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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Cooperation between p53 and p130(Rb2) in induction of cellular senescence
TL;DR: It is indicated that p53 can cooperate selectively with p130(Rb2) to induce cellular senescence, a pathway that may be relevant when the pRb/p16INK4a pathway is defunct.
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Skin senescence: mechanisms and impact on whole-body aging
TL;DR: Wang et al. as mentioned in this paper discussed the possible relevant role of skin senescence in the induction of aging phenotypes to other organs/tissues, contributing to whole-body aging.
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Senescence delay and repression of p16INK4a by Lsh via recruitment of histone deacetylases in human diploid fibroblasts
TL;DR: It is reported that Lsh overexpression delays cell senescence by silencing p16INK4a in human fibroblasts and histone deacetylase activity recruits HDAC to establish a repressive chromatin structure at the p16inks4a promoter, which in turn delays cellsenescence.
Journal ArticleDOI
Lineage-specific restraint of pituitary gonadotroph cell adenoma growth.
Vera Chesnokova,Svetlana Zonis,Cuiqi Zhou,Anat Ben-Shlomo,Kolja Wawrowsky,Yoel Toledano,Yunguang Tong,Yunguang Tong,Yunguang Tong,Kalman Kovacs,Bernd W. Scheithauer,Shlomo Melmed +11 more
TL;DR: The results point to lineage-specific pathways restricting uncontrolled murine and human pituitary gonadotroph adenoma cell growth, which may limit proliferation of benign adenomatous pituitaries.
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Conserved RB functions in development and tumor suppression
Gabriel M. Gordon,Wei Du +1 more
TL;DR: Some of the recent advances made in understanding the structure and function of pRb as they relate to tumor suppression are discussed, and research using Drosophila melanogaster that reveals important, evolutionarily conserved functions of the RB family is highlighted.
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.