Translational Control during Cellular Senescence

Senescence is a state of long-term cell cycle arrest that arises in cells that have incurred sublethal damage. While senescent cells no longer replicate, they remain metabolically active and further develop unique and stable phenotypes that are not present in proliferating cells. On one hand, senesc...

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Vydáno v:Molecular and cellular biology Ročník 41; číslo 2
Hlavní autoři: Payea, Matthew J., Anerillas, Carlos, Tharakan, Ravi, Gorospe, Myriam
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Taylor & Francis 01.02.2021
American Society for Microbiology
Témata:
aging
beta-Galactosidase - genetics
beta-Galactosidase - metabolism
biogenesis
Biomarkers - metabolism
cell cycle checkpoints
cell senescence
Cell Size
Cells, Cultured
cellular senescence
Cellular Senescence - genetics
Chemokines - genetics
Chemokines - metabolism
Cyclin-Dependent Kinase Inhibitor p21 - genetics
Cyclin-Dependent Kinase Inhibitor p21 - metabolism
DNA Damage
Humans
Mechanistic Target of Rapamycin Complex 1 - genetics
Mechanistic Target of Rapamycin Complex 1 - metabolism
Minireview
Phenotype
Protein Biosynthesis
ribosomes
RNA, Ribosomal - genetics
RNA, Ribosomal - metabolism
stress response
translation elongation
translation initiation
translational control
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
translation initiation
cellular senescence
stress response
aging
translational control
translation elongation
ISSN:1098-5549, 0270-7306, 1098-5549
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Shrnutí:Senescence is a state of long-term cell cycle arrest that arises in cells that have incurred sublethal damage. While senescent cells no longer replicate, they remain metabolically active and further develop unique and stable phenotypes that are not present in proliferating cells. On one hand, senescent cells increase in size, maintain an active mTORC1 complex, and produce and secrete a substantial amount of inflammatory proteins as part of the senescence-associated secretory phenotype (SASP). On the other hand, these progrowth phenotypes contrast with the p53-mediated growth arrest typical of senescent cells that is associated with nucleolar stress and an inhibition of rRNA processing and ribosome biogenesis. In sum, translation in senescent cells paradoxically comprises both a global repression of translation triggered by DNA damage and a select increase in the translation of specific proteins, including SASP factors.
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Citation Payea MJ, Anerillas C, Tharakan R, Gorospe M. 2021. Translational control during cellular senescence. Mol Cell Biol 41:e00512-20. https://doi.org/10.1128/MCB.00512-20.
ISSN:1098-5549
0270-7306
1098-5549
DOI:10.1128/MCB.00512-20