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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Senescence and Cancer.
Sulin Zeng,Wen Hong Shen,Li Liu +2 more
TL;DR: Early-stage senescence may protect cell from transformation, while prolongedsenescence often promotes cancer development, and the complexity of senescences that makes cancer treatment challenging is highlighted.
Journal ArticleDOI
Effects of bioactive compounds on senescence and components of senescence associated secretory phenotypes in vitro
Janubová Mária,Žitňanová Ingrid +1 more
TL;DR: This review summarizes how the biological compounds listed above affect cell morphology, cell proliferation, specific cell functions, the activity of senescence-associated β-galactosidase (SA-β-gal), the shortening of telomeres and reduction of telomerase activity, production of intracellular reactive oxygen species (ROS) and lipid peroxidation products, expression of antioxidant enzymes and expression of p53 and p21 are summarized.
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Cellular Senescence and the Kidney: Potential Therapeutic Targets and Tools.
TL;DR: The connection between CKD and senescence, the pharmacological options for targeting senescent cells, and the means to specifically target the kidney are discussed, which shows promise for the options of targetingSenescent cells in CKD.
Journal ArticleDOI
Hypoxia-Inducible Histone Lysine Demethylases: Impact on the Aging Process and Age-Related Diseases
TL;DR: The regulation of HIF-1α-dependent induction of KDMs is reviewed to clarify their role in pathological processes emphasizing that long-term stress-related insults can impair the maintenance of chromatin landscape and provoke cellular senescence and tissue fibrosis associated with aging and age-related diseases.
Journal ArticleDOI
SPOP E3 Ubiquitin Ligase Adaptor Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase
Hengrui Zhu,Shancheng Ren,Benjamin G. Bitler,Katherine M. Aird,Zhigang Tu,Emmanuel Skordalakes,Yasheng Zhu,Jun Yan,Yinghao Sun,Rugang Zhang +9 more
TL;DR: It is shown that SPOP promotes senescence, an important tumor suppression mechanism, by targeting the SENP7 deSUMOylase for degradation, which correlates with ubiquitin-mediated degradation of SENP6 and HP1α sumoylation, subcellular re-localization, and its associated gene silencing.
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.