Regular ArticleInvestigation of the Role of G1/S Cell Cycle Mediators in Cellular Senescence
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Redox control of senescence and age-related disease
2017, Redox BiologyCitation Excerpt :Cellular senescence, also termed replicative senescence, was first proposed four decades ago [31,32] and has since been proven to be a significant tumor constraining mechanism that halts the proliferation of primary mammalian cells after a finite number of population doublings [33–37] allowing the organism to antagonize the potentially detrimental effects of uncontrolled growth. Proliferation is checked by persistently arresting cell growth at the G1- [38–42], G2- [43–45], G2/M- [46] or S-phase of the cell cycle leading to failure of DNA replication. So far, senescence-associated growth arrest has been shown to depend functionally on the tumor- suppressor pathways controlled by p16INK4a and pRB (retinoblastoma protein), as well as by p53.
Luotonin-A based quinazolinones cause apoptosis and senescence via HDAC inhibition and activation of tumor suppressor proteins in HeLa cells
2015, European Journal of Medicinal ChemistryCitation Excerpt :Cellular senescence is a final common pathway for a number of DNA damage and repair pathways and appears to play a major role in processes such as aging, stress and tumor suppression [52] and is characterized by morphological changes such as blue coloration and adopted a fattened morphology with spread out cytoplasm as observed in senescence associated β-galactosidase (SA-β-gal) staining [53]. Previous studies have indicated that strong irreversible G1 cell cycle arrest might be responsible for senescence phenotype in cancer cells [54,55]. This prompted us to examine senescence as a part of tumor-suppressive mechanism in compound treated cells [56].
MAP kinase: It's been longer than fifteen minutes
2008, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Defects in ERK1 versus ERK2 activation in senescence suggest divergent functions. Serum stimulates tyrosine phosphorylation of ERK2 in young MRC-5 cells, but not in senescent MRC-5 cells [53]. These are older observations that require reexamination.
Regulation of growth arrest in senescence: Telomere damage is not the end of the story
2006, Mechanisms of Ageing and Development