Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence.
Masashi Narita,Sabrina Nuñez,Sabrina Nuñez,Edith Heard,Masako Narita,Athena W. Lin,Stephen Hearn,David L. Spector,Gregory J. Hannon,Scott W. Lowe +9 more
TLDR
A distinct heterochromatic structure that accumulates in senescent human fibroblasts is described, which is designated senescence-associated heterochROMatic foci (SAHF) and is associated with the stable repression of E2F target genes.About:
This article is published in Cell.The article was published on 2003-06-13 and is currently open access. It has received 2055 citations till now. The article focuses on the topics: Senescence-associated heterochromatin focus & E2F.read more
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A rat epigenetic clock recapitulates phenotypic aging and co-localizes with heterochromatin.
Morgan E. Levine,Ross A. McDevitt,Margarita Meer,Kathy A Perdue,Andrea Di Francesco,Theresa Meade,Colin Farrell,Kyra Thrush,Meng Wang,Christopher Dunn,Matteo Pellegrini,Rafael de Cabo,Luigi Ferrucci +12 more
TL;DR: This study aimed to generate a novel epigenetic clock in rats by incorporating behavioral data, unsupervised machine learning, and network analysis to identify epigenetic signals that not only track with age, but also relates to phenotypic aging.
Journal ArticleDOI
Deficit of circulating stem – progenitor cells in opiate addiction: a pilot study
TL;DR: Flow cytometry data are consistent with clinical data suggesting accelerated ageing in addicted humans and implicate the important stem cell pool in both addiction toxicology and ageing and suggest that the toxicity both of addiction itself and of indefinite agonist maintenance therapies may have been seriously underestimated.
Journal ArticleDOI
Epigenome rejuvenation: HP1β mobility as a measure of pluripotent and senescent chromatin ground states
Maria Manukyan,Prim B. Singh +1 more
TL;DR: The dynamics of a key epigenetic modifier can be rejuvenated without de-differentiation through an embryonic stage by introducing “reprogramming factors” into senescent fibroblasts and measuring the changes in HP1β mobility as reprogramming proceeds shows that the mobility of HP1 β in senescent cells increases and by day 9 is the same as that found in young fibro Blasts.
Journal ArticleDOI
Immortalization of Primary Keratinocytes and Its Application to Skin Research
Moonju Choi,Choongho Lee +1 more
TL;DR: In order to understand the immortalization process of a primary keratinocyte, several key biological phenomena governing its lifespan will be reviewed first and its application to a three-dimensional skin culture system will be described.
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Insights into 4E-BP1 and p53 mediated regulation of accelerated cell senescence
TL;DR: A research perspective will address these somewhat contradictory findings and summarize recent research regarding senescence and mTORC1 signaling.
References
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo
Goberdhan P. Dimri,X Lee,G Basile,Meileen Acosta,G Scott,C Roskelley,E E Medrano,Maarten H.K. Linskens,Ivica Rubelj,Olivia M. Pereira-Smith +9 more
TL;DR: It is shown that several human cells express a beta-galactosidase, histochemically detectable at pH 6, upon senescence in culture, which provides in situ evidence that senescent cells may exist and accumulate with age in vivo.
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The limited in vitro lifetime of human diploid cell strains
TL;DR: The survival curves obtained with human diploid cell strains are comparable to “multiple-hit” or “ multiple-target” curves obtain with other biological systems where an initial threshold dose is required before an exponential form of the curve is established.
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Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TL;DR: It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus.
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Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins.
TL;DR: It is shown that mammalian methyltransferases that selectively methylate histone H3 on lysine 9 (Suv39h HMTases) generate a binding site for HP1 proteins—a family of heterochromatic adaptor molecules implicated in both gene silencing and supra-nucleosomal chromatin structure.
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Selective recognition of methylated lysine 9 on histone H3 by the HP1 chromo domain.
Andrew J. Bannister,Philip Zegerman,Janet F. Partridge,Eric A. Miska,Jean O. Thomas,Robin C. Allshire,Tony Kouzarides +6 more
TL;DR: A stepwise model for the formation of a transcriptionally silent heterochromatin is provided: SUV39H1 places a ‘methyl marker’ on histone H3, which is then recognized by HP1 through its chromo domain, which may also explain the stable inheritance of theheterochromatic state.