be mimicked by expressing progerin in human cells and prevented by inhibition of farnesylation. Furthermore, serine 22 phosphorylation of non-farnesylated progerin was enhanced by a mutation that disrupts lamin A head to tail interactions. The phosphorylation of lamin A or non-farnesylated progerin was associated to the formation of spherical intranuclear lamin A droplets that accumulate protein kinases of the CDK family capable of phosphorylating lamin A at serine 22. CDK inhibitors compromised the turnover of progerin, accelerated senescence of HGPS cells and reversed the effects of FTI on progerin levels. We discuss a model of progeria where faulty serine 22 phosphorylation compromises phase separation of lamin A polymers, leading to accumulation of functionally impaired lamin A structures.
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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.