ArticleScience (New York, N.Y.)2013
Targeting isoprenylcysteine methylation ameliorates disease in a mouse model of progeria.
Article in Science (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
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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
62 citing papers in PubMed, 119 citations in OpenAlex.
- The Underexplored Mechanobiology of Lamin A Biogenesis and Homeostasis.Biology of the cell · 2026Review
- HMGA1-HP1β axis regulates premature aging in Hutchinson-Gilford progeria syndrome through chromatin remodeling.Nature communications · 2026Article
- Targeting ICMT: A promising strategy in cancer treatment (Review).Oncology letters · 2026Review
- Increased Telomere Mobility in Progeria is Restored by Isoprenylcysteine Carboxyl Methyltransferase Inhibition.bioRxiv : the preprint server for biology · 2026Article
- ICMT deficiency ameliorates weight loss and mortality, but not tumor formation in a mouse model of liver cancer.Cell communication and signaling : CCS · 2026Article
- The accumulation of progerin underlies the loss of aortic smooth muscle cells in Hutchinson-Gilford progeria syndrome.Cell death & disease · 2025Article
- Inhibition of poly(ADP-Ribosyl)ation reduced vascular smooth muscle cells loss and improves aortic disease in a mouse model of human accelerated aging syndrome.Cell death & disease · 2024Article
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
- Prelamin A and ZMPSTE24 in premature and physiological aging.Nucleus (Austin, Tex.) · 2023Review
- Progeria-a Rare Genetic Condition with Accelerated Ageing Process.Applied biochemistry and biotechnology · 2023Review
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
- Review
- Status of treatment strategies for Hutchinson-Gilford progeria syndrome with a focus on prelamin: A posttranslational modification.Basic & clinical pharmacology & toxicology · 2022Review
- Progerin modulates the IGF-1R/Akt signaling involved in aging.Science advances · 2022Article
- Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- Toward a New Therapy for Rapidly Aging Children.ACS central science · 2021Article
- Isoprenylcysteine Carboxylmethyltransferase-Based Therapy for Hutchinson-Gilford Progeria Syndrome.ACS central science · 2021Article
- Impact of Progerin Expression on Adipogenesis in Hutchinson-Gilford Progeria Skin-Derived Precursor Cells.Cells · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Several progeroid disorders, including Hutchinson-Gilford progeria syndrome (HGPS) and restrictive dermopathy (ZMPSTE24 deficiency), arise when a farnesylated and methylated form of prelamin A accumulates at the nuclear envelope. Here, we found that a hypomorphic allele of isoprenylcysteine carboxyl methyltransferase (ICMT) increased body weight, normalized grip strength, and prevented bone fractures and death in Zmpste24-deficient mice. The reduced ICMT activity caused prelamin A mislocalization within the nucleus and triggered prelamin A-dependent activation of AKT-mammalian target of rapamycin (mTOR) signaling, which abolished the premature senescence of Zmpste24-deficient fibroblasts. ICMT inhibition increased AKT-mTOR signaling and proliferation and delayed senescence in human HGPS fibroblasts but did not reduce the levels of misshapen nuclei in mouse and human cells. Thus, targeting ICMT might be useful for treating prelamin A-associated progeroid disorders.
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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.