Abstract
Senescence is an irreversible event that occurs during the G1 transition of the cell cycle and is elicited by replicative exhaustion or in response to stresses such as DNA damage, chemotherapeutic drugs, or aberrant expression of oncogenes. Senescence-associated heterochromatin foci, repress the expression of proliferation-promoting genes, thereby contributing to senescence-associated proliferation arrest. This arrest is regulated by chromatin-remodeling factors and two tumor suppressor proteins, p53 and Rb, whose expression is controlled by the CDKN2A locus. Jun dimerization protein 2 (JDP2)-deficient mouse embryonic fibroblasts are resistant to replicative senescence. Oxygen induces the expression of JDP2, which then inhibits the recruitment of polycomb repressive complexes (PRCs) 1 and 2 to the promoter of the gene encoding p16Ink4a and p19Arf, resulting in inhibition of the methylation of histone H3K27. These results suggest that the PRC controlled by JDP2 plays an important role in replicative senescence. Here we review the possible contribution of the histone chaperone JDP2 to induction of replicative senescence.
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Acknowledgments
This work was supported by grants from the NSC (NSC-102-2320-B-037-047-MY3; NSC-102-2314-B-038-004-MY2), the NHRI (NHRI-EX101-10109BI, NHRI-102AI-PDCO-03010201) of Taiwan and KMU (KMER006; KMU-EM-99-3; KMV-ER006, to KKY).
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Yokoyama, K.K., Kuo, KK. (2014). Role of Chromatin-Remodeling Factor Jun Dimerization Protein 2 (JDP2) in Cellular Senescence. In: Hayat, M. (eds) Tumor Dormancy, Quiescence, and Senescence, Volume 2. Tumor Dormancy and Cellular Quiescence and Senescence, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-7726-2_11
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DOI: https://doi.org/10.1007/978-94-007-7726-2_11
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