Biopolym. Cell. 2015; 31(5):323-337.
Reviews
Stress factor – dependent differences in molecular mechanisms of premature cell senescence
- Institute of Gene Biology, Russian Academy of Sciences
34/5, Vavilova Str., Moscow, Russian Federation, 119334 - M. V. Lomonosov Moscow State University
Leninskie Gory, 1/12, Moscow, Russian Federation, 119991
Abstract
Cell senescence is an established cell stress response in the form of a permanent proliferation arrest accompanied by a complex phenotype. Senescent cells share several crucial features, such as lack of DNA synthesis, increased senescence-associated β-galactosidase activity and upregulation of cyclin-dependent kinase inhibitors. Most of these universal senescence markers are indicative not only for cell senescence but for other types of growth arrest as well. Along with ubiquitous markers, cell senescence has accessory characteristics, which mostly depend on senescence-inducing stimulus and/or cell type. Here, we review main markers and mechanisms involved in the induction of cell senescence with a focus on stress factor-dependent differences in signaling pathways activated in senescence.
Keywords: cell senescence, telomeres, DNA damage, irradiation, reactive oxygen species, oncogenes
Full text: (PDF, in English)
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