We are analyzing https://link.springer.com/article/10.1007/s00412-007-0115-7.

Title:
Cellular senescence and chromatin structure | Chromosoma
Description:
Cellular senescence is characterized by stable cell cycle arrest that is triggered by various forms of stress stimuli. Senescent cells show a series of morphological and physiological alterations including a flat and enlarged morphology, an increase in acidic β-galactosidase activity, chromatin condensation, and changes in gene expression pattern. These features are not observed in proliferating cells or quiescent cells in vitro. Using these senescence markers, cellular senescence has been shown to occur in benign or premalignant lesions but not in malignant lesions and to act as a tumor-suppressing mechanism in vivo. The onset and maintenance of the senescent state are regulated by two tumor suppressor proteins, p53 and Rb, which mediate senescence signals through p38 mitogen-activated protein kinase and cyclin-dependent kinase inhibitors. Alterations of chromatin structure are believed to contribute to the irreversible nature of the senescent state. Senescent cells form characteristic heterochromatin structure called senescence-associated heterochromatic foci (SAHFs), which may repress the expression of proliferation-promoting genes, such as E2F target genes. Recent studies have provided molecular insights into the structure and the mechanism of SAHF formation. In this paper, we review the role of cellular senescence in tumor suppression in vivo and the molecular mechanism of stable growth arrest in senescent cells, focusing on the special form of heterochromatin, SAHFs.
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Keywords {🔍}

article, google, scholar, pubmed, cas, cell, senescence, biol, cellular, human, chromatin, cells, nature, histone, mol, genes, dna, proteins, senescent, dev, cancer, damage, res, structure, tumor, kinase, chen, heterochromatin, aging, ishikawa, wright, chromosome, fibroblasts, function, mechanism, suppressor, protein, formation, access, oncogeneinduced, narita, lowe, pathways, shay, exp, regulation, nat, replicative, zhang, privacy,

Topics {✒️}

mek-extracellular signal-regulated kinase brahma chromatin-remodelling machinery ataxia telangiectasia mutated month download article/chapter ras-induced premature senescence acidic β-galactosidase activity cyclin-dependent kinase inhibitors dna double-strand breaks p38 map kinase endogenous k-ras oncogene common senescence-signalling pathway protein kinase regulated vitro-replicative life span chromatin structure characteristic rb-related genes leads high-mobility-group proteins putative telomere-independent mechanisms dna checkpoint pathways replication-independent nucleosome assembly oncogene-induced genetic instability p53-dependent cellular senescence candidate anti-cancer barrier full article pdf ras-induced senescence replicative senescence overlapping anti-oncogenic role article chromosoma aims article funayama requires histone macroh2a1 rb-mediated heterochromatin formation dna damage checkpoint hira/asf1a-mediated formation privacy choices/manage cookies human cellular senescence assess cellular senescence induce dna damage growth arrest induced senescent cells show telomere-initiated senescence age-related decline high-mobility group mediate senescence signals dna damage response dna damage checkpoints reactive oxygen species adda di fagagna conditions privacy policy mitogenic signaling mediated tumor suppressor proteins histone chaperone asf1

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         Ataxia Telangiectasia Mutate
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         Replicative Senescence
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         Cell Biology
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         Human Genetics
         Animal Genetics and Genomics
         Eukaryotic Microbiology
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