ArticleMolecular biology of the cell2008
Suppression of proliferative defects associated with processing-defective lamin A mutants by hTERT or inactivation of p53.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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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Who cites it
77 citing papers in PubMed, 117 citations in OpenAlex.
- Current advances and future prospects of cell reprogramming in progeroid syndromes.Frontiers in cell and developmental biology · 2025Article
- Interstitial telomeric sequences promote gross chromosomal rearrangement via multiple mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genetic and pharmacological modulation of lamin A farnesylation determines its function and turnover.Aging cell · 2024Article
- Progerin, an Aberrant Spliced Form of Lamin A, Is a Potential Therapeutic Target for HGPS.Cells · 2023Review
- Adult progenitor rejuvenation with embryonic factors.Cell proliferation · 2023Article
- Review
- Inhibition of glutaminolysis restores mitochondrial function in senescent stem cells.Cell reports · 2022Article
- Lamin A to Z in normal aging.Aging · 2022Article
- Establishment and Characterization ofCells · 2022Article
- In vivo cyclic induction of the FOXM1 transcription factor delays natural and progeroid aging phenotypes and extends healthspan.Nature aging · 2022Article
- Article
- Genetic basis of cardiovascular aging is at the core of human longevity.The journal of cardiovascular aging · 2022Article
- Progerin impairs 3D genome organization and induces fragile telomeres by limiting the dNTP pools.Scientific reports · 2021Article
- Review
- Impairment of nuclear F-actin formation and its relevance to cellular phenotypes in Hutchinson-Gilford progeria syndrome.Nucleus (Austin, Tex.) · 2020Article
- Progress and trends in the development of therapies for Hutchinson-Gilford progeria syndrome.Aging cell · 2020Review
- Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS).Biochemical Society transactions · 2020Review
- Heterochromatin loss as a determinant of progerin-induced DNA damage in Hutchinson-Gilford Progeria.Aging cell · 2020Article
- Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson-Gilford Progeria Syndrome.Nature communications · 2019Article
- Transient introduction of human telomerase mRNA improves hallmarks of progeria cells.Aging cell · 2019Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare, debilitating disease with early mortality and rapid onset of aging-associated pathologies. It is linked to mutations in LMNA, which encodes A-type nuclear lamins. The most frequent HGPS-associated LMNA mutation results in a protein, termed progerin, with an internal 50 amino acid deletion and, unlike normal A-type lamins, stable farnesylation. The cellular consequences of progerin expression underlying the HGPS phenotype remain poorly understood. Here, we stably expressed lamin A mutants, including progerin, in otherwise identical primary human fibroblasts to compare the effects of different mutants on nuclear morphology and cell proliferation. We find that expression of progerin leads to inhibition of proliferation in a high percentage of cells and slightly premature senescence in the population. Expression of a stably farnesylated mutant of lamin A phenocopied the immediate proliferative defects but did not result in premature senescence. Either p53 inhibition or, more surprisingly, expression of the catalytic subunit of telomerase (hTERT) suppressed the early proliferative defects associated with progerin expression. These findings lead us to propose that progerin may interfere with telomere structure or metabolism in a manner suppressible by increased telomerase levels and possibly link mechanisms leading to progeroid phenotypes to those of cell immortalization.
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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.