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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Oncogene-induced cell senescence--halting on the road to cancer.
Wolter J. Mooi,Daniel S. Peeper +1 more
TL;DR: This review of oncogene-induced cell senescence describes a physiological mechanism that provides protection against cancer that has considerable clinical implications.
Journal ArticleDOI
Many roads lead to oncogene-induced senescence
TL;DR: This review will focus on integrating current models and will highlight data that provide new insight into the signals that function to suppress human tumor development.
Journal ArticleDOI
p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
Albert R. Davalos,Albert R. Davalos,Misako Kawahara,Gautam K. Malhotra,Nicholas Schaum,Jiahao Huang,Urvi Ved,Christian Beauséjour,Jean-Philippe Coppe,Francis Rodier,Francis Rodier,Judith Campisi,Judith Campisi +12 more
TL;DR: In addition to allowing immune cells to signal tissue damage, HMBG1 is secreted by senescent cells to initiate inflammatory cytokine secretion.
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Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer
Roman Camarda,Alicia Y. Zhou,Rebecca A. Kohnz,Sanjeev Balakrishnan,Celine Mahieu,Brittany Anderton,Henok Eyob,Shingo Kajimura,Aaron D. Tward,Gregor Krings,Daniel K. Nomura,Andrei Goga +11 more
TL;DR: It is demonstrated that MYC-overexpressing TNBC shows an increased bioenergetic reliance on FAO and the inhibition of FAO is identified as a potential therapeutic strategy for this subset of breast cancer.
Journal ArticleDOI
Anti-oncogenic role of the endoplasmic reticulum differentially activated by mutations in the MAPK pathway.
Christophe Denoyelle,George Abou-Rjaily,Vladimir Bezrookove,Monique Verhaegen,Timothy M. Johnson,Douglas R. Fullen,Jenny N. Pointer,Stephen B. Gruber,Lyndon D. Su,Mikhail A. Nikiforov,Randal J. Kaufman,Boris C. Bastian,Maria S. Soengas +12 more
TL;DR: The results argue against premature senescence as a converging mechanism of response to activating oncogenes and support a direct role of the ER as a gatekeeper of tumour control.
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.