ReviewExperimental cell research2012
Lamin A, farnesylation and aging.
Review in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 94 citations in OpenAlex.
- Article
- Why and How Are Infants with Hutchinson-Gilford Progeria Syndrome Born Without Severe Manifestations?Medical sciences (Basel, Switzerland) · 2025Review
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- Molecular Mechanisms for the Regulation of Nuclear Membrane Integrity.International journal of molecular sciences · 2023Review
- Article
- Loss of Mature Lamin A/C Triggers a Shift in Intracellular Metabolic Homeostasis via AMPKα Activation.Cells · 2022Article
- Article
- Oxidative stress-induced premature senescence and aggravated denervated skeletal muscular atrophy by regulating progerin-p53 interaction.Skeletal muscle · 2022Article
- NXP032 Ameliorates Aging-Induced Oxidative Stress and Cognitive Impairment in Mice through Activation of Nrf2 Signaling.Antioxidants (Basel, Switzerland) · 2022Article
- High-Throughput Screen Detects Calcium Signaling Dysfunction in Hutchinson-Gilford Progeria Syndrome.International journal of molecular sciences · 2021Article
- Posttranslational modifications of the cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2021Review
- A 13-Year-Old Boy from Thailand with Hutchinson-Gilford Progeria Syndrome with Coronary Artery and Aortic Calcification and Non-ST-Segment Elevation Myocardial Infarction (NSTEMI).The American journal of case reports · 2021Article
- Algae Metabolites in Cosmeceutical: An Overview of Current Applications and Challenges.Marine drugs · 2020Review
- Review
- Nuclear Lamins and Emerin Are Differentially Expressed in Osteosarcoma Cells and Scale with Tumor Aggressiveness.Cancers · 2020Article
- Discovery of Lonafarnib-Like Compounds: Pharmacophore Modeling and Molecular Dynamics Studies.ACS omega · 2020Article
- Biology, pathology, and therapeutic targeting of RAS.Advances in cancer research · 2020Review
- Dysfunction of iPSC-derived endothelial cells in human Hutchinson-Gilford progeria syndrome.Cell cycle (Georgetown, Tex.) · 2019Article
- Insulin-like growth factor-1 attenuates oxidative stress-induced hepatocyte premature senescence in liver fibrogenesis via regulating nuclear p53-progerin interaction.Cell death & disease · 2019Article
- Presence and distribution of progerin in HGPS cells is ameliorated by drugs that impact on the mevalonate and mTOR pathways.Biogerontology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lamin A is a component of the nuclear envelope that is synthesized as a precursor prelamin A molecule and then processed into mature lamin A through sequential steps of posttranslational modifications and proteolytic cleavages. Remarkably, over 400 distinct point mutations have been so far identified throughout the LMNA gene, which result in the development of at least ten distinct human disorders, collectively known as laminopathies, among which is the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). The majority of HGPS cases are associated with a single point mutation in the LMNA gene that causes the production of a permanently farnesylated mutant lamin A protein termed progerin. The mechanism by which progerin leads to premature aging and the classical HGPS disease phenotype as well as the relationship between this disorder and the onset of analogous symptoms during the lifespan of a normal individual are not well understood. Yet, recent studies have provided critical insights on the cellular processes that are affected by accumulation of progerin and have suggested that cellular alterations in the lamin A processing pathway leading to the accumulation of farnesylated prelamin A intermediates may play a role in the aging process in the general population. In this review we provide a short background on lamin A and its maturation pathway and discuss the current knowledge of how progerin or alterations in the prelamin A processing pathway are thought to influence cell function and contribute to human aging.
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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.