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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Coordinated control of senescence by lncRNA and a novel T-box3 co-repressor complex
Pavan Kumar P,Uchenna Emechebe,Richard Smith,Sarah Franklin,Barry Moore,Mark Yandell,Stephen L. Lessnick,Stephen L. Lessnick,Anne M Moon +8 more
TL;DR: The elucidation of CAPERα and UCA1 functions in vivo provides new insights into senescence induction, and the oncogenic and developmental properties of TBX3.
Journal ArticleDOI
Notch Signaling Mediates Secondary Senescence
Yee Voan Teo,Nattaphong Rattanavirotkul,Nelly Olova,Angela Salzano,Andrea Quintanilla,Núria Tarrats,Christos Kiourtis,Miryam Müller,Anthony R. Green,Peter D. Adams,Juan Carlos Acosta,Thomas G. Bird,Kristina Kirschner,Nicola Neretti,Tamir Chandra +14 more
TL;DR: It is found that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought, and global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondarysenescence point toward a functional diversification between secondary and primary senescences.
Journal ArticleDOI
A genome-wide RNA interference screen identifies putative chromatin regulators essential for E2F repression
TL;DR: A genome-wide RNAi screen in cultured Drosophila cells for genes required for repression of E2F activity suggests that potential chromatin regulation mediated by Domino and PcG-like factors plays an important role in controlling E 2F activity and cell growth.
Journal ArticleDOI
The Senescence–Stemness Alliance – A Cancer-Hijacked Regeneration Principle
TL;DR: Recent discoveries underscoring the unexpected senescence-stemness alliance are reviewed, elucidate underlying molecular mechanisms, and discuss its fundamentally different implications in normal tissue repair - to replenish the exhausted repopulation capacity - as compared to cancer biology, where usurpation of this natural principle accounts for particularly aggressive tumor behavior.
Journal ArticleDOI
Genetics of melanoma progression: the rise and fall of cell senescence.
TL;DR: Current knowledge of the genetic or epigenetic driver changes necessary to generate a cutaneous metastatic melanoma, the commonest order in which these occur, and the relation of these changes to the biology and pathology of melanoma progression are analyzed are analyzed.
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.