The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence
Open accessAbstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is a premature-aging syndrome caused by a dominant mutation in the gene encoding lamin A, which leads to an aberrantly spliced and processed protein termed progerin. Previous studies have shown that progerin induces early senescence associated with increased DNA-damage signaling and that telomerase extends HGPS cellular lifespan. We demonstrate that telomerase extends HGPS cellular lifespan by decreasing progerin-induced DNA-damage signaling and activation of p53 and Rb pathways that otherwise mediate the onset of premature senescence. We show further that progerin-induced DNA-damage signaling is localized to telomeres and is associated with telomere aggregates and chromosomal aberrations. Telomerase amelioration of DNA-damage signaling is relatively rapid, requires both its catalytic and DNA-binding functions, and correlates in time with the acquisition by HGPS cells of the ability to proliferate. All of these findings establish that HGPS premature cellular senescence results from progerin-induced telomere dysfunction.
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Cites
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin
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“The TIFs observed in response to progerin expression prompted us to investigate whether we could detect any chromosomal aberrations known to occur under conditions of telomere dysfunction (Bolzan and Bianchi, 2006; Davoli et al., 2010; Hande et al., 2001; Michishita et al., 2008).”
InfluentialSenescence Induced by Altered Telomere State, Not Telomere Loss
Karlseder, J., Smogorzewska, A., & de Lange, T. (2002) · Science · doi:10.1126/science.1069523 · Cited by 796
Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging
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Control of Human Telomere Length by TRF1 and TRF2
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Telomerase modulates Wnt signalling by association with target gene chromatin
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“For example, both wild-type and catalytically inactive mutant TERT are recruited to the promoters of growthcontrolling genes and function indistinguishably to modulate gene expression and enhance cell proliferation (Park et al., 2009; Zhou et al., 2009).”
Genomic instability in laminopathy-based premature aging
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Persistent Telomere Damage Induces Bypass of Mitosis and Tetraploidy
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Cited by
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
Lamin B1 loss is a senescence-associated biomarker
Freund, A., Laberge, R.-M., Demaria, M., & Campisi, J. (2012) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-10-0884 · Cited by 1,046
Human iPSC-based modeling of late-onset disease via progerin-induced aging
Miller, J. D., Ganat, Y. M., Kishinevsky, S., Bowman, R. L., Liu, B., Tu, E. Y., Mandal, P. K., Vera, E., Shim, J.-W., Kriks, S., et al. (2013) · Cell stem cell · doi:10.1016/j.stem.2013.11.006 · Cited by 777
Impaired immune surveillance accelerates accumulation of senescent cells and aging
Ovadya, Y., Landsberger, T., Leins, H., Vadai, E., Gal, H., Biran, A., Yosef, R., Sagiv, A., Agrawal, A., Shapira, A., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-07825-3 · Cited by 578
Induced pluripotent stem cells (iPSCs): molecular mechanisms of induction and applications
Cerneckis, J., Cai, H., & Shi, Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01809-0 · Cited by 452
Metadata
- Authors
- Benson, E. K., Lee, S. W., & Aaronson, S. A.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2010-08-01
- Volume
- 123
- Issue
- 15
- Pages
- 2605-2612
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2122983246
- Cited by
- 182
- References
- 12
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- green
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