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- W2022055712 abstract "Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DCConstitutive heterochromatin is important for maintaining chromosome stability but also delays the repair of DNA double strand breaks (DSB). DSB repair in complex mammalian genomes involves a fast phase (2-6 hrs) where most of the breaks are rapidly repaired, and a slow phase (up to 24 hrs) where the remaining damages in heterochromatin are repaired. We found that p53 deficiency delays the slow phase DNA repair after ionizing irradiation. P53 deficiency prevents down regulation of histone H3K9 trimethylation at pericentric heterochromatin after DNA damage. Moreover, p53 directly induces expression of the H3 K9 demethylase JMJD2b through promoter binding. P53 activation also indirectly down regulates expression of the H3 K9 methytransferase SUV39H1. Depletion of JMJD2b or sustained expression of SUV39H1 delays the repair of heterochromatin DNA and reduces clonogenic survival after ionizing irradiation. The results suggest that by regulating JMJD2b and SUV39H1 expression, p53 not only controls transcription but also promotes heterochromatin relaxation to accelerate a rate-limiting step in the repair of complex genomes.Citation Format: Hong Zheng, Jiandong Chen. p53 promotes repair of heterochromatin DNA by regulating JMJD2b and SUV39H1 expression. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1772. doi:10.1158/1538-7445.AM2013-1772" @default.
- W2022055712 created "2016-06-24" @default.
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- W2022055712 date "2013-04-15" @default.
- W2022055712 modified "2023-09-25" @default.
- W2022055712 title "Abstract 1772: p53 promotes repair of heterochromatin DNA by regulating JMJD2b and SUV39H1 expression." @default.
- W2022055712 doi "https://doi.org/10.1158/1538-7445.am2013-1772" @default.
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