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
Citations
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Chromatin landscape: Methylation beyond transcription
TL;DR: This Point of View emphasizes that alterations in histone modification landscapes are not only relevant to transcription but have broad range implications in chromatin structure, nuclear architecture, cell cycle, genome stability and disease progression.
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Metabolic Signaling to Chromatin
TL;DR: The biosynthetic pathways of the cofactors nicotinamide adenine dinucleotide (NAD), acetyl coenzyme A (acetyl-CoA), S-adenosyl methionine (SAM), α-ketoglutarate, and flavin adenines din nucleotide (FAD) are explored, and their role in metabolically regulating chromatin processes is explored.
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TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging.
Guoliang Lyu,Yiting Guan,Chao Zhang,Le Zong,Lei Sun,Xiaoke Huang,Li Huang,Lijun Zhang,Xiao-Li Tian,Zhongjun Zhou,Wei Tao +10 more
TL;DR: It is reported that TGF-β signaling promotes miR-29 mediated loss of H4K20me3 thus accelerating senescence, shedding light on potential therapeutic interventions in cardiac aging.
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Subversion of Autophagy by Kaposi’s Sarcoma-Associated Herpesvirus Impairs Oncogene-Induced Senescence
TL;DR: A coordinated viral gene expression program is revealed that usurps autophagy, blocks senescence, and facilitates the proliferation of KSHV-infected cells.
Journal ArticleDOI
Turning back time with emerging rejuvenation strategies
TL;DR: Four emerging rejuvenation strategies—systemic factors, metabolic manipulations, senescent cell ablation and cellular reprogramming—are reviewed and their mechanisms of action, cellular targets, potential trade-offs and application to human ageing are discussed.
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.