Stress factor - dependent differences in molecular mechanisms of premature cell senescence

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 cycli...

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Bibliographic Details
Published in:Biopolimery i kletka 2015, Vol.31 (5), p.323-337
Main Authors: Petrova, N. V., Velichko, A. K., Razin, S. V., Kantidze, O. L.
Format: Article
Language:English
Subjects:
Cell proliferation
Cellular stress response
Cyclin-dependent kinase
Cyclin-dependent kinase inhibitors
Cyclin-dependent kinases
DNA biosynthesis
Molecular modelling
Phenotypes
Senescence
β-Galactosidase
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Summary: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.
ISSN:0233-7657
1993-6842
DOI:10.7124/bc.0008F4