ArticleThe Journal of cell biology1990
Isoprenylation is required for the processing of the lamin A precursor.
Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 225 citations in OpenAlex.
- Abnormal nuclear morphology in vivo in mouse hair follicle fibroblasts expressing progerin.Biochemical and biophysical research communications · 2026Article
- Farnesylated prelamin A induces fibroblast polarity defects in premature aging disorders by inhibiting nesprin-2-SUN2 LINC complex function.Journal of cell science · 2026Article
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
- Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023Review
- Review
- Article
- Akt1-associated actomyosin remodelling is required for nuclear lamina dispersal and nuclear shrinkage in epidermal terminal differentiation.Cell death and differentiation · 2021Article
- Linking skeletal muscle aging with osteoporosis by lamin A/C deficiency.PLoS biology · 2020Article
- Review
- Progeria: A Rare Genetic Syndrome.Indian journal of clinical biochemistry : IJCB · 2020Review
- Defining substrate requirements for cleavage of farnesylated prelamin A by the integral membrane zinc metalloprotease ZMPSTE24.PloS one · 2020Article
- Vascular smooth muscle cell loss underpins the accelerated atherosclerosis in Hutchinson-Gilford progeria syndrome.Nucleus (Austin, Tex.) · 2019Review
- Prelamin A mediates myocardial inflammation in dilated and HIV-associated cardiomyopathies.JCI insight · 2019Article
- Pathogenic mutations in genes encoding nuclear envelope proteins and defective nucleocytoplasmic connections.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Presence and distribution of progerin in HGPS cells is ameliorated by drugs that impact on the mevalonate and mTOR pathways.Biogerontology · 2019Article
- Article
- Lamins and Lamin-Associated Proteins in Gastrointestinal Health and Disease.Gastroenterology · 2018Review
- The Pathogenesis and Therapies of Striated Muscle Laminopathies.Frontiers in physiology · 2018Review
- Nucleolar expansion and elevated protein translation in premature aging.Nature communications · 2017Article
- Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.Current treatment options in cardiovascular medicine · 2017Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear lamina proteins, prelamin A, lamin B, and a 70-kD lamina-associated protein, are posttranslationally modified by a metabolite derived from mevalonate. This modification can be inhibited by treatment with (3-R,S)-3-fluoromevalonate, demonstrating that it is isoprenoid in nature. We have examined the association between isoprenoid metabolism and processing of the lamin A precursor in human and hamster cells. Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by mevinolin (lovastatin) specifically depletes endogenous isoprenoid pools and inhibits the conversion of prelamin A to lamin A. Prelamin A processing is also blocked by mevalonate starvation of Mev-1, a CHO cell line auxotrophic for mevalonate. Moreover, inhibition of prelamin A processing by mevinolin treatment is rapidly reversed by the addition of exogenous mevalonate. Processing of prelamin A is, therefore, dependent on isoprenoid metabolism. Analysis of the conversion of prelamin A to lamin A by two independent methods, immunoprecipitation and two-dimensional nonequilibrium pH gel electrophoresis, demonstrates that a precursor-product relationship exists between prelamin A and lamin A. Analysis of R,S-[5-3H(N)]mevalonate-labeled cells shows that the rate of turnover of the isoprenoid group from prelamin A is comparable to the rate of conversion of prelamin A to lamin A. These results suggest that during the proteolytic maturation of prelamin A, the isoprenylated moiety is lost. A significant difference between prelamin A processing, and that of p21ras and the B-type lamins that undergo isoprenylation-dependent proteolytic maturation, is that the mature form of lamin A is no longer isoprenylated.
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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.